FORMULATIONS AND METHODS OF TREATING CONDITIONS RELATED TO THE S1P ₁ RECEPTOR Provided are formulations and methods useful in the treatment of sphingosine 1-phosphate subtype 1 (S1P ₁ or S1P ₁ ) receptor-associated disorders. The sphingosine-1-phosphate (S1P) receptors 1-5 constitute a family of G protein-coupled receptors with a seven-transmembrane domain. These receptors, referred to as S1P ₁ to S1P ₅ (formerly termed endothelial differentiation gene (EDG) receptor-1, -5, -3, -6, and -8, respectively; Chun et al., Pharmacological Reviews, 54:265-269, 2002), are activated via binding by sphingosine-1-phosphate, which is produced by the sphingosine kinase-catalyzed phosphorylation of sphingosine. S1P ₁ , S1P ₄ , and S1P5 receptors activate Gi but not Gq, whereas S1P ₂ and S1P ₃ receptors activate both Gi and Gq. The S1P3 receptor, but not the S1P ₁ receptor, responds to an agonist with an increase in intracellular calcium. In view of the growing demand for S1Pl agonists useful in the treatment of S1P ₁ receptor- associated disorders, the compound (R)-2-(7-(4-cyclopentyl-3-(trifluoromethyl)benzyloxy)-1,2,3, 4- tetrahydrocyclopenta[b]indol-3-yl)acetic acid (Compound 1, APD334) , or a pharmaceutically acceptable salt, solvate, or hydrate thereof, has emerged as an important new compound, see PCT patent application, Serial No. PCT/US2009/004265 hereby incorporated by reference in its entirety. Compound 1, or a pharmaceutically acceptable salt, solvate, or hydrate thereof, is an investigational drug candidate intended for the treatment of sphingosine 1-phosphate subtype 1 (S1P ₁ ) receptor-associated disorders. Processes for manufacturing and crystalline forms of Compound 1, or a pharmaceutically acceptable salt, solvate, or hydrate thereof, are also disclosed within PCT patent application Serial No. PCT/US2011/000153, which is incorporated by reference in its entirety, specifically, for example, Figures 5 – 8 and the related disclosure contained therein. Many S1P ₁ agonists cause side effects, and particularly cardiovascular-related adverse events, that may require that doctors titrate patients slowly to a maintenance dose. This titration period can take weeks or even a month. The complexity and length of the titration regimen may result in prematurely discontinuing therapy by patients prior to reaching the maintenance dose or result in doctors preferring other therapeutic options. There exists a need for effectively treating individuals who are in need of treatment with Compound 1, or a pharmaceutically acceptable salt, solvate, or hydrate thereof. The present disclosure satisfies this need and provides related advantages as well. Citation of any reference throughout this application is not to be construed as an admission that such reference is prior art to the present application. SUMMARY Provided is a method of treatment of a sphingosine 1-phosphate subtype 1 ( S1P ₁ ) receptor- associated disorder comprising: administering to an individual in need thereof a therapeutically effective amount of (R)-2- (7-(4-cyclopentyl-3-(trifluoromethyl)benzyloxy)-1,2,3,4-tetr ahydrocyclopenta[b]indol-3-yl)acetic acid (Compound 1), or a pharmaceutically acceptable salt, hydrate, or solvate thereof, where the individual is Japanese. Also provided is a method of treatment of a sphingosine 1-phosphate subtype 1 (S1P1) receptor- associated disorder comprising: administering to an individual in need thereof a therapeutically effective amount of (R)-2- (7-(4-cyclopentyl-3-(trifluoromethyl)benzyloxy)-1,2,3,4-tetr ahydrocyclopenta[b]indol-3-yl)acetic acid (Compound 1), or a pharmaceutically acceptable salt, hydrate, or solvate thereof, where the individual has a body mass index (BMI) less than about 25. These and other aspects of the invention disclosed herein will be set forth in greater detail as the patent disclosure proceeds. BRIEF DESCRIPTION OF DRAWINGS Figure 1: Panel A shows mean lymphocyte count over time. Panel B shows change from baseline lymphocyte count (%) over time. DETAILED DESCRIPTION As used in the present specification, the following words and phrases are generally intended to have the meanings as set forth below, except to the extent that the context in which they are used indicates otherwise. COMPOUND 1: As used herein, “Compound 1” means (R)-2-(7-(4-cyclopentyl-3- (trifluoromethyl)benzyloxy)-1,2,3,4-tetrahydrocyclopenta[b]i ndol-3-yl)acetic acid including crystalline forms thereof. As a non-limiting example, Compound 1 may be present as an anhydrous, non-solvated crystalline form as described in WO 2010/011316 (incorporated by reference herein in its entirety). As another non-limiting example, an L-arginine salt of Compound 1 may be present as an anhydrous, non- solvated crystalline form as described in WO 2010/011316 and WO 2011/094008 (each of which is incorporated by reference herein in its entirety). As another non-limiting example, a calcium salt of Compound 1 may be present as a crystalline form as described in WO 2010/011316 (incorporated by reference herein in its entirety). Compound 1, or a pharmaceutically acceptable salt, solvate, or hydrate thereof, is an orally administered, selective, synthetic sphingosine 1-phosphate (S1P) receptor 1, 4, 5 modulator. To date, Compound 1, or a pharmaceutically acceptable salt, solvate, or hydrate thereof, has been found to be safe and well-tolerated in approximately 281 adult subjects treated at various doses. Its safety and tolerability have been evaluated in Phase 1 studies with healthy adult subjects at single doses up to 5 mg and repeated doses up to 4 mg once daily (QD). In a Phase 2 dose-ranging study in UC patients, treatment with 2 mg QD for 12 weeks led to clinically meaningful and statistically significant endoscopic and symptomatic improvements versus placebo. Sustained beneficial effects of were observed for up to 46 weeks in the subsequent open-label extension study. Compound 1 may also be referred to as etrasimod (CAS Registry No.1206123-37-6). A pharmaceutically acceptable salt of Compound 1 includes the L-arginine salt of Compound 1, which may be referred to etrasimod arginine (CAS Registry No.1206123-97-8). ADMINISTERING: As used herein, “administering” means to provide a compound or other therapy, remedy, or treatment such that an individual internalizes a compound. PRESCRIBING: As used herein, “prescribing” means to order, authorize, or recommend the use of a drug or other therapy, remedy, or treatment. In some embodiments, a health care practitioner can orally advise, recommend, or authorize the use of a compound, dosage regimen or other treatment to an individual. In this case the health care practitioner may or may not provide a prescription for the compound, dosage regimen, or treatment. Further, the health care practitioner may or may not provide the recommended compound or treatment. For example, the health care practitioner can advise the individual where to obtain the compound without providing the compound. In some embodiments, a health care practitioner can provide a prescription for the compound, dosage regimen, or treatment to the individual. For example, a health care practitioner can give a written or oral prescription to an individual. A prescription can be written on paper or on electronic media such as a computer file, for example, on a hand-held computer device. For example, a health care practitioner can transform a piece of paper or electronic media with a prescription for a compound, dosage regimen, or treatment. In addition, a prescription can be called in (oral), faxed in (written), or submitted electronically via the internet to a pharmacy or a dispensary. In some embodiments, a sample of the compound or treatment can be given to the individual. As used herein, giving a sample of a compound constitutes an implicit prescription for the compound. Different health care systems around the world use different methods for prescribing and/or administering compounds or treatments and these methods are encompassed by the disclosure. A prescription can include, for example, an individual’s name and/or identifying information such as date of birth. In addition, for example, a prescription can include: the medication name, medication strength, dose, frequency of administration, route of administration, number or amount to be dispensed, number of refills, physician name, physician signature, and the like. Further, for example, a prescription can include a DEA number and/or state number. A healthcare practitioner can include, for example, a physician, nurse, nurse practitioner, or other related health care professional who can prescribe or administer compounds (drugs) for the treatment of a sphingosine 1-phosphate subtype 1 (S1P1) receptor-associated disorder. In addition, a healthcare practitioner can include anyone who can recommend, prescribe, administer, or prevent an individual from receiving a compound or drug including, for example, an insurance provider. PREVENT, PREVENTING, OR PREVENTION: As used herein, the term “prevent,” “preventing”, or “prevention” such as prevention of a sphingosine 1-phosphate subtype 1 (S1P1) receptor- associated disorder or the occurrence or onset of one or more symptoms associated with the particular disorder and does not necessarily mean the complete prevention of the disorder. For example, the term “prevent,” “preventing” and “prevention” means the administration of therapy on a prophylactic or preventative basis to an individual who may ultimately manifest at least one symptom of a disease or condition but who has not yet done so. Such individuals can be identified on the basis of risk factors that are known to correlate with the subsequent occurrence of the disease. Alternatively, prevention therapy can be administered without prior identification of a risk factor, as a prophylactic measure. Delaying the onset of at least one symptom can also be considered prevention or prophylaxis. TREAT, TREATING, OR TREATMENT: As used herein the term “treat,” “treating”, or “treatment” means the administration of therapy to an individual who already manifests at least one symptom of a disease or condition or who has previously manifested at least one symptom of a disease or condition. For example, “treating” can include alleviating, abating or ameliorating a disease or one or more condition symptoms, preventing one or more additional symptoms, ameliorating the underlying metabolic causes of one or more symptoms, inhibiting the disease or condition, e.g., arresting the development of the disease or condition, relieving the disease or condition, causing regression of the disease or condition, relieving a condition caused by the disease or condition, or stopping one or more of the symptoms of the disease or condition. For example, the term “treating” in reference to a disorder means a reduction in severity of one or more symptoms associated with that particular disorder. Therefore, treating a disorder does not necessarily mean a reduction in severity of all symptoms associated with a disorder and does not necessarily mean a complete reduction in the severity of one or more symptoms associated with a disorder. TOLERATE: As used herein, an individual is said to “tolerate” a dose of a compound if administration of that dose to that individual does not result in an unacceptable adverse event or an unacceptable combination of adverse events. One of skill in the art will appreciate that tolerance is a subjective measure and that what may be tolerable to one individual may not be tolerable to a different individual. For example, one individual may not be able to tolerate headache, whereas a second individual may find headache tolerable but is not able to tolerate vomiting, whereas for a third individual, either headache alone or vomiting alone is tolerable, but the individual is not able to tolerate the combination of headache and vomiting, even if the severity of each is less than when experienced alone. ADVERSE EVENT: As used herein, an “adverse event” is an untoward medical occurrence that is associated with treatment with Compound 1 or a pharmaceutically acceptable salt, solvate, or hydrate thereof. In one embodiment, an adverse event is selected from: leukopenia, constipation, diarrhea, nausea, abdominal pain, neutropenia, vomiting, back pain, and menstrual disorder. In one embodiment, an adverse event is heart block, for example, a first-degree atrioventricular heart block. In one embodiment, an adverse event is an acute heart rate reduction. In one embodiment, an adverse event is an abnormal pulmonary function test finding, such as an FEV1 below 80%, FVC. In one embodiment, an adverse event is an abnormal liver function test, such as an elevated ALT & AST>2X ULN. In one embodiment, an adverse event is macular edema. IN NEED OF TREATMENT and IN NEED THEREOF: As used herein, “in need of treatment” and “in need thereof” when referring to treatment are used interchangeably to mean a judgment made by a caregiver (e.g. physician, nurse, nurse practitioner, etc. in the case of humans) that an individual requires or will benefit from treatment. This judgment is made based on a variety of factors that are in the realm of a caregiver’s expertise, but that includes the knowledge that the individual is ill, or will become ill, as the result of a disease, condition or disorder that is treatable by the compounds of the invention. Accordingly, the compounds of the invention can be used in a protective or preventive manner; or compounds of the invention can be used to alleviate, inhibit or ameliorate the disease, condition or disorder. JAPANESE: As used herein, “Japanese” generally refers to an individual or individuals of Japanese descent. In some embodiments, the individual was born in Japan. In some embodiments, both of the individual’s biological parents and all four grandparents are Japanese. In some embodiments, the individual has lived no longer than 10 years outside of Japan. In some embodiments, the individual has lived no longer than 10 years outside of Japan and has had no significant change in lifestyle, including diet, since leaving Japan. BODY MASS INDEX (BMI): As used herein, “body mass index” or “BMI” refers to a measure of body fat based on height and weight that applies to adult men and women. BMI is calculated by dividing body weight (kg) by height squared (m ² ). Thus, the units of BMI are kg/m ² . Normal is defined as a BMI in the range of 18.5-24.9 kg/m ² . Underweight is defined <18.5 kg/ m ² . In some embodiments, the individual has a BMI of less than, or less than about, 25, 24.5, 24, 23.5, 23, 22.5, 22, 21.5, 21, 20.5, 20, 19.5, 19, or 18.5 kg/m ² . In some embodiments, the individual has a BMI of less than, or less than about, 25 kg/ m ² . In some embodiments, the individual has a BMI of less than, or less than about, 18.5 kg/ m ² . In some embodiments, the individual has a BMI of, or of about, 25, 24.5, 24, 23.5, 23, 22.5, 22, 21.5, 21, 20.5, 20, 19.5, 19, or 18.5 kg/m ² . DESENSITIZATION: As used herein, “desensitization” refers to induction of sustained sphingosine 1-phosphate receptor subtype 1 (S1P1) internalization by Compound 1. Prior to S1P1 internalization/desensitization, agonism of this receptor with Compound 1 may lead to activation of G protein-coupled inwardly rectifying potassium channels that regulate heart rate. DESENSITIZATION OF THE HEART: As used herein, “desensitization of the heart" refers to the absence of an acute heart rate reduction after drug administration. ACUTE HEART RATE REDUCTION: As used herein, “acute heart rate reduction” means a heart rate decrease from normal sinus rhythm of, for example, 10 or more beats per minute (bpm). NORMAL SINUS RHYTHM: As used herein, “normal sinus rhythm” means the sinus rhythm of the individual when not undergoing treatment. The evaluation of normal sinus rhythm is within the ability of a physician. A normal sinus rhythm will generally give rise to a heart rate in the range from 60- 100 bpm. DOSE: As used herein, “dose” means a quantity of Compound 1, or a pharmaceutically acceptable salt, solvate, or hydrate thereof, given to the individual for treating or preventing the disease or disorder at one specific time. MAYO CLINIC SCORE (MCS): As used herein, “Mayo Clinic Score” or “MCS” means an instrument designed to measure disease activity of ulcerative colitis and consists of up to 4 subscores: stool frequency, rectal bleeding, findings of flexible proctosigmoidoscopy, and physician global assessment with each component ranging from 0 to 3 (0=normal, 1=mild, 2=moderate, 3=severe). Total score therefore ranges from 0 to 12, with a higher score indicating more severe disease. The 6-point Mayo score is based on stool frequency and rectal bleeding PROs collected daily using electronic patient diaries and excludes the findings on endoscopy and the physician’s global assessment. The 3-point Mayo score is based on stool frequency, rectal bleeding, and findings on endoscopy and has a total score ranging from 0 to 9. The 2-point Mayo score is based on rectal bleeding and findings on endoscopy and has a total score ranging from 0 to 6. The physician’s global assessment acknowledges the three other criteria findings of the MCS, the individual’s daily record of abdominal discomfort and general sense of well-being, and other observations, such as physical findings and the individual’s performance. MILDLY TO MODERATELY ACTIVE ULCERATIVE COLITIS: As used herein, “mildly to moderately active ulcerative colitis” means ulcerative colitis characterized by a 4-component MCS of 4 to 10. MODERATELY TO SEVERELY ACTIVE ULCERATIVE COLITIS: As used herein, “moderately to severely active ulcerative colitis” means ulcerative colitis characterized by a 3-component MCS of 4 to 9 including an endoscopic subscore of ≥ 2 and a rectal bleeding score of ≥ 1. The 3- component MCS uses 3 of the 4 components of the complete MCS (endoscopic findings, rectal bleeding, and stool frequency). CLINICAL REMISSION: As used herein, “clinical remission” with respect to ulcerative colitis means a 3-component Mayo Clinic score as follows: an endoscopy score (using flexible proctosigmoidoscopy) of 0 or 1, a rectal bleeding score of 0, and a stool frequency score of 0 or 1 with a decrease of ≥ 1 point from baseline subscore. CLINICAL RESPONSE: As used herein, “clinical response” with respect to ulcerative colitis means a reduction in the 3-component Mayo Clinic score of ≥ 2 points and a decrease of ≥ 30% from baseline with an accompanying decrease in rectal bleeding subscore of ≥ 1 or absolute rectal bleeding score of 0 or 1. ENDOSCOPIC IMPROVEMENT: As used herein, “endoscopic improvement” with respect to ulcerative colitis means ulcerative colitis characterized by a Mayo endoscopic subscore (using findings of flexible proctosigmoidoscopy) of ≤ 1 point. ENDOSCOPIC REMISSION: As used herein, “endoscopic remission” with respect to ulcerative colitis means ulcerative colitis characterized by findings from flexible proctosigmoidoscopy subscore of the Mayo Clinic score = 0. IMPROVEMENT IN RECTAL BLEEDING: As used herein, “improvement in rectal bleeding” with respect to ulcerative colitis means a change from baseline < 0. HISTOLOGIC HEALING: As used herein, “histologic healing” with respect to ulcerative colitis means a score of < 3.1 on the Geboes Index. IMPROVEMENT IN STOOL FREQUENCY: As used herein, “improvement in stool frequency” with respect to ulcerative colitis means a change from baseline < 0. PHARMACEUTICAL COMPOSITION: As used here, “pharmaceutical composition” means a composition comprising at least one active ingredient, such as Compound 1; including but not limited to, salts, solvates, and hydrates of Compound 1, whereby the composition is amenable to investigation for a specified, efficacious outcome in a mammal (for example, without limitation, a human). Those of ordinary skill in the art will understand and appreciate the techniques appropriate for determining whether an active ingredient has a desired efficacious outcome based upon the needs of the artisan. EOSINOPHILIC ESOPHAGITIS: As used herein, “eosinophilic esophagitis” or “EoE” means an inflammatory disease characterized by abnormal eosinophilic inflammation within the esophagus and esophageal dysfunction. The primary symptoms of EoE include, but are not limited to, chest and abdominal pain, dysphagia, heartburn, food refusal, vomiting and food impaction. The clinicopathology of EoE is characterized by presence of ridges or trachea-like rings in the esophageal wall and eosinophilic infiltration in the esophageal mucosa. EoE is presently diagnosed by endoscopy of the esophagus followed by microscopic and biochemical analysis of the esophageal mucosal lining. EoE may be classified as allergic or non-allergic depending upon the status of the subject. The present invention includes methods to treat both allergic and non-allergic forms of EoE. ESOPHAGEAL STRICTURES: As used herein, esophageal strictures can be classified as simple or complex, based on their diameter and associated anatomic abnormalities. A simple stricture is defined as a short stricture with a symmetric or concentric lumen and a diameter of ≥12 mm that can be traversed easily with an endoscope. A complex stricture is usually longer than 2 cm, may be angulated or irregular, and has a diameter of <12 mm. It may be associated with a large hiatal hernia, esophageal diverticula, or tracheoesophageal fistula. Complex strictures have a higher rate of recurrence and an increased risk for dilation-related adverse events, compared with simple strictures. The severity of a stricture can be estimated by the resistance encountered with passage of the diagnostic endoscope, which has a typical external diameter of 9 mm. A mild stricture allows passage of the endoscope without resistance, a moderate stricture offers increased resistance, whereas a severe stricture may not be traversable. ALLERGEN: As used herein, "allergen," means any substance, chemical, particle or composition which is capable of stimulating an allergic response in a susceptible individual. Allergens may be contained within or derived from a food item such as, e.g., dairy products (e.g., cow's milk), egg, wheat, soy, corn, rye, fish, shellfish, peanuts and tree nuts. Alternatively, an allergen may be contained within or derived from a non-food item such as, e.g., dust (e.g., containing dust mite), pollen, insect venom (e.g., venom of bees, wasps, mosquitoes, etc.), mold, animal dander, latex, medication, drugs, ragweed, grass and birch. ALLERGIC RESPONSE or ALLERGIC REACTION or ALLERGIC SYMPTOM: As used herein, the phrases "allergic response," "allergic reaction," "allergic symptom," and the like, include one or more signs or symptoms selected from urticaria (e.g., hives), angioedema, rhinitis, asthma, vomiting, sneezing, runny nose, sinus inflammation, watery eyes, wheezing, bronchospasm, reduced peak expiratory flow (PEF), gastrointestinal distress, flushing, swollen lips, swollen tongue, reduced blood pressure, anaphylaxis, and organ dysfunction/failure. An "allergic response," "allergic reaction," "allergic symptom," etc., also includes immunological responses and reactions such as, e.g., increased IgE production, increased allergen-specific immunoglobulin production and/or eosinophilia. EOSINOPHILIC INFILTRATION: As used herein, "eosinophilic infiltration" refers to the presence of eosinophils in an organ or tissue including blood, esophagus, stomach, duodenum, and ileum of a subject and more specifically, to presence of eosinophils in the mucosal lining of a region of the gastro-intestinal tract including, but not limited to, esophagus and stomach. Eosinophilic infiltration is analyzed, for example, in an esophageal tissue biopsy of a subject suffering from EoE. According to some embodiments, "eosinophilic infiltration" refers to the presence of ≥15 eosinophils per high power field in the esophagus. The term "high power field" refers to a standard total magnification of 400x by a microscope used to view eosinophils in a tissue, e.g., from the esophagus of a subject. In certain embodiments, "eosinophilic infiltration" includes infiltration into a tissue by leucocytes, for example, lymphocytes, neutrophils and mast cells. The leucocyte infiltration into, e.g., esophageal tissue can be detected by cell surface markers such as eosinophil-specific markers (e.g., CD11c ^Low/Neg , SiglecF ⁺ , F4/80 ⁺ , EMR1 ⁺ , Siglec 8 ⁺ , and MBP2 ⁺ ), macrophage-specific markers (e.g., CD11b ⁺ , F4/80 ⁺ , CD14 ⁺ , EMR1 ⁺ , and CD68 ⁺ ), neutrophil-specific markers (e.g., CD11b ⁺ , Ly6G ⁺ , Ly6C ⁺ , CD11b ⁺ , and CD66b ⁺ ), and T- cell-specific markers (e.g., CD3 ⁺ CD4 ⁺ CD8 ⁺ ). REDUCTION IN ESOPHAGUS EOSINOPHILS: As used herein, “a reduction in esophagus eosinophils” means that the number of eosinophils and other leucocytes measured in the esophagus of a subject with EoE and who has been treated with Compound 1, or a pharmaceutically acceptable salt or as a solvate or hydrate thereof, is at least 5%, 10%, 20%, 50%, 70%, 80%, or 90% lower than the esophagus eosinophils measured in the same or an equivalent subject that has not been treated with Compound 1, or a pharmaceutically acceptable salt or as a solvate or hydrate thereof. In certain embodiments, reducing eosinophilic infiltration means detecting less than 15 eosinophils per high power field, such as less than 10 eosinophils, less than 9 eosinophils, less than 8 eosinophils, less than 7 eosinophils, less than 6 eosinophils, or less than 5 eosinophils per high power field in a biopsy of the esophageal mucosa. In certain embodiments, a reduction in esophagus eosinophils means that no eosinophils are detected in the esophageal mucosa of a subject. ALOPECIA AREATA: As used herein, “alopecia areata” or “AA” means a chronic T-cell mediated autoimmune skin disease leading to hair loss. Hair may be lost more diffusely over the whole scalp, in which case the condition is called diffuse alopecia areata. Alopecia areata monolocularis describes baldness in only one spot. It may occur anywhere on the head. Alopecia areata multilocularis refers to multiple areas of hair loss. Ophiasis refers to hair loss in the shape of a wave at the circumference of the head. The disease may be limited only to the beard, in which case it is called alopecia areata barbae. If the person loses all the hair on the scalp, the disease is then called alopecia areata totalis. If all body hair is lost, the diagnosis then becomes alopecia areata universalis. Severe alopecia areata refers to 50% or more involvement of the entire scalp, alopecia totalis, and alopecia universalis. Moderate alopecia areata refers to at least 30% and up to 50% involvement of the entire scalp. The present invention includes methods to treat all forms of alopecia areata. SALT SCORE: As used herein, “SALT score” refers to the Severity of Alopecia Tool which is a tool for determining degree of hair loss based on the percentage of scalp surface area involved on the top, back, and each side of the scalp. The SALT II score is an updated tool which includes smaller increments of scalp coverage to facilitate the assessment of hair loss where small patches of hair loss predominate. See, e.g., Olsen et al. (2016) J. Am. Acad. Dematol. Research Letters 1268-1270; Olsen (2001) J. Am. Acad. Dermatol.45(3 Suppl): S70-S80; and Olsen et al. (2003) Hair Science and Technology 2003:251-254, each of which is incorporated by reference for all purposes. The SALT score, using either the original SALT I or SALT II, is determined by adding the percentage hair loss in the various areas of the scalp. CLINICAL REMISSION: As used herein, with respect to alopecia areata, “clinical remission” refers to achieving 90% or greater hair re-growth from baseline, based on the SALT score at end of treatment (e.g., complete hair regrowth would confer a SALT score of 0). CLINICAL RESPONSE: As used herein, with respect to alopecia areata, “clinical response” refers to achieving 50% or greater hair re-growth from baseline, based on the SALT score at end of treatment. ALADIN: As used herein, the “Alopecia Areata Disease Activity Index” or “ALADIN” is a three-dimensional quantitative composite gene expression score for use as a biomarker for tracking disease severity and response to treatment. See, e.g., U.S. Patent Publication 2019/0072541, which is incorporated by reference for all purposes. HYDRATE: As used herein, “hydrate” means a compound of the invention or a salt thereof, that further includes a stoichiometric or non-stoichiometric amount of water bound by non-covalent intermolecular forces. SOLVATE: As used herein, “solvate” means a compound of the invention or a salt, thereof, that further includes a stoichiometric or non-stoichiometric amount of a solvent bound by non-covalent intermolecular forces. Preferred solvents are volatile, non-toxic, and/or acceptable for administration to humans in trace amounts. Alternatively, the dosage amounts of etrasimod disclosed herein can be replaced with dosage amounts for other salt or crystalline forms, formulations, and dosage regimens that exhibit bioequivalence to the specified amount of free acid etrasimod, including forms with 80-125% of the AUC and/or C _max for the specified amount of free acid etrasimod as measured by method disclosed in the FDA’s Guidance for Industry for Bioavailability and Bioequivalence (Guidance for Industry: Bioavailability and Bioequivalence Studies for Orally Administered Drug Products—General Considerations. U.S. Department of Health and Human Services, Food and Drug Administration, Center for Drug Evaluation and Research (CDER), March 2003, Revision 1, www.fda.gov/cder/guidance/index.htm). For example, the dosage amounts of etrasimod disclosed herein can be replaced with dosage amounts for other salt or crystalline forms, formulations, and dosage regimens that exhibit bioequivalence to 2 mg of free acid etrasimod in an immediate-release orally administered tablet, such as 2.8 mg of the L-arginine salt of etrasimod. The compounds according to the invention may optionally exist as pharmaceutically acceptable salts including pharmaceutically acceptable acid addition salts prepared from pharmaceutically acceptable non-toxic acids including inorganic and organic acids. Representative acids include, but are not limited to, acetic, benzenesulfonic, benzoic, camphorsulfonic, citric, ethenesulfonic, dichloroacetic, formic, fumaric, gluconic, glutamic, hippuric, hydrobromic, hydrochloric, isethionic, lactic, maleic, malic, mandelic, methanesulfonic, mucic, nitric, oxalic, pamoic, pantothenic, phosphoric, succinic, sulfiric, tartaric, oxalic, p-toluenesulfonic and the like, such as those pharmaceutically acceptable salts listed by Berge et al., Journal of Pharmaceutical Sciences, 66:1-19 (1977), incorporated herein by reference in its entirety. The acid addition salts may be obtained as the direct products of compound synthesis. In the alternative, the free base may be dissolved in a suitable solvent containing the appropriate acid and the salt isolated by evaporating the solvent or otherwise separating the salt and solvent. The compounds of this invention may form solvates with standard low molecular weight solvents using methods known to the skilled artisan. It is understood that when the phrase “pharmaceutically acceptable salts, solvates and hydrates” or the phrase “pharmaceutically acceptable salt, solvate, or hydrate” is used when referring to Compound 1, it embraces pharmaceutically acceptable solvates and/or hydrates of Compound 1, pharmaceutically acceptable salts of Compound 1, as well as pharmaceutically acceptable solvates and/or hydrates of pharmaceutically acceptable salts of Compound 1. It is also understood that when the phrase “pharmaceutically acceptable solvates and hydrates” or the phrase “pharmaceutically acceptable solvate or hydrate” is used when referring to Compound 1that are salts, it embraces pharmaceutically acceptable solvates and/or hydrates of such salts. It will be apparent to those skilled in the art that the dosage forms described herein may comprise, as the active component, either Compound 1 or a pharmaceutically acceptable salt or as a solvate or hydrate thereof. Moreover, various hydrates and solvates of Compound 1 and their salts will find use as intermediates in the manufacture of pharmaceutical compositions. Typical procedures for making and identifying suitable hydrates and solvates, outside those mentioned herein, are well known to those in the art; see for example, pages 202-209 of K.J. Guillory, “Generation of Polymorphs, Hydrates, Solvates, and Amorphous Solids,” in: Polymorphism in Pharmaceutical Solids, ed. Harry G. Britain, Vol.95, Marcel Dekker, Inc., New York, 1999. Accordingly, one aspect of the present disclosure pertains to methods of prescribing and/or administering hydrates and solvates of Compound 1 and/or its pharmaceutical acceptable salts, that can be isolated and characterized by methods known in the art, such as, thermogravimetric analysis (TGA), TGA-mass spectroscopy, TGA-Infrared spectroscopy, powder X-ray diffraction (XRPD), Karl Fisher titration, high resolution X-ray diffraction, and the like. There are several commercial entities that provide quick and efficient services for identifying solvates and hydrates on a routine basis. Example companies offering these services include Wilmington PharmaTech (Wilmington, DE), Avantium Technologies (Amsterdam) and Aptuit (Greenwich, CT). Compounds of the present invention can also be present in an appropriate crystalline form, as such form may affect the stability, release, and/or tolerability of the compound. For example, Compound 1 can be present in a crystalline form as described in PCT patent application Serial No. PCT/US2011/000153, specifically, for example, Figures 5 – 8 and the disclosure related thereto. In some embodiments, the amorphous form of Compound 1 is present in pharmaceutical formulations as described herein. In some embodiments, an L-arginine salt of Compound 1 may be present as an anhydrous, non- solvated crystalline form as described in WO 2010/011316 and WO 2011/094008. In some embodiments, the crystalline form of Compound 1 is the only form of the drug or substantially the only form present in pharmaceutical formulations as described herein. When an integer is used in a method disclosed herein, the term “about” can be inserted before the integer. Throughout this specification, unless the context requires otherwise, the word “comprise”, or variations such as “comprises” or “comprising” will be understood to imply the inclusion of a stated step or element or integer or group of steps or elements or integers but not the exclusion of any other step or element or integer or group of elements or integers. Throughout this specification, unless specifically stated otherwise or the context requires otherwise, reference to a single step, composition of matter, group of steps, or group of compositions of matter shall be taken to encompass one and a plurality (i.e. one or more) of those steps, compositions of matter, groups of steps, or groups of compositions of matter. Each embodiment described herein is to be applied mutatis mutandis to each and every other embodiment unless specifically stated otherwise. Those skilled in the art will appreciate that the invention(s) described herein is susceptible to variations and modifications other than those specifically described. It is to be understood that the invention(s) includes all such variations and modifications. The invention(s) also includes all of the steps, features, compositions and compounds referred to or indicated in this specification, individually or collectively, and any and all combinations or any two or more of said steps or features unless specifically stated otherwise. The present invention(s) is not to be limited in scope by the specific embodiments described herein, which are intended for the purpose of exemplification only. Functionally-equivalent products, compositions, and methods are clearly within the scope of the invention(s), as described herein. It is appreciated that certain features of the invention(s), which are, for clarity, described in the context of separate embodiments, can also be provided in combination in a single embodiment. Conversely, various features of the invention(s), which are, for brevity, described in the context of a single embodiment, can also be provided separately or in any suitable subcombination. For example, a method that recites prescribing and/or administering Compound 1 or a pharmaceutically acceptable salt, solvate, or hydrate thereof can be separated into two methods; one method reciting prescribing Compound 1 or a pharmaceutically acceptable salt, solvate, or hydrate thereof and the other method reciting administering Compound 1 or a pharmaceutically acceptable salt, solvate, or hydrate thereof. In addition, for example, a method that recites prescribing Compound 1 or a pharmaceutically acceptable salt, solvate, or hydrate thereof and a separate method of the invention reciting administering Compound 1 or a pharmaceutically acceptable salt, solvate, or hydrate thereof can be combined into a single method reciting prescribing and/or administering Compound 1 or a pharmaceutically acceptable salt, solvate, or hydrate thereof. Provided is a method of treatment of a sphingosine 1-phosphate subtype 1 (S1P1) receptor- associated disorder comprising: administering to an individual in need thereof a therapeutically effective amount of (R)-2- (7-(4-cyclopentyl-3-(trifluoromethyl)benzyloxy)-1,2,3,4-tetr ahydrocyclopenta[b]indol-3-yl)acetic acid (Compound 1), or a pharmaceutically acceptable salt, hydrate, or solvate thereof, wherein the individual is Japanese. In some embodiments, both of the individual’s biological parents and all four grandparents are Japanese. In some embodiments, the individual was born in Japan. In some embodiments, the individual has lived no longer than 10 years outside of Japan. In some embodiments, the individual has lived no longer than 10 years outside of Japan and has had no significant change in lifestyle, including diet, since leaving Japan. Also provided is a method of treatment of a sphingosine 1-phosphate subtype 1 (S1P ₁ ) receptor- associated disorder comprising: administering to an individual in need thereof a therapeutically effective amount of (R)-2- (7-(4-cyclopentyl-3-(trifluoromethyl)benzyloxy)-1,2,3,4-tetr ahydrocyclopenta[b]indol-3-yl)acetic acid (Compound 1), or a pharmaceutically acceptable salt, hydrate, or solvate thereof, wherein the individual has a body mass index (BMI) less than about 25. Also provided is a method of treatment of a sphingosine 1-phosphate subtype 1 (S1P1) receptor- associated disorder comprising: administering to an individual in need thereof a therapeutically effective amount of (R)-2-(7-(4- cyclopentyl-3-(trifluoromethyl)benzyloxy)-1,2,3,4-tetrahydro cyclopenta[b]indol-3-yl)acetic acid (Compound 1), or a pharmaceutically acceptable salt, hydrate, or solvate thereof, wherein the individual is Japanese and wherein the individual has a body mass