INDAZOLES AND THEIR USE IN METHODS FOR TREATING 5-HT2 RESPONSIVE CONDITIONS FIELD OF THE INVENTION In general, the invention features compositions and methods for treating 5-HT2 responsive conditions. BACKGROUND OF THE INVENTION Significant interest in the therapeutic application of 5-HT2 receptor ligands has developed, based upon evidence of possible therapeutic effects in a wide array of 5-HT2 responsive conditions (e.g., mitigating or improving conditions and disorders via 5-HT2 receptor target modulation), including psychiatric conditions, pain disorders, immunological conditions, and neurological conditions. There is a need in the field for discovery and development of small molecule 5-HT2 receptor ligands with more desirable therapeutic, absorption, distribution, pharmacokinetic, and/or safety profiles. SUMMARY OF THE INVENTION The present invention discloses a new chemotype class of ligands of the 5-HT2 receptors that have potent pharmacological properties. Also provided are methods of using the compounds or compositions of the invention, e.g., for treating an inflammatory or a neurological disorder in a subject in need thereof. An aspect of the invention features a compound of any one of formulas (I)-(III), or a pharmaceutically acceptable salt or zwitterion, hydrate, ester, co-crystal or prodrug thereof: (II) wherein, X is N for formulae (I) and (II); and N(CH3) for formula (III); ; R ³ is hydrogen, OH, optionally substituted O-alkaryl, optionally substituted O-alkyl, OPO ₃ H ₂ , O-acyl, OCH3, OCH2CH3, ; R ⁹ is C2-7 heterocyclyl, optionally substituted C6-12 aryl, optionally substituted C7-14 alkaryl, optionally substituted C _3-10 alkheterocyclyl, or optionally substituted C _1-8 heteroalkyl; R ₁₁ is H or methyl, the latter being in either the R or S stereochemical configuration; and R ¹² is H, optionally substituted C ₁ -C ₈ alkyl, optionally substituted C2-7 heterocyclyl, optionally substituted C6-12 aryl, optionally substituted C7-14 alkaryl, optionally substituted C3-10 alkheterocyclyl, or optionally substituted C1-8 heteroalkyl. In an embodiment, when R ¹² is H, R ³ is not OH. In an embodiment formula (III), does not include the compound: Compound S) For the sake of brevity, above definition (e.g. disclaiming Compounds (S)) may be referred to as compounds of formula (III) In particular embodiments, the compound of formula (I) is selected from: , , or a phar In particular embodiments, the compound of formula (I) is selected from: , or a In particular embodiments, the compound of formula (II) is selected from: , or a In , or a In a particular embodiment of formula (I), (II), or (III), R ³ is: . , , , a halogen. In some embodiments, the halogen is F, Cl, Br, I, or At. In a particular embodiment of formula (I), (II), or (III), R ³ is hydrogen, OH, O-Benzyl, or OMe. In a particular embodiment of formula (I), (II), or (III), R ³ is OPO ₃ H _2. In a particular embodiment of formula (I), (II), or (III), R ⁴ is hydrogen, or OCH ₃ . In a particular embodiment of formula (I), (II), or (III), R ⁵ is hydrogen, or OH In a particular embodiment of formula (I) or (II), R ⁹ is hydrogen, or CH3. In a particular embodiment of formula (I) or (II), R ¹⁰ is hydrogen, or CH ₃ . In a particular embodiment of formula (I) or (II), R ¹¹ is hydrogen, or CH ₃ .In a particular embodiment of formula (III), R ¹² is hydrogen, or CH3. In a particular embodiment, there is provided a compound of formula (I) or (III), or a pharmaceutically acceptable salt or zwitterion or prodrug thereof: wherein, X is N for formula (I); and N(CH3) for formula (III); R ³ is OH or OCH ₃ for formula (I); and R ³ is OH or OCH ₃ , or O-Benzyl for formula (III); R ⁴ is hydrogen; R ⁵ is hydrogen; R ⁹ is hydrogen; R ¹⁰ is hydrogen or CH ₃ ; R ¹¹ is hydrogen; and R ¹² is hydrogen or optionally substituted C1-C8 alkyl; optionally C1-C4 alkyl; further optionally CH3. For the sake of brevity, compounds meeting the above definition may be referred to as compounds of formula (I)a or (III)a respectively. In a particular embodiment, there is provided a compound of formula (I)a, wherein R ³ is OH or OCH ₃ ; and R ¹⁰ is CH ₃ . In a particular embodiment, there is provided a compound of formula (I)a, wherein R ³ is OH or OCH3; and R ¹⁰ is H. In a particular embodiment, there is provided a compound of formula (I)a, wherein R ³ is OH; and R ¹⁰ is hydrogen or CH3. In a particular embodiment, there is provided a compound of formula (III)a, wherein R ³ is OH, OCH ₃ , or O-Benzyl; and R ¹² is CH3. In a particular embodiment, there is provided a compound of formula (III)a, wherein R ³ is OH or OCH ₃ ; and R ¹² is CH ₃ . In a particular embodiment, there is provided a compound of formula (III)a, wherein R ³ is OH or O-Benzyl; and R ¹² is H. In a particular embodiment, there is provided a compound of formula (III)a wherein when R ¹² is hydrogen, R ³ is not OH. In a particular embodiment, there is provided a compound of formula (I) or (III), or a pharmaceutically acceptable salt or zwitterion or prodrug thereof: wherein, X is N for formula (I) and N(CH ₃ ) for formula (III); R ³ is OH or OCH ₃ ; R ⁴ is hydrogen; R ⁵ is hydrogen; R ⁹ is hydrogen; R ