Treatment of cognitive impairment associated with schizophrenia (CIAS) with a CNS- penetrant sGC stimulator in combination with antipsychotics RELATED APPLICATIONS [001] This application claims the benefit of priority to U.S. Provisional Application No. 63/392,643, filed on July 27, 2022. The entire contents of the above-referenced application are incorporated herein by reference. FIELD OF THE INVENTION [002] The present invention provides methods of treating cognitive impairment in patients with schizophrenia that are on anti-psychotic medication by administering specific dosage regimens of a brain-penetrant stimulator of soluble guanylate cyclase (sGC). BACKGROUND OF THE INVENTION Cognition and cognitive impairment or decline [003] Cognitive impairment and cognitive decline are broad terms describing deficits in one or more higher brain functions that generally involve aspects of thinking and information processing (i.e., cognition). Included among these functions or aspects of cognition are perception, learning, memory (short- and long-term), attention, attentional control, focus, reaction time to a stimulus (psychomotor function), concentration, language production and comprehension, decision-making, problem-solving, reasoning, planning, cognitive speed and capacity, cognitive processing, emotional recognition, visuospacial skills, and executive function. Cognitive impairment can start suddenly or gradually and can be temporary or more permanent. It may also manifest short term, or may progress and worsen in a progressive manner (i.e., cognitive decline), and this will depend on the underlying cause or causes. Some common causes of cognitive impairment may include medication side effects, metabolic imbalances, hormonal problems, vitamin or nutrient deficiencies, delirium, psychiatric illness (including schizophrenia), damage to brain neurons due to an injury (for example in stroke or in traumatic brain injury), neurodegenerative conditions or diseases, and exposure to toxins, or viral or bacterial infections. Schizophrenia and Cognitive Impairment [004] Schizophrenia is a psychiatric disorder involving chronic or recurrent psychosis. People with schizophrenia experience a spectrum of positive symptoms (eg, hallucinations, delusions, and disorganized thinking), negative symptoms (eg, blunted affect, alogia, avolition, asociality, and anhedonia), and impairments in cognition (cognitive impairment associated with schizophrenia or CIAS) , including deficiencies in learning, attention, memory, emotional recognition, reaction time, and executive function.These symptoms are associated with marked social and/or academic/occupational dysfunction. Among adults in the United States (US), the incidence of schizophrenia is estimated to be 1.5 million people per year, and worldwide prevalence is estimated to be about 1%. Schizophrenia is often diagnosed in the late teens to early 30s, with symptoms commonly presenting earlier in males than in females. Schizophrenia is associated with significant health and societal burden. The average number of years of potential life lost due to any cause for individuals with schizophrenia in the US is 28.5 years. Relative to other chronic health conditions, the financial costs of schizophrenia are disproportionately high, in the form of both direct healthcare costs and indirect costs associated with productivity loss and caregiver costs. There are numerous antipsychotic medications approved for the treatment of schizophrenia, however, they are primarily effective for the treatment of positive symptoms only. [005] Nearly all people with schizophrenia (ca.98%) exhibit cognitive deficits, including those who are treated with antipsychotic medications, which are actualy believed to have the potential to exacerbate such cognitive deficits. Cognitive impairment can manifest as deficits in speed of processing, attention/vigilance, memory deficits, verbal learning, visual learning, reasoning/problem solving, social cognition, and executive function. Impairments in memory, attention, reasoning and problem solving are worse in schizophrenia compared to bipolar disorder and major depressive disorder (Buchanan et al Schizophrenia Bulletin, Volume 31, Issue 4, October 2005, Pages 962–977, https://doi.org/10.1093/schbul/sbi028) _{. Cognitive} impairment results in functional impairments or poor functional outcomes in these patients. Although cognitive impairment is a core element of schizophrenia, there are no approved therapies to treat it. No medicines have been approved for the treatment of cognitive impairment associated with schizophrenia as of the date of this filing. The development of drugs for CIAS has been challenging and to date unsuccessful. Therefore, there is clear unmet medical need for treatments that can improve the cognitive deficits in patients with schizophrenia, including for the treatment on top of standard of care with antipsychotics. SUMMARY OF THE INVENTION [006] In a first aspect of the invention, disclosed herein is a method of treating cognitive impairment in a patient with schizophrenia who is on antipsychotic treatment by administering a total oral daily dose of 15 mg of Compound I or an equal quantity in moles of a pharmaceutically acceptable salt of Compound I to said patient. [007] In a second aspect of the invention, disclosed herein is a Compound I or a pharmaceutically acceptable salt thereof for use in treating cognitive impairment in a patient with schizophrenia who is on antipsychotic treatment by administering a total oral daily dose of 15 mg of Compound I or an equal quantity in moles of a pharmaceutically acceptable salt of Compound I to said patient. [008] In a third aspect of the invention, disclosed herein is the use of Compound I or a pharmaceutically acceptable salt thereof for the manufacture of a medicament for treating cognitive impairment in a a patient with schizophrenia who is on antipsychotic treatment, by administering a total oral daily dose of 15 mg of Compound I or an equal quantity in moles of a pharmaceutically acceptable salt of Compound I to said patient. [009] In a fourth aspect, the methods and uses of the invention involve treatment in combination with one or more additional therapeutic agents, in addition to Compound I and at least one anti-psychotic DETAILED DESCRIPTION OF THE INVENTION NO-sGC-cGMP pathway and sGC stimulation in the CNS and in schizophrenia [010] In the body, nitric oxide (NO) is synthesized from arginine and oxygen by various nitric oxide synthase (NOS) enzymes and by sequential reduction of inorganic nitrate. Three distinct isoforms of NOS have been identified: inducible NOS (iNOS or NOS II) found in activated macrophage cells of the immune system; constitutive neuronal NOS (nNOS or NOS I), involved in neurotransmission and long-term potentiation; and constitutive endothelial NOS (eNOS or NOS III), which regulates smooth muscle relaxation and blood pressure. [011] Soluble guanylate cyclase (sGC) is the primary receptor enzyme for NO in vivo. sGC can be activated via both NO-dependent and NO-independent mechanisms. In response to this activation, sGC converts guanosine-5'- triphosphate (GTP) into the secondary messenger cyclic guanosine 3’, 5’-monophosphate (cGMP). The increased level of cGMP, in turn, modulates the activity of downstream effectors including protein kinases, phosphodiesterases (PDEs), and ion channels. [012] cGMP, by activating cGMP-dependent protein kinase (PKG) and other downstream modulators, regulates vascular tone and regional blood flow, fibrosis, and inflammation. In the central nervous system (CNS), the NO-sGC-cGMP signaling pathway underlies multiple physiological processes that contribute to overall brain health, including neurotransmission, neurovascular function, cellular bioenergetics and inflammation, and has been implicated in neuronal survival and cognitive function (Ben Aissa M, Lee SH, Bennett BM, Thatcher GR. Targeting NO/cGMP Signaling in the CNS for Neurodegeneration and Alzheimer's Disease. Current medicinal chemistry; 2016;23(24):2770-88). Experimental and clinical evidence has indicated that reduced NO concentrations, reduced NO bioavailability, and/or reduced responsiveness to endogenously produced NO contributes to the development of disease, and in particular brain disease. [013] Multiple lines of evidence strongly suggest that the modulation of cGMP may be a promising target for the treatment of schizophrenia. cGMP is reduced in the CSF of schizophrenia patients (Gattaz WF, Cramer H, Beckmann H. Low CSF concentrations of cyclic GMP in schizophrenia. Br J Psychiatry.1983;142:288-291. doi:10.1192/bjp.142.3.288 and Ebstein RP, Biederman J, Rimon R, Zohar J, Belmaker RH. Cyclic GMP in the CSF of patients with schizophrenia before and after neuroleptic treatment. Psychopharmacology (Berl).1976;51(1):71-74. doi:10.1007/BF00426324). cGMP synthesis is modulated by NO and PDE inhibitors and also by N-methyl-D-aspartate (NMDA) receptors. The therapeutic effects of cGMP on schizophrenia may take place by mechanisms including cGMP signalling, oxidative stress and neuroinflammation (see Seong Shim, Michael Shuman, Erica Duncan, An emerging role of cGMP in the treatment of schizophrenia: A review, Schizophrenia Research, Volume 170, Issue 1, 2016, Pages 226-231, ISSN 0920-9964, https://doi.org/10.1016/j.schres.2015.11.015). [014] Network analysis of pathways, protein-protein interactions, and genetics also link the NO-sGC-cGMP signaling pathway specifically to schizophrenia. Compromised prefrontal and hippocampal NO signaling is implicated in cognitive deficits in schizophrenia. The positive symptoms of schizophrenia have been primarily associated with dopaminergic hyperfunction, and dopamine antagonism is the main mechanism of antipsychotic treatments. In contrast, cognitive impairment in schizophrenia has been associated with dysregulated glutamatergic neurotransmission, which is important to learning and memory and is mediated by postsynaptic NMDA receptors. [015] sGC stimulators are a class of heme-dependent agonists of the sGC enzyme that work synergistically with varying amounts of NO to increase its enzymatic conversion of GTP to cGMP. sGC stimulators are clearly differentiated from and structurally unrelated to another class of NO-independent, heme-independent agonists of sGC known as sGC activators. The benzylindazole compound YC-1 was the first sGC stimulator to be identified. Several sGC stimulators have been identified and pharmacologically characterized since then, including BAY 41-2272, BAY 41-8543, riociguat (BAY 63-2521), vericiguat, olinciguat (IW-1701), and praliciguat (IW-1973). No sGC stimulators have been approved for marketing in the field of CNS to date and, to our knowledge, Compound I, described below, is the only CNS- penetrant sGC stimulator currently in clinical development for the treatment of CNS diseases. [016] sGC stimulators may offer considerable advantages over other potential therapies that target the aberrant NO pathway or otherwise upregulate the NO pathway. For example, sGC stimulation is a more powerful approach than either the use of NO supplementation (which is associated with tachyphylaxis) or inhibition of cGMP breakdown via PDEi, which has limited effectiveness if cGMP levels are very low. In addition, the broad CNS distribution of sGC enables augmentation of signaling across brain regions, while the PDEi targets have more limited cellular and tissue expression. Compound I: CY6463 [017] Compound I (also named CY6463, IW-6463, or IWP-247) is an orally administered CNS-penetrant sGC stimulator being investigated for the treatment of CNS and mitochondrial diseases (NCT03856827, NCT04240158, NCT04475549, NCT04798989, NCT04972227). To our knowledge it is the only CNS-penetrant stimulator tested in human subjects to date. [018] As an sGC stimulator, Compound I acts as a positive allosteric modulator of sGC, by binding to sGC and amplifying downstream signaling in response to endogenous NO. In rodent studies, Compound I increased levels of cGMP in the CNS—in contrast to a peripherally restricted sGC stimulator that demonstrated a lack of target engagement and distinct pharmacology in the CNS. Compound I [019] In additional nonclinical experiments in rats, Compound I prevented the impairment of learning elicited by blockade of NMDA in a novel object recognition model, suggesting Compound I acts downstream of NMDA signaling and may be able to address upstream dysfunction in glutamatergic neurotransmission. Engagement of neurons in the hippocampus and cortex are critical for learning and memory, and long-term potentiation (LTP), a form of synaptic plasticity, underlies memory formation. In a mouse model of neurodegeneration with LTP deficits, Compound I treatment increased glutamatergic synaptic transmission assessed by LTP in hippocampal slices, suggesting that Compound I has the potential to restore neuroplasticity central to learning and memory. Furthermore, also in rodent studies, Compound I increased fMRI-BOLD signals and elevated qEEG gamma-band oscillatory power, in contrast to a peripherally restricted sGC stimulator. In models of CNS impairment in pharmacologically impaired rats, Compound I improved dendritic spine density, reversed brain metabolite N-acetyl-aspartate (NAA) + N-acetylaspartate-glutamate (NAAG) deficits, increased neurotrophic factors such as phosphorylated cAMP-response element binding (pCREB) and brain-derived neurotrophic factor (BDNF), and improved behavioral task performance (see Correia, Susana S; Iyengar, Rajesh R; Germano, Peter; Tang, Kim; Bernier, Sylvie G; Schwartzkopf, Chad D; Tobin, Jenny; Lee, Thomas W-H; Liu, Guang; Jacobson, Sarah; Carvalho, Andrew; Rennie, Glen R; Jung, Joon; Renhowe, Paul A; Lonie, Elisabeth; Winrow, C; Hadcock, J; Jones, J; Currie, MG. The CNS-Penetrant Soluble Guanylate Cyclase Stimulator CY6463 Reveals its Therapeutic Potential in Neurodegenerative Diseases. Front Pharmacol.24 May 2021 | https://doi.org/10.3389/fphar.2021.656561). [020] Safety and pharmacokinetic (PK) data from a Phase 1 study in healthy adults (clinicaltrials.gov identifier NCT03856827), together with safety, PK and pharmacodynamic (PD) data from a second Phase 1 study in healthy elderly adults (clinicaltrials.gov identifier NCT04240158) also supported clinical investigation of Compound I in the treatment of cognitive impairment associated with schizophrenia (CIAS). Definitions and general terminology [021] Unless otherwise defined, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention belongs, which is the field of medicine, and of brain medicine in particular. Methods and materials are described herein for use in the present invention; other, suitable methods and materials known in the art can also be used. The materials, methods, and examples are illustrative only and not intended to be limiting. All publications, patent applications, patents, sequences, database entries, and other references mentioned herein are incorporated by reference in their entirety. In case of conflict, the present specification, including definitions, will control. [022] As used herein, the word “a” before a noun represents one or more of the particular noun. As used herein, the singular forms “a,” “an,” and “the” include plural referents unless the context clearly dictates otherwise. [023] As used herein, the terms “subject” and “patient” are used interchangeably. A subject or a patient is a human patient or human subject. [024] For the terms “for example” and “such as,” and grammatical equivalences thereof, the phrase “without limitation” or “and without limitation” is understood to follow unless explicitly stated otherwise. [025] “Functional capacity” refers to a person’s capability or ability to perform tasks and activities that people find necessary or desirable in their lives in different circumstances or situations. Functional capacity is most appropriately examined with reference to particular life-cycle tasks that an individual may need to perform. For instance, for children, functional requirements include learning at school, participating in play, and involvement in family life. For adults, functional abilities in the labor force are important, as well as activities related to living independently or rearing and interacting with their children. There are many tools known in the field that examine capabilities to perform certain age-related tasks in detail. Some assessment tools, especially those used in large-scale research, attempt to use questions that work for all age groups. The most common approach is to consider ability to perform each in a list of specific tasks or activities that are most relevant to the population being studied. Some assessments of functional capacity focus, for instance, on activities related to cardiovascular capacity, or activities related to muscle strength or balance, or activities related to exercise capacity, or most relevant to this disclosure, the can focus on cognitive abilities. In the last few years, functional capacity measures have particularly been emphasized for people who need long-term care, including elderly people, but also younger people suffering from certain chronic diseases or disability, including patients suffering with schizophrenia. With reference to those needing long-term care, two common terms have emerged to characterize functional capacity: ability to perform "activities of daily living" (ADLs) and ability to perform "instrumental activities of daily living" (IADLs) (see for example Lara-Ruiz J, Kauzor K, Nakhala M, et al. The Functional Ability of MCI and Alzheimer's Patients Predicts Caregiver Burden. GeroPsych (Bern).2019; 32(1):31-39 and references cited therein; and https://www.acc.org/latest-in- cardiology/articles/2018/07/10/07/16/prioritizing-the-import ance-of-functional-capacity- assessments-among-the-older-population). Reduced functional capacity is also associated with reduced quality of life (QOL) and increased caretaker burden. Both QOL and caretaker burden can also be measured and tools for their assessment and quantification have been developed in the field. [026] ADLs are the most basic of self-care functions. These include things like bathing, dressing, using the toilet, transferring in and out of beds or chairs, and eating. When ADL is measured dichotomously, people are usually considered independent if they can do the function without help (even if they depend on equipment) and dependent if they need human help. Depending on the level of detail sought, some ADL measures use more graduated scales to measure degrees of dependency; some break down the tasks (e.g., dressing can include upper body, lower body, putting on shoes); and some add some quantitative measures (e.g., walking a certain number of feet, climbing a certain number of stairs). [027] IADLs are functions that may be needed for independence depending on task allocation in a family unit or demands made specific to a person's life or age. They may include things like cooking, cleaning, laundry, shopping, making and receiving telephone calls, driving or using public transportation, taking medicines or being able to perform certain work-related tasks. [028] Functional capacity can be measured by questions about what a person can do, or by demonstrations of actual ability (e.g., getting up from a chair, demonstrating ability to hold food on a spoon and bring it to one's mouth, opening a medicine bottle and taking out the correct number of pills, or carrying out more complex tasks). Sometimes, the measure focus more on questions about what a person actually does do (sometimes these are addressed by caretakers rather than patient themselves). In this case one is measuring more the “functional performance” rather than the functional capacity. [029] Thus, the specific measurement strategy should be tailored to the aspects of functional outcomes that one intends to measure (Applegate, W. B.; Blass, J. P.; and Williams, T. E. (1990), Instruments for the Functional Assessment of Older Patients. New England Journal of Medicine 322(17): 1132–1148; Kane, R. L., and Kane, R. A. (2000), Assessing Older Persons: Measurement, Meaning, and Practical Applications. New York: Oxford University Press; McDowell, I.; and Newell, C. (1996), Measuring Health: A Guide to Rating Scales and Questionnaires, 2nd edition. New York: Oxford University Press). [030] Low functional capacity or performance in general, and in ADL or IADL tasks in particular, can result from any combination of physical problems, lack of social resources, lack of motivation (e.g., because of depression) and, most importantly for the purposes of this disclosure, they can be the result of cognitive impairment. Decline or negative changes in cognitive parameters have been shown to be associated with diminished functional capacity and performance, as well as QOL. Conversely, improvements or positive changes in cognitive parameters have been shown to be positively linked to improvements in functional capacity, functional performance and QOL in many patients. [031] Functional capacity and functional performance are different ways to look at “functional outcomes”. The relationship between cognitive status and functional outcomes has been examined in diverse patient populations with different levels of clinical or subclinical cognitive impairment, including in patients with schizophrenia. [032] In general, in diverse populations, it has been observed that cognitive impairment appears to be positively correlated with worse functional outcome measurements and that better cognition is associated with better functional outcome measurements (see for example: Jing Ee Tan, David F. Hultsch & Esther Strauss, Cognitive abilities and functional capacity in older adults: results from the modified Scales of Independent Behavior–Revised. The Clinical Neuropsychologist, 23:3, 479-500, 2009; McClure MM, Harvey PD, Bowie CR, Iacoviello B, Siever LJ, Functional outcomes, functional capacity, and cognitive impairment in schizotypal personality disorder. Schizophr Res.2013;144(1-3):146-150; McLennan SN, Mathias JL, Brennan LC, Russell ME, Stewart S. Cognitive impairment predicts functional capacity in dementia-free patients with cardiovascular disease. J Cardiovasc Nurs. 2010;25(5):390-397; Zielonka D, Ren M, De Michele G, et al. The contribution of gender differences in motor, behavioral and cognitive features to functional capacity, independence and quality of life in patients with Huntington's disease. Parkinsonism Relat Disord. 2018;49:42-47; Ott C, Miné H, Petersen JZ, Miskowiak K. Relation between functional and cognitive impairments in remitted patients with bipolar disorder and suggestions for trials targeting cognition: An exploratory study. J Affect Disord.2019;257:382-389; Clark JMR, Jak AJ, Twamley EW. Cognition and functional capacity following traumatic brain injury in veterans. Rehabil Psychol.2020;65(1):72-79). [033] Further, some approaches (both pharmacological and non-pharmacological) that improve brain health or improved brain performance in general, and cognition in particular, have been shown to also result in improved functional outcomes (see, for example, Bherer L, Cognitive plasticity in older adults: effects of cognitive training and physical exercise. Ann N Y Acad Sci.2015;1337:1-6; Holzapfel SD, Ringenbach SD, Mulvey GM, et al., Improvements in manual dexterity relate to improvements in cognitive planning after assisted cycling therapy (ACT) in adolescents with down syndrome. Res Dev Disabil.2015;45- 46:261-270; Winblad B, Kilander L, Eriksson S, et al., Donepezil in patients with severe Alzheimer's disease: double-blind, parallel-group, placebo-controlled study [published correction appears in Lancet.2006 Jun 17; 367(9527):1980] [published correction appears in Lancet.2006 Nov 11;368(9548):1650]. Lancet.2006;367(9516):1057-1065). [034] “Functional outcome” is to be distinguished from “clinical outcome”, as being focused on an individual’s recovery in areas such as vocational and social functioning rather than symptom resolution (see for example (2015) Functional Outcome. In: Stolerman I.P., Price L.H. (eds) Encyclopedia of Psychopharmacology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-36172-2_200676). Its measurement speaks to the impact of severe and chronic illnesses, such as schizophrenia, and a growing awareness that functional and clinical recovery do not necessarily parallel each other. [035] In schizophrenia, for instance, it was held for many years that the positive symptoms (e.g., delusions, hallucinations) were central to the gradual decline in functioning commonly seen over the course of the illness. However, more recent evidence suggests that other features of this illness, for example, negative symptoms and neurocognitive changes, may play a more critical role in compromising functional recovery. This has diminished focus on positive symptoms and the implicit assumption that their resolution ensures a return to premorbid level of functioning and shifted the focus to addressing also negative and cognitive aspects of the disease. The present disclosure focuses on improvements to the cognitive aspects of schizophrenia in patients that are already receiving treatment for their positive symptoms in the form of antipsychotics. [036] A pharmacological approach that improves the neurophysiology of the brain or that improves measures of brain performance that are known to be related to one or more aspects of cognition would be expected to also result in improved functional outcomes in patients with schizophrenia. [037] For example, a pharmacological approach that improves measures of brain performance related to aspects of cognition such as attention, focus, reaction time to a stimulus, processing speed, psychomotor function, learning (e.g. visual or verbal learning), memory, emotional or social cognition, problem solving and reasoning or executive function is likely to be useful in patients with reduced functional capacity or performance. [038] The term “therapeutically effective amount” or “pharmaceutically effective amount” as used herein means that amount of active compound or pharmaceutical agent that elicits the medicinal response in a human that is being sought by a medical doctor or other clinician. The therapeutically or pharmaceutically effective amount of a compound is at least the minimum amount necessary to ameliorate, palliate, lessen, delay, reduce, alleviate, or cure a disease, disorder, or syndrome or one or more of its symptoms, signs or causes. In another embodiment, it is the amount needed to bring abnormal levels of certain clinical markers of the disease, disorder, or syndrome closer to the normal values or levels. In another embodiment, it is the amount needed to bring the levels of certain clinical markers displayed by a subject closer to those of a normal subject of the same age (normalization) or closer to those of a younger subject. An effective amount can be administered in one or more administrations throughout the day. [039] As used herein, a dose that does not “result in a significant incidence of adverse events (AEs) or serious adverse events (SAEs) associated with symptomatic hypotension” is one that does not result in excessive orthostatic hypotension, excessive dizziness, excessive postural dizziness, excessive pre-syncope, or excessive syncope in patients. Excessive orthostatic hypotension, excessive dizziness, excessive postural dizziness, excessive pre- syncope, or excessive syncope in patients are those that would warrant discontinuation of treatment by the patient or a recommendation of discontinuation by the practitioner. [040] The terms “administer”, “administering” or “administration” in reference to a compound or pharmaceutical agent, mean introducing the compound into the body of the patient in need of treatment. When Compound I or a pharmaceutically acceptable salt thereof is used in combination with one or more other therapeutic agents, “administration” and its variants are each understood to encompass concurrent and/or sequential introduction of Compound I and the other therapeutic agents into the patient. [041] The term “disorder”, as used herein refers to any deviation from or interruption of the normal structure or function of any body part, organ, or system that is manifested by a characteristic set of symptoms and signs and whose etiology, pathology, and prognosis may be known or unknown. The term disorder encompasses other related terms such as disease and condition (or medical condition) as well as syndromes, which are defined as a combination of symptoms resulting from a single cause or so commonly occurring together as to constitute a distinct clinical picture. In some embodiments, the term disorder refers to a psychiatric disorder. As used herein the terms “disorder”, “disease”, “condition” or “syndrome” are used interchangeably. [042] “Treat”, “treating” or “treatment” with regard to a disorder, disease, condition, symptom or syndrome, refers to abrogating or improving the cause and/or the effects (i.e., the symptoms, physiological, physical, psychological, emotional or functional manifestations, or any of the clinical parameters or observations) associated with the disorder, disease, condition or syndrome. As used herein, the terms “treat”, “treatment”, and “treating” also refer to the delay or amelioration or slowing down or prevention of the progression (i.e., the known or expected progression of the disease), severity, and/or duration of the disease or delay or amelioration or slowing down or prevention of the progression of one or more clinical parameters associated with the disease (i.e., “managing” without “curing” the condition), resulting from the administration of one or more therapies. [043] Treating cognitive impairment according to the invention may involve improving cognition or improving cognitive function as determined by tools used in the field. It may involve total or partial reversal of congitive dysfunction. It may also involve attenuation or stopping the progression of cognitive decline. [044] The phrase "pharmaceutically acceptable salt," as used herein, refers to pharmaceutically acceptable organic or inorganic salts of Compound I. The pharmaceutically acceptable salts of Compound I may be used in medicine. Salts that are not pharmaceutically acceptable may, however, be useful in the preparation of Compound I or of other Compound I pharmaceutically acceptable salts. A pharmaceutically acceptable salt may involve the inclusion of another molecule such as an acetate ion, a succinate ion or other counter ion. The counter ion may be any organic or inorganic moiety that stabilizes the charge on the parent compound. Furthermore, a pharmaceutically acceptable salt may have more than one charged atom in its structure. Instances where multiple charged atoms are part of the pharmaceutically acceptable salt can have multiple counter ions. Hence, a pharmaceutically acceptable salt can have one or more charged atoms and/or one or more counter ion. [045] Pharmaceutically acceptable salts of Compound I described herein include those derived from Compound I with inorganic acids, organic acids or bases. In some embodiments, the salts can be prepared in situ during the final isolation and purification of the compounds. In other embodiments the salts can be prepared from the free form of Compound I in a separate synthetic step. [046] When a compound such as Compound I is acidic or contains a sufficiently acidic moiety , suitable "pharmaceutically acceptable salts" refers to salts prepared from pharmaceutically acceptable non-toxic bases including inorganic bases and organic bases. Salts derived from inorganic bases include aluminum, ammonium, calcium, copper, ferric, ferrous, lithium, magnesium, manganic salts, manganous, potassium, sodium, zinc and the like. Particular embodiments include ammonium, calcium, magnesium, potassium and sodium salts. Salts derived from pharmaceutically acceptable organic non-toxic bases include salts of primary, secondary and tertiary amines, substituted amines including naturally occurring substituted amines, cyclic amines and basic ion exchange resins, such as arginine, betaine, caffeine, choline, N, N’dibenzylethylenediamine, diethylamine, 2- diethylaminoethanol, 2-dimethylaminoethanol, ethanolamine, ethylenediamine, N- ethylmorpholine, N-ethylpiperidine, glucamine, glucosamine, histidine, hydrabamine, isopropylamine, lysine, methylglucamine, morpholine, piperazine, piperidine, polyamine resins, procaine, purines, theobromine, triethylamine, trimethylamine tripropylamine, tromethamine and the like. [047] When a compound such as Compound I is basic or contains a sufficiently basic moiety, salts may be prepared from pharmaceutically acceptable non-toxic acids, including inorganic and organic acids. Such acids include acetic, benzenesulfonic, benzoic, camphorsulfonic, citric, ethanesulfonic, fumaric, gluconic, glutamic, hydrobromic, hydrochloric, isethionic, lactic, maleic, malic, mandelic, methanesulfonic, mucic, nitric, pamoic, pantothenic, phosphoric, succinic, sulfuric, tartaric, p-toluenesulfonic acid and the like. Particular embodiments include citric, hydrobromic, hydrochloric, maleic, phosphoric, sulfuric and tartaric acids. Other exemplary salts include, but are not limited, to sulfate, citrate, acetate, oxalate, chloride, bromide, iodide, nitrate, bisulfate, phosphate, acid phosphate, isonicotinate, lactate, salicylate, acid citrate, tartrate, oleate, tannate, pantothenate, bitartrate, ascorbate, succinate, maleate, gentisinate, fumarate, gluconate, glucuronate, saccharate, formate, benzoate, glutamate, methanesulfonate, ethanesulfonate, benzenesulfonate, p-toluenesulfonate, and pamoate (i.e., 1,1'-methylene-bis-(2-hydroxy-3- naphthoate)) salts. [048] The preparation of the pharmaceutically acceptable salts described above and other typical pharmaceutically acceptable salts is more fully described by Berg et al., "Pharmaceutical Salts," J. Pharm. Sci., 1977:66:1-19, incorporated here by reference in its entirety. Clinical assessments and functional outcome measurements tools [049] The assessment of cognitive function and functional capacity or performance and the assessment of the corresponding pathology underlying the observed dysfunction, decline, or symptoms, may be carried out using a number of different assessment tools or clinical measurements known and used in the field. [050] These range from imaging tools (e.g., MRIs, PET, CT scans), to laboratory measurements (e.g., fluid biomarkers measured in blood, cerebro-spinal-fluid (CSF), urine, plasma, serum, skin, saliva), to clinical outcome assessment tools or instruments (e.g., using patient- caretaker- or clinician-reported outcome instruments or performance outcome measures, such cognitive assessments using Cogstate batteries of tests, Standford Sleepiness Scale, etc), digital assessments (e.g., those obtained with wearable devices, sensor- or camera-based asessments) and electrophysiological assessements (e.g., EEG). Some of these are described in the Examples section below. Others are known in the art and could be used in the hospital or clinical setting. For example, the American Association of Family Physicians (AAFP), in its webpage, describes and provides links to a number of potential cognitive assessment tools, such as MiniCog, MoCA, SLUMS Examination, CPCoG, MIS and MMSE and others (https://www.aafp.org/patient-care/public-health/cognitive- care/cognitive-evaluation.html). [051] Some measurements are carried out to help in diagnosis and or patient selection. Others are carried out to help in assessing prognosis. Others may be carried out to assess pharmacological responses to a certain intervention (pharmacodynamic or PD assessments) such as described herein with Compound I. Others may be carried out to assess susceptibility to or risk of decline or response to a certain intervention (e.g., assessment of genetic markers or other biomarkers ) or to assess disease progression in a patient. [052] Electroencephalography (EEG) is an electrophysiology technique that measures electrical activity in the brain by using electrodes placed on the scalp. EEG-power spectral signals may be analyzed at different frequencies or frequency bands. They were analyzed at the following frequency bands in the experiments described in Example 1. Oscillatory bands: Delta- ≥2 to <4 Hz (typically associated with sleep), Theta- ≥4 to <8 Hz (associated with waking/falling asleep, some association with cognition), Alpha1- ≥8 to <10 Hz and Alpha2- ≥10 to <12 Hz (associated with passive wakefulness, and with cognitive processing), Beta1- ≥12 to <15 Hz, Beta 2- ≥15 to <18 Hz and Beta-3 ≥18 to <25 Hz (associated with alertness and concentration) . Fractal bands: Delta- ≥2 to <4 Hz, Theta- ≥4 to <8 Hz, Alpha ≥8 to <12 Hz, Beta- ≥12 to <30 Hz, Gamma ≥30 to <50 Hz (associated with higher cognitive function). [053] qEEG stands for quantitative electroencephalography. qsEEG stands for quantitative sleep EEG, if the qEEG is obtained during the subject’s sleep. [054] An “event-related potential” or ERP is a time-locked measure of electrical activity of the cerebral surface representing a distinct phase of cortical processing for example, in response to an auditory or visual stimulus (Patel and Azzam (2005), Characterization of N200 and P300: Selected Studies of the Event-Related Potential. International Journal of Medical Sciences 2(4):147-154). ERPs are time-locked and represent the average of the electrical responses observed after multiple recordings of EEG in response to repeated stimuli. ERPs are an objectively non-invasive approach for studying information processing and cognitive functions in the brain. [055] During EEG-ERP experiments such as those described in Example 1 in the Examples section, several key waveforms may be evaluated following a stimulus: N200 (associated with stimulus identification and distinction), P300 (associated with selective attention, information processing and cognitive speed/capacity), P200 (associated with aspects of selective attention or stimulus encoding), P50 (associated with sensory gating, or the reduced neurophysiological response to redundant stimuli), and N100 (associated with early perceptual processes). [056] Two key parameters are used to quantify each response: latency (how long after the stimulus is the peak signal) and amplitude (how strong is the peak signal). [057] P300 is a component of the ERP named for its polarity and approximate latency. It is a large positive waveform reaching a maximum at ~300ms after stimulus. It is most commonly elicited in an "oddball" paradigm when a subject detects an occasional "target" stimulus in a regular train of standard stimuli. The P300 wave only occurs if the subject is actively engaged in the task of detecting the targets. Its amplitude varies with the improbability of the targets. Its latency varies with the difficulty of discriminating the target stimulus from the standard stimuli. A typical peak latency when a young adult subject makes a simple discrimination is 300 ms. In patients with decreased cognitive ability, the P300 is smaller and later than in age-matched normal subjects. P300 is disrupted in a variety of neuropsychiatric and neurodegenerative disorders associated with cognitive impairment, including schizophrenia. [058] N200 is a negative waveform at ~200ms after stimulus, associated with stimulus identification and distinction. Mismatch negativity (MMN) is an alternative terminology used for N200 abnormal activity on an auditory ERP that occurs when a sequence of repetitive sounds is interrupted by an occasional “oddball” sound that differs in frequency or duration. MMN or N200 is not dependent upon active engagement on the part of the subject. Both terms are used interchangeable throughout this disclosure. The investigation of MMN in monkeys has shown that NMDA antagonists block the generation of the MMN response, suggesting that NMDA receptors play an important role in this index of information processing and working memory. Consequently, MMN is one of a family of EEG signals that may hold promise as a translational biomarker for CNS diseases, as do other markers of neuronal network activity such as gamma-band oscillation that are aberrant in these patients. Network oscillations may be valuable tools in pharmacological and translational studies that are aimed at developing and refining new treatment interventions for CNS diseases. N200 has been shown to be altered in AD subjects, other neurodegenerative diseases and psychiatric diseases. [059] Changes in EEG power spectra have been detected in neuropsychiatric and neurodegenerative disorders and have been correlated with cognitive performance (see for example: Herrmann CS, Demiralp T, Human EEG gamma oscillations in neuropsychiatric disorders. Clin Neurophysiol.2005 Dec;116(12):2719-33; K. van der Hiele, A.A. Vein, R.H.A.M. Reijntjes, R.G.J. Westendorp, E.L.E.M. Bollen, M.A. van Buchem, J.G. van Dijk, H.A.M. Middelkoop, EEG correlates in the spectrum of cognitive decline. Clinical Neurophysiology. Volume 118, Issue 9, 2007, Pages 1931-1939). [060] Meta-analyses have shown that latency and amplitude of P300, N200, P200, N100 and P50 waveforms are impacted in numerous CNS diseases, are associated with disease progression/severity, may be useful in the analysis of cognitive deterioration and treatment response, and change with aging (see for example van Dinteren R, Arns M, Jongsma MLA, Kessels RP, P300 Development across the Lifespan: A Systematic Review and Meta-Analysis. PLoSONE, 2014, 9(2): e8734; Howe AS, Meta-analysis of the endogenous N200 latency event-related potential subcomponent in patients with Alzheimer's disease and mild cognitive impairment. Clin Neurophysiol.2014 Jun;125(6):1145-51; Ishii R, Canuet L, Aoki Y, Hata M, Iwase M, Ikeda S, Nishida K, Ikeda M, Healthy and Pathological Brain Aging: From the Perspective of Oscillations, Functional Connectivity, and Signal Complexity. Neuropsychobiology 2017;75:151-161; Patel and Azzam (2005), Characterization of N200 and P300: Selected Studies of the Event-Related Potential. International Journal of Medical Sciences 2(4):147-154). [061] The Cogstate schizophrenia battery (CSB) is an established scale for the measurement of cognitive performance in schizophrenia. General cognition is measured based on a composite score that is the mean of scores of 8 individual tests. In addition, 3 domains of cognition can also be measured based on composite scores of subsets of the individual tests. These 3 domains of cognition are attention, memory, and executive function. Several types of measurements are carried out within each of these domains. Within the attention domain, both psycho-motor function and visual attention are measured. Within the memory domain, both verbal and visual learning are measured. And within the executive function domain, working memory and reasoning and problem solving are measured. In addition, social cognition is also measured using a social emotional cognition test as described below. The general cognition score for each participant is a composite or mean of 8 tests results for said participant. In the trial described in the Examples section, cognition using the CSB was assessed at multiple timepoints across the study including at screening, check-in (day -3), baseline (day -1), and on days 2, 7, and 14. [062] In the trial described in the Examples section, the following Cogstate battery of cognitive function tests was completed digitally. The total estimated time to complete the tests is approximately 38 minutes. [063] Detection test (3 min; measures simple reaction time/psychomotor function, attention domain): In this test, playing cards all depict the same joker. The participant were asked to press the “Yes” key as soon as the card in the center of the computer screen turned face up. The software measured the speed and accuracy of each response. This test measures processing speed. [064] Identification test (3 min; measures visual attention - attention domain): In this test, playing cards are all jokers, red or black. The participant was asked whether the card displayed in the center of the screen is red. The participant responded by pressing the “Yes” key when the joker card was red, and the “No” key when it was black. The participant was asked to work as quickly and accurately as possible. The software measured the speed and accuracy of each response. [065] One card learning test (6 min; measures visual learning -memory domain): In this test, the playing cards are identical to a standard deck of 52 playing cards (without the joker cards). The participant was aked whether the card displayed in the center of the screen was seen previously in this test. Accordingly, the participant pressed the “Yes” or “No” key as quickly and accurately as possible. The software measured the speed and accuracy of each response. [066] International shopping list test (5 min; measures verbal learning memory domain): A shopping list (high frequencies, high imagery, concrete nouns) was read to the participant by the test supervisor at the rate of 1 word every 2 seconds. Once all 12 words had been read, the participant was asked to recall as many items from the list as he/she could as quickly as possible. The test supervisor recorded on the testing device the words recalled by the participant. When the participant was able to recall no more words, the same list was read a second time. The test supervisor recorded the words recalled by the participant on this second trial. The test was the repeated a third time. The software measured the number of correct responses as recorded by the test supervisor. [067] One back test (4 min; measures working memory – executive function domain): In this test, the playing cards are identical to a standard deck of 52 playing cards (without the joker cards). The participant was asked whether the card displayed in the center of the screen was the same as the card presented immediately previously. The participant responded by pressing the “Yes” or “No” key. Because no card had been presented yet on the first trial, a correct first response is always “No.” The participant ws encouraged to work as quickly and as accurately as possible. The software measured the speed and accuracy of each response. [068] Two back test (4 min; measures working memory -executive function domain): In this test, the playing cards are identical to a standard deck of 52 playing cards (without the joker cards). The participant was asked whether the card displayed in the center of the screen was the same as the 2 cards presented previously. The participant responded by pressing the “Yes” or “No” key. Because no card had been presented two-back on the first and second trials, a correct response on these trials was always “No.” The software measured the speed and accuracy of each response. [069] Modified Groton maze learning test (7 min; measures reasoning and problem solving- executive function domain): A 10×10 grid of boxes is presented on the computer screen. A 28-step pathway is hidden among these locations. Each box represents move locations, and the grid refers to the box array (ie, 10×10). The participant was asked to find the hidden pathway, guided by 3 search rules: do not move diagonally; do not move more than 1 box (ie, do not jump); do not move back on the pathway. The participant did not need to return to the last correct location after making an error before continuing the search for the next correct box. Feedback was given with visual and auditory cues (green check marks and red crosses) to indicate whether the selected box was correct or incorrect. All correctly selected boxes remained ticked with a green check, keeping the revealed pathway displayed until the round was completed. There were 21 well-matched alternate pathways available. The software recorded each move as either an error or as a correct move. [070] Social emotional cognition test (6 min; measures emotional recognition): This test uses a well-validated odd-man-out paradigm based on pictures of faces. In this test, 4 pictures were presented on the screen such that 1 of them differs from all the others in 1 key aspect (ie, the emotion being expressed). In this regard, all but 1 picture established a communal context that was violated by 1 and only 1 of the pictures, causing this to be seen as unusual or atypical. The participant was to click on the 1 picture that did not match the rest. The software measured the speed and accuracy of each response. Prior Clinical Data with Compound I [071] As indicated above, in pre-clinical models, sGC stimulation by Compound I was shown to lead to changes in qEEG signals (Meeting abstracts from the 9th International Conference on cGMP: Generators, Effectors and Therapeutic Implications, Journal of Translational Medicine volume 17, Article number: 254 (2019) S 1-02 Evaluating soluble guanylate cyclase stimulation for serious central nervous system diseases). These studies were performed in rats with telemetry devices implanted in the frontal cortical and front- parietal regions of the brain. Rats were dosed with a suspension of Compound I orally, a suspension of a peripherally restricted sGC stimulator orally, or a solution of donepezil by subcutaneous injection. Compound I altered qEEG measurements including increasing gamma oscillations while the peripherally restricted sGC stimulator reduced gamma power compared to vehicle dosing. Compound I given to rats orally at 10 mg/kg increased gamma power and the signal was further increased in combination with 1 mg/kg donepezil at 1-2 hours post-dose. [072] In a Phase 1 clinical trial with elderly subjects [NCT04240158; described in a prior patent application publication WO 2022/081610 and in “A Phase I Translational Pharmacology Study in Healthy Elderly Volunteers Evaluating the Safety, Tolerability, Pharmacokinetics, and CNS Activity of IW-6463, a CNS-penetrant, Soluble Guanylate Cyclase Stimulator” Chad Glasser, Jacob Donoghue, Phillip Alday, Alex Arslan, Emily Florine, Chris Winrow, Chris Wright Neurology Apr 2021, 96 (15 Supplement) 4701)], Compound I increased the amplitude and decreased the latency of the ERP N200 signal in the auditory oddball task. N200 is a neurophysiological biomarker associated with stimulus identification and distinction (i.e., in the attention domain) that is altered in aging and cognitive impairment associated with a number of diseases. Latency was significantly shorter with Compound I treatment at day 14 at a dose of 15 mg QD, compared with placebo treatment, an effect that improved with age of participants (i.e. older participants displayer larger drug effect). Similarly, the effect was also greater in participants who, at baseline, had slower individual alpha frequencies, a marker of cognitive function/capacity (i.e. the more dysfunction the person showed at baseline, the larger the drug effect). Latency response was greater in subjects older than 70 years old when compared with those 65-69 years old. The narrowing of variance for older patients supported a drug effect. [073] In the NCT04240158 trial, Compound I also increased alpha band power, a parameter known to be decreased in AD and with aging, after 15 mg QD dosing. Alpha band power is also correlated with cognitive decline, APOE4 mutation status, and hippocampal atrophy. A positive impact on EEG (posterior) alpha power, with a 13.7% increase from baseline, in the Compound I treatment group compared to a 3.7% decrease in the placebo group (17.4% treatment effect) was again observed. Furthermore, trend increases in (anterior) alpha power (17.5% in subjects when treated with Compound I, 4.4% in subjects when treated with placebo, providing a 13.1% treatment effectas well as (anterior) gamma power (45% in subjects when treated with Compound I, -0.1% in subjects when treated with placebo, 44.9% treatment effect) were also observed. [074] Also in the NCT04240158 trial, in an exploratory CSF biomarker analysis, positive trends on some important CSF neuroinflammatory markers were observed in subjects after two weeks of treatment with 15 mg of Compound I QD as compared with placebo. In particular, potentially relevant reductions in the concentrations of Alpha 2 macroglobulin (A2M) and complement C3 (C3) biomarkers were observed. The largest reductions in concentrations of these biomarkers were observed in subjects older than 70 years old. [075] Finally, in the NCT04240158 trial, the NeuroCart® battery of CNS assessments was also employed. NeuroCart® is a full battery of tests for measuring a wide range of CNS functions that was developed by the Center of Human Drug Research (CHDR). NeuroCart can be used to correlate a compound’s CNS effects with drug concentration, helping determine whether an effect is due to the compound specifically. NeuroCart provides both objective (e.g. neurophysiology, brain performance) and subjective (e.g. cognitive function, memory, mood, etc.) measures of CNS function. NeuroCart measurements were performed in a quiet room with ambient illumination. Per session, only one participant was allowed in the same room. NeuroCart included EEG, discussed above and saccadic eye movement (SEM) assessments in addition to several other assessments of brain performance. Saccadic peak velocity and latency may be reflective of attention/focus, passive/attentive state, and brain processing time. Clinically relevant increases in SEM peak velocity and decreases in latency/reaction time were observed for Compound I in the NCT04240158 trial using a 15 mg oral daily dose. Thus positive effects in this objective SEM performance task related to attention and cognitive processing were observed. These were consistent with improvements observed in other attentional/reaction time neurophysiological measures discussed above in the EEG studies (gamma power and ERP N200 and P300). Saccadic reaction times were significantly shorter following treatment with Compound I compared with placebo treatment. Trends towards increases in saccadic peak velocities were also observed in response to treatment. [076] Although changes in the assessment of brain physiology and performance were observed in the NCT04240158 trial (EEG alpha power, ERP and SEM parameters), no changes in any of the cognitive function assessments were observed. Compound I in patients with schizophrenia [077] Thus, as summarized in the previous section, in a prior Phase 1 clinical trial with Compound I, changes in EEG paramenters (alpha power and N200/P300 ERP), changes in a SEM assessment, as well as a tendency towards improvement in two neuroinflammation parameters were observed. However, no improvements were detected in assessments of cognitive function. No changes were observed in other ERP parameters. Since the subjects on those trials were healthy and did not display any specific pathologies, it may not have been expected to see effects on cognitive tests, but improvements on brain physiology consistent with potential positive effects were observed. All of the changes observed in the EEG and SEM measurements were consistent with and pointed to effects on attention, focus and brain processing time and supported a potential of Compound I for the treatment of at least those aspects of cognition (i.e. in the attention domain) in patients with a variety of pathologies. [078] The compound had never been tested in a population of schizophrenia patients that are already receiving treatment with anti-psychotics. [079] A goal of the study described in the Examples section (Example 1) was to assess the effect of a range of oral daily dosages of Compound I on a number of parameters or measures related to brain health and cognitive function or ability in patients with schizophrenia on stable treatment with anti-psychotics. Some of the patients were also on other medications, including ACE inihibitors (lisinopril), anilides (acetaminophen), azaspirodecandione derivatives (buspirone), benzodiazepine derivatives (lorazepam, alprazolam), benzodiazepine-related drugs (zolpidem), beta blocking agents (propranolol), dihydropyridine derivatives (amlodipine), statin drugs (atorvastatin), anticonvulsants (gabapentin), muscle relaxants (cyclobenzaprine hydrochloride), proprionic acid derivatives (ibuprofen), beta-2-adrenoreceptor agonists (salbutamol), SSRIs (paroxetine, escitalopram), serotonin antagonists (ondansetron) anddiuretics (hydrochlorothiazide). [080] Some of the assessments carried out were described in prior sections. The different assessments and measurements carried out are further described in the Examples section. [081] The primary objective of the trial was to evaluate the safety and tolerability of Compound I when administered to a patient population of subjects with schizophrenia on stable antipsychotic medications, by measuring AEs, SAEs and TEAEs leading to drug discontinuation at a range of dosages. [082] The secondary objective was to evaluate the plasma PK of the compound. [083] In addition, exploratory endpoints were aimed at evaluating the effect of Compound I on brain neurophysiology and cognitive function. In particular, change from baseline to each postdose timepoint in ERP (e.g. MMN) parameters was assessed, as well as change from baseline to each postdose timepoint in qEEG parameters and overnight EEG parameters. Other exploratory endpoints included change from baseline to each postdose timepoint in cognitive performance paramenters as assessed with the Cogstate Schizophrenia Battery (CSB) and change in day 15 plasma inflammatory biomarker parameters. [084] The present invention is based on the surprising finding that Compound I, administered at a total oral dosage of 15-60 mg per day, to a population of patients with schizophrenia on stable antipsychotic medication was not only safe and well tolerated but, in the case of the 15 mg dose also showed clear and strong evidence of improvements in general cognitive performance measures after only two weeks of treatment. Effect sizes on general cognition in the CSB were greater than those showed by other agents in much longer studies. For example BI425809, a GlyT1 inhibitor, dosed at 10 mg daily showed an effect size of 0.34 in the MATRICS consensus cognitive battery (MCCB) of tests after 12 weeks of treatment (Fleishhacker et al, 2021, Phase III study ongoing). Encenicline, an alpha-7 partial agonist, after 12 weeks at 0.27 mg daily showed an effect size in the CSB of 0.26 (Keefe et al, 2015). GSK239512, an H3R antagonist/inverse agonist, after 7 weeks at maximum dose of 80 μg per day showed aneffect size in the CSB of 0.29 (Jarskog et al, 2015) . In comparison, Compound I, at 15 mg daily, showed a large effect size of 0.60 in the general cognition composite score of the CSB after a much shorter treatment course of only two weeks (14 days). Effect size for the CSB composite score in this trial is defined as (mean change from baseline Compound I- mean change from baseline placebo)/pooled baseline standard deviation. Changes from baseline (CFB) were determined by a MMRM analysis (mixed-effect model repeated measure) with change from baseline as the response variable, treatment, time point, and treatment-by-visit interaction as fixed effects and the respective baseline value as the covariate with an appropriate variance-covariance structure. The effect size of the general cognition composite score at day 2 was 0.16 and at day 7 was 0.31, indicating that the effect size increases over time as the participant achieves steady-state levels of Compound I. Steady state had not yet been achieved at day 7, but it was achieved by day 14. A 0.6 value is an effect size that is substantially greater than 0.3, which is generally accepted as clinically meaningful in the field of neuropsychiatry. [085] It is expected that benefit will be durable, which would be consistent with the pharmacological effects of other compounds with this mechanism and may further increase with longer treatment, which would be consistent with other trials in CIAS. [086] Unexpectedly, no changes were observed on the 30 and 60 mg dosages in the general cognition composite score of the CSB. Pharmacodynamic cognition signals were less pronounced at these higher doses. A positive effect was observed at these dosages only in the memory domain. [087] The 15 mg dose also showed antiinflammatory effects on a broad panel of plasma inflammatory markers, including biomarkers with links to schizophrenia and cognition. Examples include a reduction from baseline relative to placebo in interleukin (IL)-6, which has been shown to be elevated in schizophrenia and associated with cognitive impairment, and an increase in IL-2, which has been shown to be decreased in schizophrenia and positively correlates with cognitive performance. These anti-inflammatory effects extend results observed in preclinical and earlier clinical studies of Compound I. [088] For biomarkers levels changes, ANCOVA (analysis of covariance) change from baseline as the response variable, treatment group as the main effect, and the respective baseline value as the covariate was used. Effect sizes for biomarkers changes are defined as Effect size: (Mean CFB CY6463 – mean CFB placebo)/pooled SD. [089] Preliminary analysis of additional exploratory endpoints looking at a wide range of EEG parameters showed changes in neurophysiology. However, in this trial, based on prespecified analyses (MMRM model; p <0.05), no significant changes in awake resting-state alpha or gamma power measurements in the daytime qEEG or in any of the ERP measurements were correlated with cognitive performance measures. [090] If one analyzes specific composite scores for the different cognition domains, the larger effects at the 15 mg dosage were observed for the executive function and memory subdomains (0.44 size effects in both cases). The attention domain showed smaller effects (0.15 size effect). Even though the general cognition scores are lower at 30 and 60 mg dosages (0.13 and 0.12, respectively), a potentially relevant effect size was observed at all dosages in the memory domain (0.44 at 15 mg, 0.53 at 30 mg and 0.37 at 60 mg). This is in contrast with the effects observed in previous trials in which the results pointed to effects mostly in attention. In the 30 and 60 mg dosages, negative effect sizes were observed for attention. In the trial herein described, the effects of 15 daily mg of Compound I in attention were the least pronounced and the effects on memory and executive function were the most pronounced, something that could not have been predicted based on prior trial results. [091] The results obtained at the 15 mg daily dose are consistent with a broad procognitve effect and an anti-inflammatory effect of Compound I in these patients. Therapeutic methods [092] In some embodiments of the methods and uses of the invention, a therapeutically effective amount of Compound I is a total oral daily dose of 15 mg of Compound I. In some embodiments, a pharmaceutically acceptable salt of Compound I can be used in the methods and uses of the invention described herein. When a pharmaceutically acceptable salt of Compound I is used, the dose for the pharmaceutically acceptable salt depends on the molecular weight of the salt and has an equal quantity in moles to the dose of Compound I described herein. Accordingly, in some embodiments, the present invention is a method of treating cognitive impairment in a patient with schizophrenia who is being treated with antipsychotics in need thereof by administering a total oral daily dose of Compound I of 15 mg or an equal quantity in moles of a pharmaceutically acceptable salt of Compound I to said patient. [093] In some embodiments of the above methods and uses of the invention, treatment with Compound I or a pharmaceutically acceptable salt thereof does not result in an adverse event (AE) associated with symptomatic hypotension. [094] In some embodiments of the methods and uses of the invention, the human patient is between 16 and 100 years old. In other embodiments, the patient is between 16 and 90 years old. In still other embodiments, the patient is between 16 and 80 years old. In still other embodiments the patient is between 16 and 75 years old. In some embodiments, the human patient is 16 years or older. In other embodiments, the human patient is 18 years or older. In some embodiments, the human patient is between 18 and 50 years old. In still other embodiments, the patient is younger than 65 years old. In yet other embodiments, the patient is an adult. [095] In certain embodiments, the methods and uses of the present invention described herein comprise administering to the patient a total oral daily dose of 15 mg of Compound I. [096] In certain embodiments, the methods and uses of the present invention described herein comprise administering to the patient a single oral daily dose of 15 mg of Compound I or an equal quantity in moles of a pharmaceutically acceptable salt of Compound I. [097] In some embodiments, the methods and uses of the invention described herein comprise administering an initial total oral daily dose of 15 mg of Compound I or an equal quantity in moles of a pharmaceutically acceptable salt of Compound I to the patient followed by a down-titration to a total oral daily dose of between 7 and 10 mg of Compound I or an equal quantity in moles of a pharmaceutically acceptable salt of Compound I if the patient does not tolerate 15 mg daily as assessed by a medical practitioner. In some embodiments, the dose can be increased back up to 15 mg once the patient tolerates the lower dose. [098] In some embodiments, the maintenance dose continues indefinitely as long as the patient continues to experience clinical benefit. [099] In some embodiments, the methods and uses of the present invention described herein improve overall cognition of the patient. [0100] In some embodiments, the methods and uses of the present invention described herein improve executive function and/or memory of the patient. Combination Therapies [0101] The treatment of cognitive impairment associated with schizhophrenia with Compound I or a pharmaceutically acceptable salt thereof in patients that are being treated with antipsychotics can be carried out using Compound I and the antipsychotic alone or in combination therapy with one or more additional therapeutic agents. In some embodiments, Compound I or a pharmaceutically acceptable salt thereof and antipsychotics can be used for the treatment of cognitive impairment in combination with one or more additional therapeutic agents. Examples of other therapeutic agents that may be combine with Compound I and the antipsychotics include, but are not limited to: (1) Blood pressure lowering medications (also known as anti-hypertensive medications), including, but not limited to: diuretics such as thiazide diuretics, chlorothiazide, chlorthalidone, hydrochlorothiazide, bendroflumethiazide, cyclopenthiazide, methyclothiazide, polythiazide, quinethazone, xipamide, metolazone, indapamide, cicletanine, furosemide, toresamide, amiloride, spironolactone, canrenoate potassium, eplerenone, triamterene, acetazolamid and carperitide; beta blockers such as propranolol, acebutolol, atenolol, metoprolol, and nebivolol; angiotensin-converting enzyme (ACE) inhibitors such as sulfhydryl-containing agents (for example, captopril, zofenopril), dicarboxylate-containing agents (for example, enalapril, quinapril, ramipril, perindopril, lisinopropil, and benazepril), phosphonate- containing agents (for example fosinopril), naturally occurring ACE inhibitors (for example, casokinins, lactokinins, lactotripeptides Val-Pro-Pro and Ile-Pro-Pro), alacepril, delapril, cilazapril, imidapril, temocapril, moexipril, lisinopril, combinations of lisinopril with hydrochlorothiazide, trandolapril and spirapril; angiotensin II receptor blockers (ARBs) such as candesartan, losartan, losartan potassium-hydrochlorothiazide, valsartan, candesartan cilexetil, eprosaran, irbesartan, telmisartan, olmesartan medoxomil (or olmesartan), azilsartan medoxomil, azilsartan, amlodipine besylate combined with irbesartan, azilsartan combined with amlodipine besilate, cilnidipine combined with valsartan, fimasartan, irbesartan combined with atorvastatin, irbesartan combined with trichlormethiazide, losartan potassium combined with hydrochlorothiazide and/or amlodipine besylate, pratosartan, atorvastatin calcium combined with losartan potassium, nifedipine and candesartan cilexetil, sacubitril combined with valsartan or LCZ-696, angiotensin AT2 antagonist and TAK-591 and olmesartan medoxomil; endothelin Receptor antagonists (ERAs) such as atrasentan, bosentan, sitaxentan, ambrisentan, actelion-1 (macitentan), Cyclo(D-trp-D-asp-L-pro-D-val-L-leu) (BQ-123), sparsentan and tezosentan disodium; mineralocorticoid receptor antagonists (MRAs) such as spironolactone, amiloride hydrochloride combined with spironolactone, apararenone or MT-3995, eplerenone, and finerenone (BAY-94-8862); calcium channel blockers such as amlodipine, aranidipine, azelnidipine, barnidipine, benidipine, cilnidipine, clevidipine, diltiazem, efonidipine, felodipine, lacidipine, lercanidipine, manidipine, nicardipine, nifedipine, nilvadipine, nimodipine, nisoldipine, nitrendipine, pranidipine, isradipine, verapamil, gallopamil, diltiazem, mibefradil, bepridil, fluspirilene and fendiline; renin inhibitors such as aliskiren; alpha blockers such as doxazosin and prazosin; alpha-beta blockers such as carvedilol and labetalol; central-acting agents such as clonidine, guanfacine and methyldopa; vasodilators such as nitroglycerine, hydralazine and minoxidil; and aldosterone antagonists such as finerenone, spironolactone and eplerenone (2) Anti-hyperlipidemic medications, including but not limited to: statins such as atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, and simvastatin; combinations of statins with another agent such as amlodipine/atorvastatin, aspirin/pravastatin, ezetimibe/simvastatin, niacin/simvastatin, lovastatin/niacin, simvastatin/sitagliptin and atorvastatin/ezetimibe; fibrates or fibric acid derivatives. Examples include, but are not limited to, fenofibrate, gemfibrozil, bezafibrate, ciprofibrate, clinofibrate and clofibrate; niacin (or nicotinic acid); bile acid sequestrants such as cholestyramine, colesevelam, colestilan and colestipol; ezetimibe, lomitapide, phytosterols or orlistat; and PCSK9 inhibitors such as alirocumab and evolocumab (3) Non-steroidal anti-inflammatory agents (NSAIDs), including, but not limited to: propionic acid derivatives like alminoprofen, benoxaprofen, bucloxic acid, carprofen, fenbufen, fenoprofen, fluprofen, flurbiprofen, ibuprofen, indoprofen, ketoprofen, miroprofen, naproxen, oxaprozin, pirprofen, pranoprofen, suprofen, tiaprofenic acid and tioxaprofen; acetic acid derivatives such as indomethacin, acemetacin, alclofenac, clidanac, diclofenac, fenclofenac, fenclozic acid, fentiazac, furofenac, ibufenac, isoxepac, oxpinac, sulindac, tiopinac, tolmetin, zidometacin and zomepirac; fenamic acid derivatives such as flufenamic acid, meclofenamic acid, mefenamic acid, niflumic acid and tolfenamic acid; biphenylcarboxylic acid derivatives such as diflunisal and flufenisal; oxicams such as isoxicam, piroxicam, sudoxicam and tenoxican; salicylates such as acetyl salicylic acid and sulfasalazine; and pyrazolones such as apazone, bezpiperylon, feprazone, mofebutazone, oxyphenbutazone and phenylbutazone. (4) Anilides such as acetaminophen (5) Treatments for epilespsy or seizures (anticonvulsants) including, but not limited to, phenytoin, valproic acid, phenobarbital, lamotrigine, carbamazepine, topiramate, oxcarbazepine, zonisamide, gabapentin, levetiracetam, pregabalin, clonazepam, lacosamide, rufinamide, and vigabatrin (6) Drugs used for the treatment of mood or affective disorders or OCD such as the following types: tricyclic antidepressants such as amitriptyline, desipramine , imipramine , amoxapine, nortriptyline, doxepin and clomipramine; selective serotonin reuptake inhibitors (SSRIs) such as paroxetine, escitalopram (Lexapro), fluoxetine, sertraline, trazodone and citralopram; atypical antidepressants such as agomelatine; selective norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine, reboxetine and atomoxetine; dopaminergic antidepressants such as bupropion and amineptine (7) Drugs used for the treatment of anxiety disorders or insomnia: azaspirodecandione derivatives such as buspirone; benzodiazepine derivatives such as lorazepam and alprazolam (Xanax); benzodiazepine-related drugs such as zolpidem (Ambien); diphenylmethane derivatives such as hydroxyzine; (8) Bronchodilators, including, but not limited to: short acting β2 agonists, such as albutamol or albuterol and terbutaline; long acting β2 agonists (LABAs) such as salmeterol and formoterol; anticholinergics such as pratropium and tiotropium; and theophylline, a bronchodilator and phosphodiesterase inhibitor. (9) Others: calcium compounds such as tums; muscle relaxants such as cyclobenzaprine hydrochloride; serotonin antagonists (ondansetron); colace. [0102] In some embodiments of the methods and uses of the invention, the one or more additional therapeutic agents are selected from ACE inhibitors, anilides, drugs used for treating anxiety disorders or insomnia (e.g., azaspirodecandione derivatives, benzodiazepine derivatives, benzodiazepine-related drugs), beta blocking agents, calcium channel blockers (e.g., dihydropyridine derivatives), statin drugs, anticonvulsants, muscle relaxants, non- steroidal anti-inflammatory agents (e.g., proprionic acid derivatives), beta-2-adrenoreceptor agonists, selective serotonin reuptake inhibitors, serotonin antagonists, and diuretics. [0103] In some embodiments of the methods and uses of the invention, one or more additional therapeutic agents are selected from lisnopril, acetaminophen, ibuprofen, lorazepam, alprazolam, zolpidem, propranolol, amlodipine, buspirone, atorvastatin, gabapentin, cyclobenzaprine hydrochloride, salbutamol, paroxetine, escitalopram, ondansetron and hydrochlorothiazide. [0104] In some embodiments of the methods and uses of the invention, the anti-psychotics patients are being treated with, while taking Compound I are selected from a list comprising, quetiapine, olanzapine, risperidal, aripiprazole and paliperidone. [0105] As used herein, the terms “in combination” (as in the sentence “in combination therapy”) or “co-administration” can be used interchangeably to refer to the use of more than one therapy. The use of the terms does not restrict the order in which therapies are administered to a subject. [0106] The sGC stimulator Compound I or a pharmaceutically acceptable salt thereof can be used in combination therapy with one or more additional therapeutic agents (e.g., additional therapeutic agents described herein) in addition to the antipsychotics the patients with schizophrenia will already be on. For combination treatment with more than one therapeutic agents where the therapeutic agents are in separate dosage formulations, or dosage forms, the therapeutic agents may be administered separately or in conjunction (i.e., at the same time). In addition, when administered separately, the administration of one therapeutic agent may be prior to or subsequent to the administration of the other agent. [0107] When Compound I or a pharmaceutically acceptable salt thereof is used in combination therapy with other additional therapeutic agents on top of the antipsychotics, a therapeutically effective amount of the other therapeutic agent or each of the other therapeutic agents and a therapeutically effective amount of the antipsychotic will depend on the type of drug used. Suitable dosages are known for approved therapeutic agents and can be adjusted by the skilled artisan according to the condition of the subject, the type of condition(s) being treated and the amount of a Compound I or a pharmaceutically acceptable salt thereof being used. In one embodiment of this invention, Compound I or a pharmaceutically acceptable salt thereof, and the additional therapeutic agent, including the antipsychotic, are each administered in an therapeutically effective amount (i.e., each in an amount which would be therapeutically effective if administered alone). In other embodiments, Compound I or a pharmaceutically acceptable salt thereof and the additional therapeutic agent, including the antipsychotic, are each administered in an amount which alone does not provide a therapeutic effect (a sub-therapeutic dose). In yet another embodiment, Compound I or a pharmaceutically acceptable salt thereof can be administered in an effective therapeutic amount, while the additional therapeutic agent, including the antipsychotic, is administered in a sub-therapeutic dose. In still another embodiment, Compound I or a pharmaceutically acceptable salt thereof can be administered in a sub-therapeutic dose, while the additional therapeutic agent, including the antipsychotic, is administered in a therapeutically effective amount. [0108] When co-administration involves the separate administration of a first amount of Compound I or a pharmaceutically acceptable salt thereof and a second amount of an additional therapeutic agent, including antipyschotics, and potentially additional therapeutic agents, the compounds are administered sufficiently close in time to have the desired therapeutic effect. For example, the period of time between each administration which can result in the desired therapeutic effect, can range from minutes to hours and can be determined taking into account the properties of each compound such as potency, solubility, bioavailability, plasma half-life and pharmacokinetic profile. For example, Compound I or a pharmaceutically acceptable salt thereof and the second or additional therapeutic agent can be administered in any order within 24 hours of each other, within 16 hours of each other, within 8 hours of each other, within 4 hours of each other, within 1 hour of each other, within 30 minutes of each other, within 5 minutes of each other, simultaneously or concomitantly. [0109] More, specifically, a first therapy can be administered prior to (e.g., 5 minutes, 15 minutes, 30 minutes, 45 minutes, 1 hour, 2 hours, 4 hours, 6 hours or 12 hours before)), concomitantly with, or subsequent to (e.g., 5 minutes, 15 minutes, 30 minutes, 45 minutes, 1 hour, 2 hours, 4 hours, 6 hours, 12 hours after), the administration of a second or third or fourth, etc, therapy to a subject. EXAMPLES [0110] For this invention to be better understood, the following examples are set forth. These examples are for purposes of illustration only and are not be construed as limiting the scope of the invention in any manner. All references provided in the Examples are herein incorporated by reference. Example 1: A double-blinded (investigator and participant), sponsor unblinded , randomized, placebo-controlled, multiple-ascending-dose study to assess the safety and pharmacokinetics of Compound I (alias CY6463) in participants with stable schizophrenia on antipsychotic treatment. Abbreviation/Term Definition AASM American Academy of Sleep Medicine AE adverse event AESI adverse event of special interest AIMS Abnormal Involuntary Movement Scale ASSR auditory steady-state response AUC area under the concentration-time curve AUC ^0-24 area under the concentration-time curve from time zero (predose) to 24 hours postdose AUCtau area under the concentration-time curve during a dosing interval AVWT average wavelet amplitude BARS Barnes Akathisia Rating Scale BCRP breast cancer-resistance protein BP blood pressure Cavg average concentration during a dosing interval cGMP cyclic guanosine 3’,5’-monophosphate CI confidence interval CL/F apparent systemic clearance Cmax maximum observed concentration C ^min minimum observed concentration CNS central nervous system C-SSRS Columbia-Suicide Severity Rating Scale CY6463 IW-6463 = Compound I DRC Data Review Committee DSM-5 Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition ECG electrocardiogram EEG electroencephalography ERP event-related potential ICD-10 International Classification of Diseases, 10 ^th revision ICF informed consent form ITPC inter-trial phase coherence IWRS interactive voice/web response system LAI long-acting injectable LTP long-term potentiation MCCB MATRICS™ Consensus Cognitive Battery MDMA methamphetamine, 3,4-methylenedioxymethamphetamine min minute(s) MINI Mini-International Neuropsychiatric Interview MMN mismatch negativity MMRM mixed-effect model repeated measures NMDA N-methyl-D-aspartate NO nitric oxide PANSS Positive and Negative Syndrome Scale PD pharmacodynamic(s) PDE5 phosphodiesterase 5 PK pharmacokinetic(s) QD once daily qEEG quantitative electroencephalography QT the time between the beginning of the QRS (ventricular polarization) complex and the end of the T-wave QTcF QT interval corrected for heart rate using Fridericia’s formula RAUC accumulation ratio based on a comparison of AUC values after single and multiple dosing RCmax accumulation ratio based on a comparison of Cmax values after single and multiple dosing REM rapid eye movement SAE serious adverse event SAS Simpson Angus Scale sGC soluble guanylate cyclase SOA stimulus-onset asynchrony SPL sound pressure level SSS Stanford Sleepiness Scale TEAE treatment-emergent adverse event T ^max time to maximum observed concentration TSC Trial Safety Committee US United States Study objectives and outcome measures [0111] This study was a multicenter, placebo-controlled, multiple-ascending-dose, investigator- and participant-blinded, sponsor-unblinded study evaluating the safety, tolerability, PK, and PD of Compound I in participants with schizophrenia who were on stable treatment regimen with antispychotics. [0112] 48 participants (divided into 4 cohorts) were randomized in a 2:1 ratio (2 active: 1 placebo) to receive 14 sequential days of once-daily (QD) Compound I or placebo, respectively. Participants were confined to the study center from Day -3 to Day 15. The total study duration from Screening through the Follow-up visit for each participant was approximately 2 months (Clinical Trials.gov identifier NCT04972227). [0113] To minimize risk to participants, sentinel dosing was used for Cohort 1 and for any subsequent cohorts if the dose selected for that cohort was greater than that of any preceding cohort(s). For these cohorts, the first 3 participants were randomized (preferably all at one site) and dosed for ≥10 days. Randomization and dosing of the remainder of the respective cohort was allowed to begin if, per judgment of the Trial Safety and Data Review committees, no pattern of study drug-related AEs of concern had been reported (eg, serious and/or severe study drug-related TEAEs) in the sentinel participants. [0114] A goal of the study described below was to assess the effect of specific dosages of Compound I on a number of parameters or measures related to brain health and cognition in patients with schizophrenia on stable treatment with antipsychotics. [0115] The primary objective of the trial was to evaluate the safety and tolerability of Compound I when administered to a patient population of subjects with schizophrenia on stable antipsychotic medications, by measuring TEAEs, SAEs and TEAEs leading to drug discontinuation. [0116] The secondary objective was to evaluete the plasma PK of the compund. [0117] In addition, exploratory endpoinds were aimed at evaluating the effect of Compound I on brain neurophysiology and cognitive function. In particular, change from baseline to each postdose timepoint in ERP (e.g. MMN) parameters was assessed, as well as change from baseline to each postdose timepoint in qEEG parameters and overnight EEG parameters. Other exploratory endpoints including change from baseline to each postdose timepoint in cognitive performance paramenters as measured with the Cogstate battery of cognitive assessments and change in plasma day 15 blood inflammatory biomarker parameters. Additional details regarding the different assessments carried out as part of the trial are included below. Psychiatric Assessments Mini International Neuropsychiatric Interview [0118] The Mini International Neuropsychiatric Interview (MINI, Version 7.02) is a short, structured diagnostic interview administered by trained personnel. The instrument captures the major Axis I psychiatric disorders in DSM-IV and the International Classification of Diseases, 10 ^th revision (ICD-10). Each module begins with screening questions that are answered “Yes” or “No.” A negative response in the screening algorithm advances the interview to the next module, whereas a positive response will prompt additional questions that ask the participant to characterize behavior with “Yes” or “No” responses. Some questions contain a recall period (eg, “Past Two Weeks,” “Past Episode,” and “Current Episode”). After completion of the additional questions, the clinician indicates whether or not the diagnostic criteria have been met based on the instrument scoring criteria. In the clinical trial described in Example 1, The MINI was completed at Screening by trained site personnel, in accordance with the structured interview requirements. Positive and Negative Syndrome Scale (PANSS) [0119] The PANSS was developed based on patient interviews and has been widely used in schizophrenia trials. The validity and reliability of the PANSS has been extensively studied and established, including its ability to assess positive and negative symptoms in individuals with recent onset of schizophrenia. The PANSS contains 30-items rated on 7-point Likert scales and is scored to assess 3 subscales: positive symptoms, negative symptoms and psychopathological symptoms. A 5-factor structure has also been identified to explore changes in the traditional subscales, and also those that may align with disorganized (or cognitive) factors, as well as excited and depression/anxiety factors. [0120] In the clinical trial described in Example 1 below, The PANSS was completed by the investigator or qualified delegate. Data from the PANSS were enhanced when the participant identified a person who could serve as an informant for its completion. Although not required for study inclusion, identification of a reliable individual (eg, family member, social worker, or case manager) who had spent sufficient time with the participant to be able to provide information to PANSS raters and who had interacted with the participant during the previous 7 days was highly encouraged. The informant had to be able and willing to attend clinic visits or to provide input via telephone and had to be considered reliable by the site. The same informant was recommended to be used throughout the study whenever possible. Extrapyramidal Symptoms [0121] The safety assessments listed below were be performed by the investigator or qualified delegate. When possible, continuity of raters was recommended to be maintained across scales for each participant. Simpson Angus Scale (SAS) [0122] The SAS is a 10-item scale used to broadly rate adverse neurological effects of antipsychotic medications. It involves direct observation and a brief neurological examination. The investigator must observe the participant’s gait and check for tremor, excessive salivation, and for rigidity in the arms, shoulder, and neck. Each item is rated from 0 to 4 to obtain a total score. Barnes Akathisia Rating Scale (BARS) [0123] The BARS is used to assess the severity of drug-induced akathisia. Abnormal Involuntary Movement Scale (AIMS) [0124] The AIMS checklist aids in the early detection of tardive dyskinesia and provides a method for ongoing surveillance. The AIMS uses a 5-point rating scale for recording scores for 7 body areas: face, lips, jaw, tongue, upper extremities, lower extremities, and trunk. Suicidal Risk Monitoring (C-SSRS) [0125] Compound I is considered to be a CNS-active investigational drug. Although Compound I and other similar drugs in this class have not been associated with an increased risk of suicidal thinking or behavior, it was considered important to monitor for such ideation or behavior before and during the study described in Example 1. The C-SSRS was administered by an individual with appropriate clinical training. The “Baseline” version of the C-SSRS was used at the first Screening visit. For all subsequent time points, the “Since Last Visit” version was used. If at any post-Screening visit there were “Yes” answers on Items 4, 5 or on any behavioral question of the C-SSRS, an immediate risk assessment was to be conducted with the CRO-based medical monitor to determine whether it was safe for the participant to continue in the study. Physical Examination and Vital Signs [0126] At Screening, a complete physical examination was performed by the investigator. All other examinations may be symptom directed at the investigator’s discretion. [0127] A complete physical examination was to include examination and assessment of the following: general appearance, lymph nodes, nervous system; cardiovascular system; head, eyes, ears, nose, throat and skin; respiratory system, neck, mental status, abdomen/liver/spleen and musculoskeletal system. Breast, genitourinary, and rectal examinations were optional and were to be performed at the discretion of the investigator. Clinically relevant findings that were present before study drug initiation on Day 1 were recorded as part of the participant’s medical history. Beginning after study drug initiation on Day 1, new clinically relevant findings or worsening of an earlier finding were recorded as an AE. Height (cm) was measured only at Screening. Weight (kg) was recorded throughout the study. Body mass index was calculated and recorded at Screening. [0128] Vital signs were measured before blood collection(s) and included respiratory rate, peripheral oxygen saturation, oral temperature (°C), and seated-to-standing BP and pulse rate. [0129] Oxygen saturation measurements were taken by pulse oximeter on room air. [0130] BP and pulse were measured using a completely automated device. The same device (make/model) was used for an individual participant throughout the study, if possible. Manual techniques were used only if an automated device was not available. BP and pulse measurements were preceded by ≥5 minutes of rest for the participant in a quiet setting without distractions (eg, television, cell phones). For supine BP and pulse measurements, 3 consecutive BP and pulse readings measured at intervals of ≥1 minute were recorded in the source documents. The average of the 3 BP and pulse readings were recorded. For rrthostatic BP and pulse measurements, after supine measurements were collected, the participant had to stand for 3 (-1) minutes before the standing BP and pulse values were measured. The sitting averages and the standing values were used to calculate and record orthostatic BP and pulse. Stanford Sleepiness Scale (SSS) [0131] TheSSS was applied to subjects in this trial. The SSS is a participant-rated scale designed to quickly assess how alert a participant is feeling. Degrees of sleepiness and alertness are rated on a scale of 1 to 7, where the lowest score of 1 indicates the participant is “feeling active, vital, alert, or wide awake” and the highest score of 7 indicates the participant is “no longer fighting sleep, sleep onset soon; having dream-like thoughts.” Electrocardiograms (ECGs) [0132] All ECGs were obtained using an ECG machine that automatically calculated the heart rate and measured PR, QRS, QT, and QTc intervals. The ECG was obtained after the participant had rested supine for ≥5 minutes. [0133] If a QTc result (corrected using Fridericia’s formula) was considered to be outside of the normal range (>450 ms formen; >470 ms for women), the ECG was to be repeated twice and the average of the 3 results calculated. [0134] All ECGs were evaluated by an investigator or qualified designee for the presence of abnormalities. Results were reported as “normal,” “abnormal clinically significant,” or“abnormal not clinically significant.” An abnormality of clinical significance was to be recorded as an AE. [0135] If a confirmed clinically significant abnormal result was obtained, the study center was to follow standard institutional procedure until the result resolved to baseline. If concerns remained, the issue was to be escalated to the study’s designated CRO-based medical monitor. Adverse Events, SAEs, and Other Safety Reporting [0136] Participant safety was monitored by the sponsor who reviewed emerging safety data, including clinical laboratory parameters and AEs at appropriate intervals. They also met on an ad hoc basis during the study if an unanticipated trend or signal emerges. [0137] Immediate safety concerns were to be discussed with the medical monitor upon occurrence or awareness. Changes in the participant’s health status since the previous visit or previous study drug administration were to be checked, including laboratory results, as applicable. AEs, AESIs, and SAEs were recorded starting from the signing of the ICF until the Follow-up visit after the final study drug dose. [0138] After the initial AE/SAE report, the investigator was required to proactively follow each participant at subsequent visits/contacts. All SAEs and AESIs were to be followed until resolution, stabilization, the event was otherwise explained, or the participant was lost to follow-up. The investigator was to submit any updated SAE information within 24 hours of it becoming available. [0139] Investigators were not obligated to actively seek information on AEs or SAEs after conclusion of an individual’s study participation. However, if the investigator learned of any SAE, including a death, at any time after a participant had been discharged from the study and considered the event to be reasonably related to the study drug or study participation, he/she was to promptly notify the sponsor. [0140] AEs were to be reported by the participant spontaneously and/or in response to open- ended questioning from the study personnel or revealed by observation. Open-ended and nonleading verbal questioning of the participant was to be the preferred method to inquire about AE occurrences. Care was to be taken not to introduce bias when detecting events. Pregnancy Reporting and Monitoring [0141] Study drug was to be immediately discontinued in a female participant upon confirmation of a positive pregnancy test result and was to be reported to the sponsor within 24 hours of the investigator’s first awareness. Pregnancy in a partner of a male participant was to be reported to the sponsor within 24 hours after obtaining the necessary signed ICF from the female partner. The participant/consenting pregnant female partner was to be followed to determine the outcome of the pregnancy. [0142] While pregnancy itself was not considered to be an AE or SAE, any pregnancy complication or elective termination of a pregnancy for medical reasons was to be reported as an AE or SAE. Abnormal pregnancy outcomes (eg, spontaneous abortion, fetal death, stillbirth, congenital anomalies, ectopic pregnancy) were considered SAEs and were reported as such. Elective abortions without complication did not need to be handled as AEs. [0143] Any post-study pregnancy-related SAE considered reasonably related to the study drug by the investigator was to be reported to the sponsor. While the investigator was not obligated to actively seek this information in former study participants or their female partners, he or she may learn of an SAE through spontaneous reporting. Other assessments [0144] A variety of laboratory assessments for safety, drug testing, and otherwise required by protocol were carried out in all subjects. A single blood sample for potential assessment of genetic factors that may be related to underlying disease and/or inter-individual differences in drug disposition, BP, or other PD responses was also collected from participants who provided specific written consent for sample collection, storage, and potential post-study analysis. Plasma PK and Biomarker Evaluations [0145] Samples were collected for PK and biomarker evaluations. Collected samples were to be stored for future analysis for not more than 15 years. [0146] Whole-blood samples were collected for measurement of plasma concentrations of Compound I. The samples were analyzed using a validated liquid chromatography-tandem mass spectrometry (MS/MS) bioanalytical method. [0147] PK parameters were derived using noncompartmental methods. PK parameters of interest include but are not limited to: • Single-dose (Day 1) parameters: AUC0-24: area under the concentration-time curve from time zero (predose) to 24 hours postdose; Cmax: maximum observed concentration; Tmax: time to maximum observed concentration • Multiple-dose (Day 13) parameters: AUCtau: area under the concentration-time curve during a dosing interval; C _max ; T _max ; C _min : minimum observed concentration; C _avg : average concentration during a dosing interval, calculated as AUC _tau/tau ; CL/F: apparent total clearance; RAUC: accumulation ratio based on a comparison of AUC values after single and multiple dosing, calculated as AUCtau/AUC0-24; RCmax: accumulation ratio based on a comparison of C _max values after single and multiple dosing calculated as C (Day 13) / C (Day 1) [0148] For biomarker evaluations, blood samples were collected to measure changes in concentrations of select disease and PD biomarkers. The samples were analyzed to further understand the schizophrenia disease process, pathways associated with the disease state, and/or the mechanism of action of Compound I and its PD effect. Biomarkers were assessed at a single postbaseline timepoint, at pre-dose time on day 15. Cognitive Performance Assessments [0149] The Cogstate schizophrenia battery (CSB) is a established scale for the measurement of cognitive performance in schizophrenia. [0150] The following Cogstate battery of cognitive function tests was completed digitally in the trial herein described. The total estimated time to complete the tests is approximately 38 minutes. Details pertaining to each of the tests were described above in the “clinical assessments and functional outcome measurements” section. [0151] The following Cogstate battery of cognitive function tests was completed digitally. The total estimated time to complete the tests is approximately 38 minutes. Detection test Identification test One card learning test One back test Two back test International shopping list test Social emotional cognition test Modified Groton maze learning test Neurophysiological Assessments by EEG qEEG and ERP Recording Parameters [0152] All qEEG and ERP assessments were performed by registered EEG technicians using individually applied gold cup electrodes and state-of-the-art EEG recording systems. All tests were performed with the participant seated comfortably in a sound-attenuated room. In addition to the standard 19 EEG leads of the International 10/20 system, the left earlobe and right ear lobe were recorded as active leads, and the vertical and horizontal electro- oculograms were recorded as bipolar pairs. The reference electrode was amplifier-dependent but was usually placed over bony scalp areas near the FCz or FC3 electrode positions. The same montage was used for both qEEG and ERP analyses. Digital referencing to linked ears was done offline. [0153] For ERP analyses, an additional electrode on the nose was required for accurate identification of mismatch negativity (MMN). Resting State qEEG (Eyes Open/Closed) [0154] A 5-minute resting qEEG with eyes closed and a 5-minute resting qEEG with eyes open was performed with the participant seated comfortably in a sound-attenuated room. The participant viewed a fixation cross on a video monitor during the eyes-open periods and was instructed not to move their eyes or blink excessively. The resting qEEGs was evaluated by means of spectral analysis, coherence analysis, and frequency analysis. After artifact rejection or correction, the mean absolute amplitude spectra (square root of power spectral density function) was computed. The qEEG endpoints includef, but were not limited to, changes from predose baseline in the band amplitudes in oscillatory and fractal spectral estimates, coherences at selected pairs of electrodes, and several derived frequency measures. Overnight EEG [0155] EEGs and electro-oculograms were recorded per American Academy of Sleep Medicine (AASM) sleep recording standards. Electromyography recorded at 3 chin placements was added to enable rapid eye movement (REM) sleep staging. Recordings from these 3 modalities was used to score sleep into 5 stages (wake, REM, N1, N2, N3) per the AASM sleep scoring rules. Trained sleep scorers manually scored each 30-sec sleep segment. Sleep staging was used to construct sleep hypnograms and to derive standard sleep measures, including sleep efficiency, sleep latency, and the percentage of sleep in each stage. In addition, the qEEG analysis considered the EEG records of each scored sleep stage separately. Targeted endpoints matched those considered in the eyes open/eyes closed qEEG analysis. Finally, sleep spindles were detected in a semi-automatic way; endpoints including sleep spindle density, duration, amplitude, and frequency were derived and analyzed as factors of between-group and treatment-related changes. Event-Related Potential (ERP) Assessments Hearing Screen for Auditory ERP Assessments [0156] A brief hearing test was performed during Screening to determine if the participant had adequate hearing to measure and interpret endpoints for the planned auditory ERP tasks. The test presented 2 types of stimulus tones—standard (70%) and target (30%)—in a random sequence, for a total of 100 stimuli. Both tone types were brief 75-ms binaural sound stimuli, which differed in pitch but not in loudness (80-dB sound pressure level [SPL]). The participant was instructed to listen to the tones, which occured every 1.2 seconds, and to respond when and only when a target tone was heard. A participant who passed with at least 80% correct responses (hits) and no more than 20% incorrect responses (false positives) was considered to have hearing adequate for the auditory ERP assessments. The procedure could be repeated 1 time if the 80%/20% criterion was not met on the first attempt. 