index (BMI) less than about 25 kg/m ² . In some embodiments, the individual has a BMI of between about 18.5 and about 24.9 kg/ m ² . In some embodiments, the individual has a BMI of <18.5 kg/m ² . In some embodiments, the therapeutically effective amount is equivalent to about 0.5 to about 5.0 mg of Compound 1. In some embodiments, the therapeutically effective amount is in an amount equivalent to about 1 mg of Compound 1. In some embodiments, the therapeutically effective amount is in an amount equivalent to 1 mg of Compound 1. In some embodiments, the therapeutically effective amount is in an amount equivalent to about 2 mg of Compound 1. In some embodiments, the therapeutically effective amount is in an amount equivalent to 2 mg of Compound 1. In some embodiments, the administration of the Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof occurs following dose interruption. In some embodiments, the administration of the Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof is re- initiation of Compound 1 dosing. In some embodiments, the dose interruption was at least, or at least about, 2, 3, 4, 5, 6, 7, or 8 days. In some embodiments, the dose interruption was at least 1, 2, 3, 4, 5, 6, 7, or 8 doses. In some embodiments, the individual is administered the same daily dose of Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, on the first and second days of administration. In some embodiments, the individual is administered the same daily dose of Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof on at least each of the first 2, 3, 4, 5, 6, or 7 days of administration. In some embodiments, the individual is administered the same daily dose of Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, throughout treatment of a sphingosine 1-phosphate subtype 1 (S1P ₁ ) receptor-associated disorder. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof is not titrated. In some embodiments, the unit dosage form provides a therapeutically effective plasma concentration for a S1P ₁ receptor-associated disorder. In some embodiments, the S1P ₁ receptor-associated disorder is chosen from diseases and disorders mediated by lymphocytes; transplant rejection; autoimmune diseases and disorders; inflammatory diseases and disorders; cancer; conditions that have an underlying defect in vascular integrity or that are associated with angiogenesis; diseases and disorders mediated by lymphocytes; conditions that have an underlying defect in vascular integrity; autoimmune diseases and disorders; inflammatory diseases and disorders; acute or chronic rejection of cells; tissue or solid organ grafts; arthritis; diabetes; demyelinating disease; ischemia-reperfusion injury; inflammatory skin disease; hyperproliferative skin disease; inflammatory bowel disease; systemic lupus erythematosus; asthma; uveitis; myocarditis; allergy; atherosclerosis; brain inflammation; ankylosing spondylitis; central nervous system disease; pathologic angiogenesis; rheumatoid arthritis; diabetic retinopathy, atherosclerosis; cancer; chronic pulmonary disease; acute lung injury; acute respiratory disease syndrome; sepsis; microbial infections, and viral infections or diseases. In some embodiments, the S1P1 receptor-associated disorder is chosen from a disease or disorder mediated by lymphocytes, an autoimmune disease or disorder, an inflammatory disease or disorder, ankylosing spondylitis, biliary cirrhosis, cancer, psoriasis, psoriatic arthritis, rheumatoid arthritis, Crohn’s disease, transplant rejection, multiple sclerosis, systemic lupus erythematosus, inflammatory bowel disease, ulcerative colitis, type I diabetes, hypertensive nephropathy, glomerulosclerosis, myocardial ischemia-reperfusion injury and acne. In some embodiments, the S1P1 receptor-associated disorder is chosen from wherein the S1P1 receptor-associated disorder is chosen from eosinophilic esophagitis, alopecia areata, inflammatory bowel disease, and moderate to severe atopic dermatitis. Inflammatory Bowel Disease In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in endoscopic improvement, e.g., improving endoscopic appearance of the mucosa. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in inducing clinical remission. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in maintaining clinical remission. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in inducing and maintaining clinical remission. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in inducing clinical response. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in maintaining clinical response. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in inducing and maintaining clinical response. In some embodiments, the treatment reduces a lymphocyte count in the individual by at least 40%. In some embodiments, the treatment reduces a lymphocyte count in the individual by at least 45%, 50%, 55%, 60%, or 65%. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in corticosteroid-free remission. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in endoscopic remission. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in an improvement in rectal bleeding. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in histologic healing. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment results in an improvement in stool frequency. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment further comprises monitoring the level of fecal calprotectin. In some embodiments of the method of treatment of inflammatory bowel disease, e.g., ulcerative colitis, such as moderately to severely active ulcerative colitis, the treatment further comprises monitoring the level of C-reactive protein (CRP). In some embodiments, treating is reducing a sign and/or symptom of ulcerative colitis. In some embodiments, treating is reducing a sign of ulcerative colitis. In some embodiments, treating is reducing a symptom of ulcerative colitis. In some embodiments, treating is reducing a sign and/or symptom of Crohn’s disease. In some embodiments, treating is reducing a sign of Crohn’s disease. In some embodiments, treating is reducing a symptom of Crohn’s disease. In some embodiments, prior to said administering the individual has a 3-component Mayo Clinic Score of at least 6. In some embodiments, the administering results in an improvement of the individual’s 3- component Mayo Clinic Score. In some embodiments, the administering results in an improvement of the individual’s 2- component Mayo Clinic Score. In some embodiments, the administering results in an improvement of the individual’s Total Mayo Clinic Score. In some embodiments, the administering results in improvement in the endoscopic appearance of the mucosa of the individual. In some embodiments, the administering results in inducing clinical remission in the individual. In some embodiments, the administering results in maintaining clinical remission in the individual. In some embodiments, the administering results in inducing and maintaining clinical remission in the individual. In some embodiments, the administering results in inducing clinical response in the individual. In some embodiments, the administering results in maintaining clinical response in the individual. In some embodiments, the administering results in inducing and maintaining clinical response in the individual. In some embodiments, ulcerative colitis has been diagnosed using a 2-component Mayo Clinic Score. For example, in some embodiments, ulcerative colitis has been diagnosed using a score ranging from 0 to 9 for rectal bleeding and endoscopic findings. In some embodiments, ulcerative colitis has been diagnosed using a 3-component Mayo Clinic Score. For example, in some embodiments, ulcerative colitis has been diagnosed using a score ranging from 0 to 9 for stool frequency, rectal bleeding, and endoscopic findings. In some embodiments, ulcerative colitis has been diagnosed using a Total Mayo Score. For example, in some embodiments, ulcerative colitis has been diagnosed using a score ranging from 0 to 12 for stool frequency, rectal bleeding, endoscopic findings, and Physicians Global Assessment. In some embodiments, improvement in ulcerative colitis is measured using a 2-component Mayo Clinic Score. In some embodiments, improvement in ulcerative colitis is measured using a 3-component Mayo Clinic Score. In some embodiments, improvement in ulcerative colitis is measured using a Total Mayo Score. In some embodiments, improvement in ulcerative colitis is measured by clinical remission. In some embodiments, improvement in ulcerative colitis is measured by lymphocyte reduction. In some embodiments, improvement in ulcerative colitis is measured by endoscopic improvement. In some embodiments, improvement in ulcerative colitis is measured by 6-point Mayo Score. For example, in some embodiments, improvement in ulcerative colitis is measured by stool frequency and rectal bleeding. In some embodiments, improvement in ulcerative colitis is statistically significant. In some embodiments, the S1P1 receptor-associated disorder is ulcerative colitis. In some embodiments, the S1P ₁ receptor-associated disorder is moderately to severely active ulcerative colitis. In some embodiments, the S1P ₁ receptor-associated disorder is moderately active ulcerative colitis. In some embodiments, the S1P1 receptor-associated disorder is severely active ulcerative colitis. In some embodiments, the S1P1 receptor-associated disorder is mildly to moderately active ulcerative colitis. In some embodiments, the S1P1 receptor-associated disorder is mildly active ulcerative colitis. Eosinophilic Esophagitis In some embodiments, the S1P1 receptor-associated disorder is eosinophilic esophagitis. In some embodiments, the individual is selected on the basis of exhibiting ≥15 eosinophils per