2-Stimulus Auditory Oddball Task [0157] In the 2-stimulus auditory oddball task, brief tone bursts (standard tone, probability 0.8, pitch 1000 Hz, 50-msec duration, 5-msec rise/fall time, 80-dB SPL) were presented binaurally through headphones with a constant SOA (stimulus-onset asynchrony) of 1.2 seconds, randomly interrupted by higher-pitch tone bursts (target tones, probability 0.2, pitch 1500 Hz, 50-msec duration, 5-msec rise/fall time, 80-dB SPL). The total number of stimuli presented was 600, of which 480 was standard tones and 120 was target tones. The task was divided into 2 blocks of 300 trials each, with a short break (20 seconds) between blocks. Each block lasted for 6 minutes, for a total task time of approximately 12.5 minutes. The participant was asked to press a button on a response device (Cedrus response pad) as quickly as possible each time a target tone burst was heard. Artifact-free ERP responses were averaged for standard, target, and novel tones (all novel tones averaged together). Peak latencies and amplitudes of the target N200 and P300B (P3b) components as well as of the standard N100 and P200 components were determined. Sensory Gating Task [0158] The Sensory Gating task consists of 2 blocks of 150 paired click (brief noise burst) stimuli with a fixed 500-ms SOA and a fixed 4.0-s inter-trial interval. Both blocks were 80- dB SPL, 1-ms white noise stimulus. The participant sat comfortably with eyes open and listen to the series of stimuli. No responses were required. The amplitudes and associated latencies of the P50 and N100 components of the average ERPs for the first (S1) and the second stimuli (S2) were measured. Measurement were performed at the electrode with the maximal ERP component amplitude. Endpoints included but were not limited to P50 ratio (the ratio of P50 amplitude for S2 to S1) and the difference in amplitudes (S1−S2). Mismatch Negativity (MMN) with Duration Deviant Task [0159] In the MMN task, 1 standard tone (probability 0.9, 1000 Hz, 50-ms duration, 5-ms rise/fall time, 80-dB SPL) was presented binaurally through headphones with a constant interstimulus interval of 0.5 s, randomly interrupted by longer-duration deviant tone bursts (deviant tone, probability 0.1, 1000 Hz, 125 msec duration, 5 msec rise/fall time, 80 dB SPL). The total number of tone bursts presented was 1000, of which 100 were deviant tones. Total task duration was approximately 8.3 minutes. The participant was seated comfortably in a chair facing a monitor and viewed a slowly changing slide show of nature scenes (landscapes, animals). The participant was instructed to ignore the tones and to silently count the number of different nature scenes shown. No responses were required during the MMN task. The participant was asked to report the number of slide show scenes they counted; this number was recorded by the task software. Including an additional electrode on the nose was required for accurate identification of the MMN. Endpoints for the MMN task included but were not limited to N100 and P200 for standards and deviants, MMN and P3a for deviant-standard ERP difference waves, and peak amplitudes and latencies for each ERP component at the key electrode (location of maximum amplitude). Auditory Steady-State Response (ASSR) Task [0160] The ASSR task consisted of 2 blocks of 150 stimuli consisting of 500-ms trains of 1- ms white noise bursts (clicks) at 80 dB SPL with a fixed 1.0-s SOA. The participant sat comfortably with eyes open and listened to the series of click trains. No responses were required. Peak-to-peak amplitude in time domain, averaged wavelet amplitude (AVWT), and inter-trial phase coherence (ITPC) endpoints of the ASSR task were measured at the electrode with the maximal ASSR response. Endpoints included but were not limited to root mean square amplitude of the sustained portion of average ERP in time domain at the key electrode (location of maximum amplitude); the AVWT and ITPC of the sustained portion of the continuous Morlet wavelet based time-frequency average at the key electrode (location of maximum amplitude); and AVWT and ITPC, measured separately for the fundamental frequency and 2nd and 3rd harmonics of the response at the key electrode (location of maximum amplitude). Study design: [0161] This study was conducted in two study centers in the US.48 participants were randomized to receive study drug (Compound I or placebo). To minimize risk to participants, sentinel dosing was used for Cohort 1 and for any subsequent cohorts if the dose selected for that cohort was greater than that of any preceding cohort(s). For these cohorts, the first 3 participants were randomized (preferably all at 1 site) and dosed for ≥10 days. Randomization and dosing of the remainder of the respective cohort was allowed to begin if, per judgment of the Trial Safety and Data Review committees, no pattern of study drug- related AEs of concern had been reported (eg, serious and/or severe study drug-related TEAEs) in the sentinel participants. [0162] An investigator- and participant-blinded, placebo-controlled, randomized design was selected to provide comparable treatment groups and to minimize selection and investigator bias. Placebo was chosen as the control to determine the rate of spontaneously occurring treatment-emergent adverse events (TEAEs), and to reduce the potential for bias in the reporting of AEs. [0163] This study had a 14-day dosing period to explore the effects of Compound I compared with placebo control. In addition, the study included a Follow-up visit approximately 2 weeks after the final dose of study drug to monitor any AEs that were ongoing at the time of Check- out as well as any delayed-onset AEs. Two weeks represents an interval longer than 5 half- lives of the study drug. [0164] This study was designed to select participants with stable schizophrenia who were on a stable treatment regimens to increase the ability to detect effects associated with Compound I administration. See study design schematic below. The study was composed of three different phases: Screening phase: [0165] The Screening period began with the execution of the informed consent form (ICF). After signing the ICF, each participant’s study eligibility was assessed according to the Inclusion Criteria and Exclusion Criteria described below. Collection of adverse events (AEs) began after the ICF was signed and continued through the Follow-up period/discontinuation from the study (whichever occured first). [0166] After the Screening visit, participants who were eligible for enrollment had to begin complying with the Lifestyle Restrictions also detailed below. The end of the Screening period coincided with the start of the In-Clinic period. In-Clinic period: [0167] The In-Clinic period began on Day -3 when participants checked in to the study center and began undergoing baseline assessments. Those who remained eligible for study participation on Day 1 (there was no “Day 0”) were randomized and received their first QD dose of study drug (Compound I or placebo). Participants remained confined at the study center until they were discharged per investigator discretion on Day 15. Follow-up period: [0168] The Follow up period began immediately after participants were discharged from the study center on Day 15 and continued until the Follow-up visit was conducted. During this period, participants had to continue complying with all Lifestyle Restrictions. Study Schematic Dosage administration, randomization procedures: [0169] Participants who were eligible per the Inclusion Criteria were randomized on Day 1 to study drug in a 2:1 ratio (Compound I:placebo) via central randomization using an interactive voice/web response system (IWRS). The computer-generated randomization schedule was prepared by an independent statistician not otherwise associated with the study. [0170] Sentinel dosing was used. Sentinel participants were also randomized in a 2:1 ratio (Compound I:placebo). Cohorts 1 through 3 each included 12 participants (8 randomized to Compound I and 4 randomized to placebo) and the optional Cohort 4 also included 12 participants at the same randomization ratio and the same dose level as Cohort 3. Participants took their daily study drug dose each morning at a consistent time (preferably ±1 hour) throughout the In-Clinic period. Participants received study drug under medical supervision, directly from the investigator or study center designee who will examine the participant’s mouth to ensure that study drug was ingested. The study drug dose and the participant's identification was to be confirmed at the time of dosing by a member of the study site staff other than the person administering the study drug. [0171] Study drug could be taken with or without food. Because each dosage required the swallowing of multiple tablets, the tablets could be swallowed within a ≤10-minute period. Water could be consumed as needed. The date and time of each administered dose was recorded. Deviation(s) from the assigned regimen were recorded, including dates for dosing delays. Study drug and Dose Levels [0172] Compound I dose levels did not exceed 60 mg QD in this study. Dose levels indicated for Cohorts ≥2 could be substituted with lower or intermediate dose levels or with a dose level repeated from an earlier cohort, if warranted based on review of safety, PK, and other available data. Cohort 1 dosed active participants with 15 mg of an oral dosage form daily. Cohort 2 dosed them with 30 mg orally per day and Cohorts 3 and 4 dosed them with 60 mg orally per day. [0173] Compound I and Placebo to match Compound I tablets were used in this study. They were administered as white to off-white solid round tablets for oral administration, each with a unit dose strength of 5-mg per tablet. Cohort 1 participants were dosed with 15 mg QD Compound I (3×5-mg tablets) or 3×Placebo 5-mg tablets QD. Cohort 2 participants were dosed with 30 mg QD Compound I (6×5-mg tablets) or 6×Placebo 5-mg tablets QD. Cohort 3 participants were dosed with 60 mg QD (12×5-mg tablets) or 12×Placebo 5-mg tablets QD. Cohorts 4 and 5 (optional) TBD, not to exceed 60 mg QD [0174] The Trial Safety Committee (TSC) reviewed blinded safety data (AEs, clinical laboratory test results, vital signs, and 12-lead ECGs) and available, relevant, de-identified participant PK data on a cohort-by-cohort basis. For Cohorts 2 and 3, the TSC was to recommend proceeding either with dose escalation as planned or with a lower (repeated or intermediate) dose. For the optional Cohorts 4 and 5, the TSC was to recommend a dose level(s) that was not exceed 60 mg QD or the maximum dose tolerated in a preceding cohort, whichever was higher. [0175] Additionally, the DRC reviewed the blinded data and may also review unblinded safety data and available PK and PD data. If a recommendation of the DRC differed from that of TSC, the sponsor’s senior medical designee made a final decision. [0176] In all instances, escalation to a higher dose level was only allowed to proceed if ≥8 of the 12 participants in each of the preceding dose-level cohort(s) had completed all 14 days of dosing and only after review by the TSC and DRC. Escalation was not allowed to proceed if there was a pattern of AEs or other safety data that represented a potential safety or tolerability concern, with particular attention on symptomatic hypotension- and gastrointestinal-related AEs. [0177] The planned escalation from 15 to 30 to 60 mg QD across sequential cohorts of participants with stable schizophrenia on stable treatment regimens was supported by Compound I Phase 1 safety and PK data, nonclinical toxicology data, and the In-Clinic safety measures planned for the study. [0178] The 15-mg Compound I QD dose was selected for Cohort 1 based on safety, tolerability, PK, and PD data from repeated dosing at this level in two Phase 1 studies conducted in healthy adults aged 18 to 79 years. Among the healthy participants who received 15 mg Compound I QD for up to 15 days, there were no discontinuations due to AEs and no serious adverse events (SAEs) reported. All AEs were considered mild or moderate by the investigator. Across the Phase 1 studies, no safety concerns were identified. PK data were linear and were supportive of QD dosing, and were not impacted by food. Additionally, after 14 days of dosing in healthy elderly participants, 15 mg Compound I QD demonstrated modest impacts on neurophysiological parameters by EEG and no impact on cognitive performance measures. [0179] The higher 30- and 60-mg Compound I QD doses were selected to evaluate safety, tolerability, and the potential for greater PD activity of these higher dose levels in this new patient population, never before exposed to Compound I. Selection of these dose levels was supported by the clinical safety profile of the 15-mg Compound I QD regimen, which was well tolerated in healthy participants. The free plasma exposure levels after repeated dosing of 15 mg QD in a Phase 1b study had approximately a 2-fold margin below the no-observed- adverse-effectsdose level (NOAEL) determined in dogs in nonclinical toxicological with dosing of up to 90 days of oral administration; the anticipated exposure of the 30-mg QD clinical dose was expected to be approximately equivalent to the NOAEL. Nonclinical and clinical exposures were generally dose proportional, with a low volume of distribution and no accumulation observed after steady state. The main Compound I-related nonclinical findings were target-related BP decreases and compensatory increases in heart rate without arrythmias or ECG waveform changes, and gastrointestinal intolerability; the findings were observed to be reversible during the recovery phase of the studies. In the In-Clinic setting of this study, BP and gastrointestinal effects were monitored throughout the dosing period. Additionally, appropriate safety measures were planned, including sentinel dosing , within-cohort stopping rules, and between-cohort safety and PK data reviews so that potential new safety signals could be addressed appropriately . Participant Selection and Lifestyle Restrictions Inclusion Criteria [0180] Each participant had to meet each of the following criteria to be eligible for entering this study. [0181] 1. To have capacity per the opinion of the investigator, being willing and able to provide written consent for study participation, and signed ICF before any study procedure was performed. [0182] 2. Age between 18 to 50 years (inclusive) on the day of Consent. [0183] 3. Resident in a stable living situation, in the opinion of the investigator, for ≥12 weeks before Screening and expected to remain in a stable living situation for the duration of the study. [0184] 4. Body mass index of 18 to 40 kg/m ² . [0185] 5. Able to complete the cognitive battery on Day -3. [0186] 6. Fluent English speaker. [0187] 7. Diagnosed with schizophrenia as defined by the Mini-International Neuropsychiatric Interview (MINI) for Psychotic Disorders and the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). The initial diagnosis to be ≥1 year before Screening. The MINI was to be used to exclude comorbid diagnoses. [0188] 8. Evidence of stable schizophrenia symptomatology ≥3 months before Screening (eg, no hospitalizations for schizophrenia, no increase in level of psychiatric care due to worsening of schizophrenia symptoms). [0189] 9. No more than moderate (≤4) rating on any 1 of the following Positive and Negative Syndrome Scale (PANSS) items: delusions, conceptual disorganization, hallucinatory behavior, excitement, grandiosity, and suspiciousness/persecution, unusual thought content (P1, P2, P3, P4, P5, P6, G9, respectively); total PANSS score ≤70 at Screening and Check-in. [0190] 10. Receiving primary background atypical antipsychotic therapy (except clozapine) on a stable regimen for ≥6 weeks before Screening (and ≥8 weeks before Day -1), including concomitant psychotropic treatments. In addition: a. If taking long-acting injectable (LAI) antipsychotic(s), no dose change within 4 months before Screening; b. No increase in dose, and no more than 25% decrease in dose for tolerability; c. Permitted atypical antipsychotics and doses include the following: aripiprazole (10–30 mg/day; any dose of LAI monthly), brexpiprazole (1–4 mg/day), paliperidone (3–12 mg/day or any dose of LAI monthly or quarterly), risperidone (1–6 mg/day or any dose of LAI every 2 or 4 weeks), quetiapine (immediate release only; 150–300 mg/day), rurasidone (40–120 mg/day), olanzapine (10–20 mg/day); d. Second atypical antipsychotic was not required and was permitted only if used for a targeted symptom (eg insomnia) or for an adverse effect from the primary maintenance antipsychotic treatment. A second atypical antipsychotic was prohibited if used for refractory psychotic symptoms. Treatment regimen stability and dose ranges as defined above apply to the second antipsychotic also. Participant should be taking no more than 2 antipsychotics; e. Note: Hypnotics are an exception to the treatment regimen stability requirement; prohibited hypnotics may be substituted with allowed hypnotics. [0191] 11. If female, met 1 of the 2 following: a. Confirmed as being not of reproductive potential or b. If of reproductive potential: not breastfeeding at the time of the Screening visit, negative serum pregnancy test results at the Screening visit and at Check-in, and agreed to use effective contraception for the study duration and for ≥90 days after taking the final study drug dose. [0192] 12. Male and female participants of reproductive potential must have agree to use effective contraception methods starting from the date of signing the ICF until ≥90 days after taking his/her final study drug dose. [0193] 13. If male, must have agreed to refrain from donating sperm from the Screening visit through 90 days after the final dose of study drug. [0194] 14. Agreed to not receive an investigational therapy or device in any other study while participating in this study until after the