high powered field (hpf) in the esophagus prior to or at the time of the treatment ("baseline"). In some embodiments, the individual exhibits at least 50% decrease in the number of eosinophils per hpf from baseline at day 10 following the administration of Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof. In some embodiments, the individual is selected on the basis of exhibiting an eotaxin-3 level of greater than about 50 pg/mL prior to or at the time of initiation of treatment ("baseline"). In some embodiments, the individual exhibits at least 50% decrease in eotaxin-3 level from baseline at day 10 following the administration. In some embodiments, the individual is susceptible to an allergen. For example, the subject may exhibit one of the following characteristics: (a) is prone to allergic reactions or responses when exposed to one or more allergens; (b) has previously exhibited an allergic response or reaction to one or more allergens; (c) has a known history of allergies; and/or (d) exhibits a sign or symptom of an allergic response or anaphylaxis. In certain embodiments, the subject is allergic to an allergen associated with EoE or that renders the subject susceptible and/or prone to developing EoE. In some embodiments, the individual exhibits an allergic reaction to a food allergen. For example, the subject may have an allergy to an allergen contained in a food item including, but not limited to, a dairy product, egg, wheat, soy, corn, rye, fish, shellfish, peanut, a tree nut, beef, chicken, oat, barley, pork, green beans, and fruits such as apple and pineapple. In some embodiments, the individual is allergic to a non-food allergen such as allergens derived from dust, mold, insects, plants including pollen, and pets such as cats and dogs. Examples of non-food allergens (also known as environmental allergens or aeroallergens) include, but are not limited to, house dust mite allergens, pollen allergens, animal dander allergens, insect venom, grass allergens, and latex. In some embodiments, the symptom or indication of EoE is selected from eosinophilic infiltration of the esophagus, thickening of the esophageal wall, food refusal, vomiting, abdominal pain, heartburn, regurgitation, dysphagia and food impaction. In some embodiments, the individual, prior to treatment, exhibits (or have exhibited) one or more indications of EoE such as, e.g., esophageal overexpression of pro-inflammatory mediators such as mast cells, eosinophilic infiltration of the esophagus, thickening of the esophageal wall, dysphagia, food impaction and chest and abdominal pain and/or an elevated level of an EoE-associated biomarker. In some embodiments, the individual is more susceptible to EoE or may show an elevated level of an EoE-associated biomarker. For example, the individual is suffering from an atopic disease or disorder such as food allergy, atopic dermatitis, asthma, allergic rhinitis and allergic conjunctivitis. In some embodiments, the subject has an inherited connective tissue disorders. In some embodiments, prior to treatment, the individual shows the presence of ≥15 eosinophils per high power field in the esophagus. In some embodiments, prior to treatment, the individual shows an elevated peripheral eosinophil counts (>300 cells/up or elevated serum IgE (>150 kU/L). In some embodiments, prior to treatment, the individual shows the presence of ≥15 eosinophils per high power field in the esophagus and an elevated peripheral eosinophil counts (>300 cells/up or elevated serum IgE (>150 kU/L). In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof reduces migration of tissue dendritic cells to a lymph node. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof reduces infiltrating TH2 and CD8 T cells. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof reduces circulating T cells. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof reduces tissue cytokines. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof reduces eosinophil infiltration. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, reduces eosinophil tissue accumulation. In some embodiments, the individual, prior to or at the time of administration of Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, has or is diagnosed with a disease or disorder selected from atopic dermatitis, asthma, allergic rhinitis and allergic conjunctivitis. Alopecia Areata In some embodiments, the S1P ₁ receptor-associated disorder is alopecia areata. In some embodiments, the individual has severe alopecia areata. In some embodiments, the individual has moderate alopecia areata. In some embodiments, the individual has diffuse alopecia areata. In some embodiments, the individual has alopecia areata monolocularis. In some embodiments, the individual has alopecia areata multilocularis. In some embodiments, the individual has ophiasis. In some embodiments, the individual has alopecia areata barbae. In some embodiments, the individual has alopecia areata totalis. In some embodiments, the individual has is alopecia areata universalis. In some embodiments, the S1P1 receptor-associated disorder is inflammatory bowel disease is ulcerative colitis. In some embodiments, the inflammatory bowel disease is moderately to severely active ulcerative colitis. In some embodiments, the S1P1 receptor-associated disorder is moderate to severe atopic dermatitis. In some embodiments, treating is inducing and/or maintaining clinical remission. In some embodiments, treating is inducing and maintaining clinical remission. In some embodiments, treating is inducing and/or maintaining clinical remission and/or clinical response. In some embodiments, treating is inducing and maintaining clinical remission and clinical response. In some embodiments, treating is inducing clinical remission and/or clinical response. In some embodiments, treating is maintaining clinical remission and/or clinical response. In some embodiments, treating is inducing clinical remission and clinical response. In some embodiments, treating is maintaining clinical remission and clinical response. In some embodiments, treating is inducing and/or maintaining clinical remission and/or mucosal healing. In some embodiments, treating is inducing and maintaining clinical remission and mucosal healing. In some embodiments, treating is inducing and maintaining mucosal healing. In some embodiments, treating is inducing and maintaining clinical remission. In some embodiments, treating is inducing clinical remission. In some embodiments, treating is inducing mucosal healing. In some embodiments, treating is maintaining clinical remission. In some embodiments, treating is maintaining mucosal healing. In some embodiments, treating is achieving and/or sustaining clinical remission in induction responders. In some embodiments, treating is achieving and sustaining clinical remission in induction responders. In some embodiments, treating is achieving clinical remission in induction responders. In some embodiments, treating is sustaining clinical remission in induction responders. In some embodiments, treating is inducing and/or maintaining clinical response. In some embodiments, treating is inducing and maintaining clinical response. In some embodiments, treating is inducing clinical response. In some embodiments, treating is maintaining clinical response. In some embodiments, treating is inducing endoscopic improvement. In some embodiments, treating is maintaining endoscopic improvement. In some embodiments, treating is achieve endoscopic improvement. In some embodiments, treating is improving endoscopic remission. In some embodiments, treating is maintaining endoscopic remission. In some embodiments, treating is inducing histologic healing. In some embodiments, treating is maintaining histologic healing. In some embodiments, treating is improving stool frequency. In some embodiments, treating is maintaining improvement in stool frequency. In some embodiments, treating is improving endoscopic appearance of the mucosa. In some embodiments, treating is maintaining endoscopic improvement of the mucosa. In some embodiments, treating is improving endoscopic appearance of the mucosa during induction. In some embodiments, treating eliminates the need for corticosteroid use. In some embodiments, treating allows for reduced corticosteroid use. In some embodiments, treating allows for the use of a lower dose of a corticosteroid. In some embodiments, treating is achieving corticosteroid-free remission. In some embodiments, treating is sustaining corticosteroid-free remission. In some embodiments, treating is improving rectal bleeding. In some embodiments, treating is maintaining improvement in rectal bleeding. In some embodiments, treating is improving endoscopic subscore. In some embodiments, treating is maintaining improvement in endoscopic subscore. In some embodiments, the individual had demonstrated an inadequate response to, loss of response to, or intolerance of at least one of agent selected from oral 5-aminosalicylates, corticosteroids, immunosuppressives, TNFα antagonists, and integrin antagonists. In some embodiments, the dosage form is administered under fasted conditions. In some embodiments, the dosage form is administered under fed conditions. In some embodiments, the method is non-gender specific. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, is administered orally. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, is formulated as a capsule or tablet suitable for oral administration. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, is selected from: Compound 1; a calcium salt of Compound 1; and an L-arginine salt of Compound 1. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, is an L-arginine salt of Compound 1. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, is an anhydrous, non-solvated crystalline form of an L-arginine salt of Compound 1. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, is an anhydrous, non-solvated crystalline form of Compound 1. In some embodiments, the method further comprises monitoring for adverse events during the administration of Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, and optionally, interrupting or terminating the administration of Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof. In some embodiments, the method further comprises monitoring for adverse events during the administration of Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof. In some embodiments, the individual does not experience a cardiovascular-related adverse event during the administration of the Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof. In some embodiments, the cardiovascular-related adverse event is heart rate reduction. In some embodiments, the cardiovascular-related adverse event is acute heart rate reduction. In some embodiments, the cardiovascular-related adverse event is a transient decrease in heart rate. In some embodiments, the cardiovascular-related adverse event is bradycardia. In some embodiments, the cardiovascular-related adverse event is a reduction in heart rate of more than, or more than about, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, or 30 bpm. In some embodiments, heart rate reduction is mitigated in a patient population. In some embodiments, heart rate reduction is mitigated in an individual. In some embodiments, heart rate reduction is decreased to less than or equal to 5, 4, 3, 2, or 1 bpm compared to the baseline heart rate. In some embodiments, average heart rate reduction is decreased to less than or equal to 5, 4, 3, 2, or 1 bpm compared to the baseline heart rate. In some embodiments, heart rate is decreased by less than, or less than about, 20, 15, 10, or 5 bpm from baseline heart rate. In some embodiments, activation of the cardiac GIRK channel is decreased in the individual. In some embodiments, the risk of first-dose conduction delay is decreased in the individual. In some embodiments, first-dose effects of Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof are decreased. In some embodiments, first- dose effects of Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, are decreased while maintaining overall lymphocyte sequestration. In some embodiments, the method further comprises monitoring heart rate during the administration, monitoring pulmonary function during the administration, or monitoring liver function during the administration. In some embodiments, the treatment further comprises monitoring heart rate during the administration. In some embodiments, the treatment further comprises monitoring pulmonary function during the administration. In some embodiments, the treatment further comprises monitoring liver function during the administration. In some embodiments, heart rate reduction is measured using a heart rate monitor. In some embodiments, heart rate reduction is measured with a 12-lead Holter recording. In some embodiments, heart rate reduction is measured using an ECG. In some embodiments, heart rate reduction is measured by pulse. In some embodiments, the method reduces the incidence and severity of adverse events resulting from the treatment of a condition described herein. In some embodiments, the adverse event is a serious adverse event. In some embodiments, the serious adverse event is selected from leukopenia, constipation, diarrhea, nausea, abdominal pain, neutropenia, vomiting, back pain, and menstrual disorder. In some embodiments, the method results in no serious adverse events. In some embodiments, the dose is administered without substantially inducing an acute heart rate reduction or heart block in the individual. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, is administered without causing a reduction of more than 6 bpm in heart rate. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, is administered without a first-dose effect on heart rate as seen with other S1P receptor modulators. In some embodiments, Compound 1, or a pharmaceutically acceptable salt, hydrate, or solvate thereof, is administered without a first-dose effect on AV conduction as seen with other S1P receptor modulators. Also provided are pharmaceutical compositions comprising a therapeutically effective amount of Compound 1, or, a pharmaceutically acceptable salt, a hydrate or solvate thereof and, optionally, one or more pharmaceutically acceptable carriers. Also provided are pharmaceutical compositions comprising Compound 1, or, a pharmaceutically acceptable salt, a hydrate or solvate thereof, optionally, one or more pharmaceutically acceptable carriers. The carrier(s) must be “acceptable” in the sense of being compatible with the other ingredients of the formulation and not overly deleterious to the recipient thereof. In some embodiments, Compound 1, or, a pharmaceutically acceptable salt, a hydrate or solvate thereof, is administered as a raw or pure chemical, for example as a powder in capsule formulation. In some embodiments, Compound 1, or, a pharmaceutically acceptable salt, a hydrate or solvate thereof, is formulated as a pharmaceutical composition further comprising one or more pharmaceutically acceptable carriers. Pharmaceutical compositions may be prepared by any suitable method, typically by uniformly mixing the active compound(s) with liquids or finely divided solid carriers, or both, in the required proportions and then, if necessary, forming the resulting mixture into a desired shape. Conventional excipients, such as binding agents, fillers, acceptable wetting agents, tabletting lubricants and disintegrants may be used in tablets and capsules for oral administration. The compounds described herein can be formulated into pharmaceutical compositions using techniques well known to those in the art. Suitable pharmaceutically acceptable carriers, outside those mentioned herein, are known in the art; for example, see Remington, The Science and Practice of Pharmacy, 20 ^th Edition, 2000, Lippincott Williams & Wilkins, (Editors: Gennaro et al.) For oral administration, the pharmaceutical composition may be in the form of, for example, a tablet or capsule. The pharmaceutical composition is preferably made in the form of a dosage unit containing a particular amount of the active ingredient. Examples of such dosage units are capsules, tablets, powders, granules or suspensions, with conventional additives such as lactose, mannitol, corn starch or potato starch; with binders such as crystalline cellulose, cellulose derivatives, acacia, corn starch or gelatins; with disintegrators such as corn starch, potato starch or sodium carboxymethyl-cellulose; and with lubricants such as talc or magnesium stearate. Solid form preparations include powders, tablets, pills, capsules, cachets, suppositories, and dispersible granules. A solid carrier can be one or more substances which may also act as diluents, flavoring agents, solubilizers, lubricants, suspending agents, binders, preservatives, tablet disintegrating agents, or encapsulating materials. In powders, the carrier is a finely divided solid which is in a mixture with the finely divided active component. In tablets, the active component is mixed with the carrier having the necessary binding capacity in suitable proportions and compacted to the desired shape and size. The powders and tablets may contain varying percentage amounts of the active compound. A representative amount in a powder or tablet may be from 0.5 to about 90 percent of the active compound. However, an artisan would know when amounts outside of this range are necessary. Suitable carriers for powders and tablets include magnesium carbonate, magnesium stearate, talc, sugar, lactose, pectin, dextrin, starch, gelatin, tragacanth, methylcellulose, sodium carboxymethyl cellulose, a low melting wax, cocoa butter, and the like. The term “preparation” includes the formulation of the active compound with encapsulating material as carrier providing a capsule in which the active component, with or without carriers, is surrounded by a carrier, which is thus in association with it. Similarly, cachets and lozenges are included. Tablets, powders, capsules, pills, cachets, and lozenges can be used as solid forms suitable for oral administration. The pharmaceutical preparations are preferably in unit dosage forms. In such form, the preparation is subdivided into unit doses containing appropriate quantities of the active component. The unit dosage form can be a packaged preparation, the package containing discrete quantities of preparation, such as packeted tablets or capsules. Also, the unit dosage form can be a capsule or tablet itself, or it can be the appropriate number of any of these in packaged form. Further embodiments include the embodiments disclosed in the following Examples, which is not to be construed as limiting in any way. EXAMPLES EXAMPLE 1 Formulations composed of immediate-release tablets containing Compound 1 were prepared as shown below. EXAMPLE 2 A phase 1 study was conducted in 12 men (10 administered etrasimod; 2 administered placebo) in each of 4 groups: 1.) Japanese individuals (for which both of the individual’s biological parents and all four grandparents were Japanese) administered 1 mg of Compound 1; 2.) Japanese individuals administered 2 mg of Compound 1; 3.) Caucasian individuals (of North American, South American, European, or Middle Eastern descent) administered 1 mg of Compound 1; and 4.) Caucasian individuals administered 2 mg of Compound 1. The table below shows the demographic and baseline characteristics of the individuals. Mean total body weight (TBW) of individuals receiving Compound 1 was lower in individuals of Japanese descent compared with individuals of Caucasian descent. SD = Standard deviation; BMI = Body-Mass Index Compound 1 or matching placebo was administered once daily (QD) from Days 1 to 7, followed by a 7-day washout and a single dose on Day 15. Blood was sampled on Days 1 and 7 for plasma PK and collected each morning on Days 1 to 15 to assess lymphocyte counts and calculate lymphocyte PD parameters, e.g., the minimum and maximum observed response values after dosing (Rmin and Rmax, respectively) and net area under the effect curve (AUEC _Net ). AUEC _Net is equal to the area that is both above baseline and below the curve minus the area that is both below baseline and above the curve. Dose-dependent decreases in median lymphocyte counts were observed in both ethnicities from Days 2 to 8 and increased back to near baseline levels during the washout period. Only LS mean Rmin and AUECNet values were dose dependent in both ethnicities with none of the evaluated lymphocyte PD parameters being statistically different between Japanese and Caucasian individuals. Statistical Analysis of Observed Lymphocyte Count PD Parameters AUEC _net = net area under the effect curve after subtracting the area below from that above the baseline lymphocyte count; R _min and R _max = minimum and maximum observed lymphocyte count, respectively. Compound 1 peak concentration (Cmax) and total plasma exposure (AUC0-τ) values in both ethnic groups were dose-proportional following either a single dose or multiple doses. Compound 1 mean Cmax and AUC0-τ were slightly to moderately higher in Japanese individuals compared with Caucasian individuals following either a single dose or multiple doses. There was low to moderate inter-subject variability. Summary of Compound 1 Single Dose and Multiple Dose Plasma PK Parameters in Japanese and Caucasian Male Individuals Data are presented as mean (SD); t _1/2 , elimination half-life Geometric mean ratio (GMR) point estimates for Compound 1 plasma exposure measures between Japanese and Caucasian individuals ranged from 120–146%. After dose-body weight normalization of Compound 1 Cmax and AUC0-τ, the GMR point estimates between Japanese and Caucasian individuals were near 100%, which indicates that the Compound 1 plasma exposure difference between the two ethnic groups appears mainly attributable TBW rather than ethnicity. Summary of Japanese / Caucasian GMR of C _max and AUC _0-τ After Single and Multiple Doses Data are presented as % (90% confidence interval) GMR J/C, geometric mean ratio of Japanese (J) to Caucasian (C) subjects; DWN, dose-body weight normalized Dose-dependent, progressive decreases in mean absolute and percent change from baseline lymphocyte count were observed across all four treatment groups from Day 2 to Day 8, followed by a subsequent increase to near baseline levels during the 7-day washout period (see Figure 1) consistent with the half-life of Compound 1. Absolute and change from baseline nadir lymphocyte counts were dose-dependent and comparable across ethnic groups. Time to nadir (T _min ) was similar between the Compound 1 treatment groups. Summary of Baseline and Nadir Lymphocyte Counts and Time to Nadir Data are presented as mean (SD), except for Tmin shown as median (min, max) CFB, change from baseline; T _min time to nadir No statistically significant differences were seen between Japanese and Caucasian individuals for lymphocyte R _min , R _max , or AUECNet based on least square (LS) mean values. Summary of Lymphocyte PD Parameters in Subjects Treated with Compound 1 (Day 1 to Day 15) Data are presented as LS mean (90% confidence interval) Single and multiple dose Compound 1 mean peak (C _max ) and total plasma exposure (AUC) measures were slightly to moderately higher in individuals of Japanese descent compared with Caucasian descent, but were similar after dose-body weight normalization. No statistically significant differences were observed between individuals of Japanese and Caucasian descent in lymphocyte PD parameters of Rmin, Rmax, or AUECNet upon administration of multiple doses of Compound 1. These results demonstrate a lack of clinically meaningful PK or PD (lymphocyte response) ethnic differences between healthy male individuals of Japanese and Caucasian descent. EXAMPLE 3 A multicenter, randomized, double-blind, placebo-controlled, dose-ranging study will be conducted to evaluate the efficacy and safety of 1 and 2 mg of Compound 1 in Japanese subjects with moderately to severely active UC. The study will include a 28-Day screening period, a 12-week induction treatment period, and a 4-week follow-up period. The target subject population will include those who have had an inadequate response, loss of response, or intolerance to the following: 1. Conventional therapy, and are naïve to biologic or Janus kinase (JAK) inhibitor therapy 2. Biologic or JAK inhibitor (subjects in this category may have received prior conventional therapy) Subject eligibility will be determined during a four-week (28-Day) Screening Period. Entry criteria will be based on confirmation of moderately to severely active UC, defined by a modified Mayo score (MMS) of 4 to 9, which includes an endoscopic score (ES) ≥ 2 and rectal bleeding (RB) score ≥ 1. Eligible subjects will be randomized (1:1:1 ratio) in a double-blind fashion to receive an oral tablet of 1 mg of Compound 1, 2 mg of Compound 1, or matching placebo) once daily for 12 weeks. The formulations provided of 1 mg or 2 mg of Compound 1 may be prepared as described in Example 1. At the end of the 12-week Induction Treatment Period, subjects will undergo the Week 12 study assessments. Subjects will then have the option to enter an open-label extension (OLE) study following completion of week 12 study procedures provided they meet all eligibility criteria for the OLE. Subjects must complete week 12 to be eligible for the OLE. Subjects who do not participate in the OLE study will have two-week and four-week Follow-Up visits after the last treatment administration. Inclusion criteria: Subjects must meet ALL of the following inclusion criteria to be eligible for enrollment into the study: • Japanese ancestry • 20 to 80 years of age, inclusive, at the time of consent • Ability to provide written informed consent and to be compliant with the schedule of protocol assessments Disease-specific inclusion criteria: • Diagnosed with UC ≥ 3 months prior to screening. The diagnosis of UC must be confirmed by endoscopic and histologic evidence. The endoscopy and histology report should be present in the source documents; however, if not available, the screening endoscopy and histology may serve as such. • Active UC confirmed by endoscopy with ≥ 10 cm rectal involvement • Moderately to severely active UC defined as MMS of 4 to 9, including an ES ≥ 2 and RB ≥ 1 • Received a surveillance colonoscopy (performed according to local standard) within 12 months before baseline to rule out dysplasia in subjects with pancolitis > 8 years duration or subjects with left-sided colitis > 12 years duration. Subjects without a surveillance colonoscopy within the prior 12 months will have a colonoscopy at screening (ie, in place of screening proctosigmoidoscopy). Any adenomatous polyps must be removed according to routine practice prior to their first dose of study treatment. Prior treatment: • Demonstrated an inadequate response to, loss of response to, or intolerance to at least one of the following therapies as defined below: Conventional therapy a. Oral 5-aminosalicylic acid (5-ASA) compounds b. Corticosteroids c. Thiopurines Biologic therapy or JAK inhibitor therapy a. Anti-tumor necrosis factor alpha (TNFα) antibodies (eg, infliximab, adalimumab, golimumab, or biosimilars) b. Anti-integrin antibodies (eg, vedolizumab) c. Anti-interleukin 12/23 antibodies (eg, ustekinumab) d. JAK inhibitors (eg, tofacitinib) Note: The medication used to qualify the subject for entry into this category must be approved for the treatment of UC in Japan and the subject must have received an adequate course of therapy based on local guidelines for that therapy. Concomitant treatments: • Subjects are permitted to be receiving a therapeutic dose of the following drugs: • Oral 5-ASA compounds provided the dose has been stable for ≥ 2 weeks immediately prior to randomization • Oral corticosteroid therapy (prednisone at a stable dose ≤ 20 mg/day or equivalent steroid) provided the dose has been stable for the 4 weeks immediately prior to the screening endoscopy assessment • Immunosuppressive agents such as oral azathioprine (AZA) or 6-mercaptopurine (6-MP) must be discontinued ≥ 2 weeks prior to randomization • Probiotics (eg, Saccharomyces boulardii) provided the dose has been stable for the 2 weeks immediately prior to randomization If oral 5-ASA or corticosteroids have been recently discontinued, they must have been stopped for at least 2 weeks prior to the endoscopy used for the baseline MMS. The MMS and its component subscores will be used to assess efficacy. The MMS is a composite of three assessments, each rated from 0 to 3: stool frequency (SF), RB, and ES. The ES will be determined by central reading. Primary efficacy endpoint: • Proportion of subjects achieving clinical remission at week 12 Secondary efficacy endpoints: • The proportion of subjects achieving endoscopic improvement at week 12 • The proportion of subjects achieving symptomatic remission at week 12 • The proportion of subjects with mucosal healing at week 12 • The proportion of subjects achieving clinical response at week 12 • The proportion of subjects achieving endoscopic normalization at week 12 Other uses of the disclosed methods will become apparent to those in the art based upon, inter alia, a review of this patent document.