Follow-up visit. [0195] 15. Agreed to adhere to all study requirements, including lifestyle restrictions. Exclusion Criteria [0196] A participant who met any one of the following criteria was excluded from entering this study. [0197] 1. Participated in other study of an investigational drug within 60 days or 5 half-lives (whichever is longer) of that drug before Randomization. [0198] 2. Within 3 months of Check-in: participated in a trial using the MATRICS™ Consensus Cognitive Battery (MCCB™) or a Cogstate battery. [0199] 3. Within 6 months before Check-in: a. received electroconvulsive therapy –or– b. participated in cognitive remediation therapy. [0200] 4. Had ever received Compound I in a clinical study. [0201] 5. Positive drug or alcohol screen at Screening or at Check-in for disallowed substances, including amphetamines, barbiturates, cocaine, marijuana, methadone, methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA), phencyclidine, or nonprescribed benzodiazepines or opiates. Note: Individuals testing positive for marijuana or other cannabinoids at Screening or at Check-in may be eligible for the study provided that the investigator’s clinical assessment (after consultation with and approval from the sponsor/designee) indicates that the participant is not a regular user of marijuana. Under thiscircumstance, a urine dipstick drug screen will be performed at Check-in; results must be negative to be eligible for Randomization. [0202] 6. Had any of the following per DSM-5: a. Diagnosis of schizoaffective disorder per the MINI for Psychotic Disorders; b. Recent (within 6 months before Screening) diagnosis of major depressive episode, manic and hypomanic episode, panic disorder, agoraphobia, social anxiety disorder, obsessive-compulsive disorder, posttraumatic stress disorder, and/or generalized anxiety disorder per the MINI for Psychotic Disorders; c. Lifetime diagnosis of antisocial personality disorder, anorexia nervosa, bulimia nervosa, and/or binge-eating disorder per the MINI for Psychotic Disorders; d. Diagnosis of moderate or severe substance use disorder (excluding nicotine dependence) per the MINI for Psychotic Disorders within 12 months before Screening; e. Diagnosis of intellectual disability (intellectual developmental disorder) or mental retardation or borderline IQ (per medical history and investigator discretion; IQ test not required). [0203] 7. Any severe, acute, or chronic medical or psychiatric condition or laboratory abnormality that may increase the risk associated with study participation or study drug administration or that may interfere with the interpretation of study results and, in the judgment of the investigator, would make the individual inappropriate for study entry. [0204] 8. History of seizures or of a condition with risk of seizures. Exception: History of 1 febrile seizure in childhood. [0205] 9. Lifetime history of head injury with clinically significant sequelae (eg, loss of consciousness for >15 minutes). [0206] 10. History of neuroleptic malignant syndrome as determined by the investigator. [0207] 11. Significant extrapyramidal symptoms that have not been stabilized with anticholinergics at a dose not greater than the equivalent of 1 mg benztropine twice daily. [0208] 12. Considered by the investigator to be at imminent risk of suicide or injury to self, others, or property, or has attempted suicide within the past year before Screening. Note: Individuals with positive answers on Item 4 or 5 on the Columbia-Suicide Severity Rating Scale (C-SSRS) in the 12 months before Screening (“Baseline” version) and/or at Check-in (“Since Last Visit” version) will be excluded. [0209] 13. Onset of symptoms of schizophrenia before the age of 12. [0210] 14. History of resistance to antipsychotic treatment as determined by either of the following: a. failed to show even minimal response to ≥2 antipsychotic medications given at dose range listed in approved product labeling for adequate length of time (failure to tolerate a medication does not constitute failure to respond) –or–b. history of treatment with clozapine for refractory psychosis. [0211] 15. Use of clozapine within 1 year before Screening. [0212] 16. Current use of prohibited treatment. Note: Psychotropic treatments other than hypnotics cannot be discontinued to address this criterion, due to treatment regimen stability requirements. [0213] 17. History in the 3 months before Day -3 of heavy smoking (>40 cigarettes/2 packs/day) or nicotine replacement therapy (eg, nicotine patches, Chantix, or similar therapeutic agent). [0214] 18. Would be unable to refrain from using nicotine and/or caffeine for approximately 1.5 hours before each cognitive and electroencephalography (EEG) assessment. [0215] 19. Supine systolic BP ≤90 mmHg or >160 mmHg, or diastolic BP ≤60 mmHg or >100 mmHg at Screening or Check-in (Each supine BP value recorded was the average of 3 consecutive readings measured at intervals of ≥1 minute). [0216] 20. Orthostatic hypotension, defined as a decrease in systolic BP of ≥20 mmHg or a decrease in diastolic BP of ≥10 mmHg when measured 3 (-1) minutes after assuming a standing position from a sitting position. [0217] 21. Clinically significant cardiac involvement or an ECG with corrected QT interval using Fridericia’s formula (QTcF interval) >450 ms for men or >470 ms for women. Note: If the first ECG QTcF interval obtained is out of range, the ECG should be repeated twice; the average of the 3 results should be used to determine eligibility. [0218] 22. History of platelet dysfunction, hemophilia, von Willebrand disease, coagulation disorder, other bleeding diathesis condition(s), or significant, nontraumatic bleeding episode(s). [0219] 23. Donated or lost >500 mL blood within 3 months of the Screening visit and/or donated any plasma within 2 weeks of the Screening visit [0220] 24. Positive results on hepatitis panel (hepatitis B surface antigen, hepatitis B core antigen antibody, the antihepatitis C virus), and/or the human immunodeficiency virus antibody [0221] 25. Visual impairment that may affect the ability to complete study assessments as determined by the investigator, or auditory impairment as determined by a hearing screen [0222] 26. Clinically significant hypersensitivity or allergy to any of the inactive ingredients contained in the active or placebo drug product (lactose monohydrate, microcrystalline, cellulose, croscarmellose sodium, silicon dioxide, magnesium stearate, talc, polyethylene glycol, polyvinyl alcohol, and titanium dioxide). [0223] 27. Study center staff member directly involved in the conduct of this study or otherwise supervised by the investigator, or sponsor employee directly involved in the conduct of the study, or family member of any of these individuals Lifestyle restrictions Meals and Diet [0224] Participants were to fast (water was allowed) for at least 4 hours before clinical laboratory assessments except the Screening visit. Caffeine, Tobacco/Nicotine, and Alcohol [0225] Participants were not allowed to consume any caffeine-containing products (eg, coffee, tea, cola drinks, chocolate) for approximately 1.5 hours before each cognitive and event-related potential (ERP) / quantitative electroencephalography (qEEG) / sleep EEG assessment until completion of the assessment. Daily caffeine intake (including time, type, and estimated amount) was collected during the In-Clinic period and at the Follow-up visit. Participants were also not allowed to consume alcohol within 24 hours of the Screening and Follow-up visits. Consumption of alcohol was not permitted at all during the In-Clinic period. Concomitant Drugs/Combination therapy and Prohibited Medications and Supplements [0226] Any medication or vaccine (including over-the-counter or prescription medicines, recreational drugs, vitamins, and/or herbal supplements, or other specific categories of interest) that the participant received/used was recorded along with the reason for use, the dates of administration including start and end dates and the dosage information including dose and frequency. Therapies, medications, vaccinations, surgeries, etc., administered to the participant before initiation of study drug were differentiated from concomitant therapies (those administered after initiation of study drug) to facilitate understanding of any AEs that occured after the start of study drug. [0227] Participants were not permitted to initiate the use of additional medications (including nonprescription “overthe-counter” preparations) for treatment of schizophrenia during the study other than the study drug, with the exception of the medications allowed as indicated below. [0228] Caffeine and/or tobacco/nicotine use was be recorded on a daily basis during the In- Clinic period and at the Follow-up visit. Details included time, type/form (eg, coffee, cola, chocolate, cigarette, e-cigarette, patch), and estimated amount. Prohibited Medications and Supplements [0229] The following drugs, classes of drugs, and supplements are prohibited as concomitant treatments after the Screening visit through the Follow-up visit, unless noted otherwise. [0230] COVID-19 vaccine doses were prohibited within 4 days before Check-in on Day -3 until after Check out on Day 15 Enrollment/check in of participants who required a second vaccine dose should be timed accordingly. The vaccination was recorded as medical history if administered before Check-in, and as a concomitant medication if administered during the Follow-up period. [0231] Other sGC stimulators, including riociguat and vericiguat; specific inhibitors of phosphodiesterase 5 (PDE5), including sildenafil, tadalafil, vardenafil; nonspecific inhibitors of PDE5, including dipyridamole, theophylline; any supplement for the treatment of erectile dysfunction; nitrates such as nitroglycerin, isosorbide mononitrate, isosorbide dinitrate, sodium nitroprusside, amyl nitrate; aspirin ≥325 mg/day; any anticoagulant medication; any P2Y12 inhibitor, including cangrelor, clopidogrel, prasugrel, ticagrelor, ticlopidine; any “illicit drug” beginning 1 month before Screening through the Follow-up visit; marijuana or other cannibinoids (regardless of whether legal or prescribed); BCRP (breast cancer- resistance protein) substrates as Compound I may have the potential to increase the exposures of these medications (Examples of BCRP substrates include azidothymidine, bisantrene, camptothecin derivates, canertinib, cimetidine, diflomotecan, flavopiridol, gefitinib, glyburide, imatinib mesylate, indolocarbazole, irinotecan, lamivudine, lapatinib, methotrexate, mitoxantrone, nilotinib, nitrofurantoin, pantoprazole, prazosin, rosuvastatin, SN-38, sulfasalazine, and topotecan; inhibitors of BCRP transporters, including curcumin, cyclosporine A, eltrombopag [0232] Other Prohibited Medications in this trial included typical (ie, first-generation) antipsychotic treatment, including but not limited to prochlorperazine, haloperidol, loxapine, thioridazine, molindone, thiothixene, pimozide, fluphenazine, trifluoperazine, chlorpromazine, and perphenazine; treatment with clozapine; treatment with anticholinergic activity medication, including but not limited to hydroxyzine, hyoscyamine, methscopolamine, scopolamine, amitriptyline, imipramine, doxepin, diphenhydramine, atropine, cyclobenzaprine hydrochloride, orphenadrine citrate, benztropine mesylate, and trihexyphenidyl (Note that treatment with anticholinergics for extrapyramidal motor symptoms was permitted at not more than the equivalent of 1 mg benztropine twice daily.); antidepressants; anticonvulsants, including but not limited to valproate, carbamazepine, phenytoin, oxycarbamazepine, and phenobarbital (note that pregabalin and gabapentin were permitted if not being used as antiseizure treatments—a stable regimen must be followed for ≥2 months before Screening and maintained throughout study treatment); antiemetics with dopamine antagonist action (eg, metaclopramide, prochlorperazine); herbal supplements (must be discontinued ≥28 days before Day 1) or Lithium. Permitted Medications and Supplements Maintenance Schizophrenia Treatment [0233] All efforts should be made to maintain background permitted psychotropic medications (see Inclusion 10) at consistent doses throughout the In-Clinic period. Permitted exceptions to this rule include the following: in the case of primary background antipsychotic medication, minor adjustments (no increase; ≤25% decrease) were permitted to manage drug- specific tolerability issues if required to support the participant’s continued study participation. Rescue Medications [0234] Use of the following rescue medications was permitted, with the stated caveats and limitations:treatment of insomnia as needed was permitted with nonbenzodiazepine hypnotics (eg, zolpidem up to 10 mg/day, zaleplon up to 20 mg/day, or eszopiclone up to 3 mg/day) within their respective recommended dose ranges, but these medications could not be taken within 12 hours before EEG and/or cognitive performance assessments; treatment of anxiety or agitation as needed was permitted with up to 2 mg/day lorazepam (or the equivalent dose of another benzodiazepine) up to 3× per week, but could not be taken within 12 hours before EEG and/or cognitive performance assessments; treatment of extrapyramidal motor symptoms as needed was permitted with up to 2 mg/day benztropine (or the equivalent dose of another anticholinergic), up to 2× per week, but could not be taken within 12 hours before EEG and/or cognitive performance assessments; occasional use of an additional dose of the background antipsychotic medication, as sometimes occurs during standard-of-care treatment was also permitted. Baseline characteristics [0235] Patients enrolled in this trial were on backgrounds of a single anti-psychotic regimen and they had been stably on it for at least 8 weeks. The anti-psychotics they were on included, but were not limited to aripiprazole, paliperidone, risperidone or quetiapine and olanzapine. A large proportion of the patients were African-American (79%) and the remaining where white (21%).23 % were Hispanic or latino. The means age of the patients was 36.7 years old. The means BMI was 29.5. the mean number of years since diagnosis was about 15 years. The means PANSS score was about 55. The means cognitive composite score at baseline was consistent with chronic schizophrenia (means is approximately 0.5-2 standard deviations lower than that of age-matched controls from a normative database). [0236] Patients in this trial were on the following background antipsychotics: risperidone 21 (43.8 %) aripiprazole 13 (27.1 %) quetiapine 9 (18.8 %) paliperidone 3 (6.3 %) olanzapine 2 (4.2 %) Study Assessments/Results a) Safety [0237] Compound I was found to be safe and well tolerated in participants with schizophrenia on standard-of care medications up to 60 mg daily. No SAEs, or severe AEs or treatment discontinuations as a result of AEs were observed. The most common AE was headache. No safety signals were observed on clinical labs, vital signs, ECGs, PANSS, SAS, AIMS, BARS or C-SSRS. b) Pharmacokinetics [0238] PK at 15 mg was consistent with clinical predictions based on previous clinical trial, with approximately dose proportional exposure at 30 and 60 mg. Intersubject variability was fairly low. Accumulation of about three times was similar across all dose levels. The patients were at or near steady state by Day 13. c) Pharmacodynamics i) Biomarkers [0239] Inflammatory biomarkers were measured in plasma as part of the comprehensive InflammationMAP® panel. MAP stands for Multi-Analyte profile. Table I below summarizes the observed effect sizes for changes observed on some relevant biomarkers. A negative effect size is associated with a reduction and a positive effect size with an increase. ii) Cognitive Assessments [0240] The mean difference from placebo in the CSB general cognition composite score for the 15mg dose in this population was consistent with a strong procognitive profile of Compound I. [0241] Effect sizes in this assessment are described as (Mean CFB Compound I- mean CFB placebo)/pooled baseline SD. Where CFB (change from baseline) was in the Cogstate Schizophrenia Battery measured with a MMRM analysis. [0242] Positive effects relative to placebo were observed on general cognition at 15 mg, but not at 30 or 60 mg. The positive effect observed at 15 mg, was positive in both the memory and executive function domains, but little effect was observed in attention. Even though a positive effect was not observed in general cognition at 30 and 60 mg, positive effects were observed at these doses in the domains of memory (with both 30 and 60 mg). No effect in executive function was observed at 30 and 60 mg. A negative effect was observed in the psychomotor attention domain at 30 and 60 mg. [0243] General cognition, as measured by the change from baseline in Cogstate Schizophrenia Battery composite score, increased over14 days of dosing with, with an effect size of 0.60 at day 14. The cognitive performance at 15 mg improved over time from day 2, to 7 and then 14. This effect is consistent with the PK observations, as levels of drug are increasing and finally achieve steady state before day 14.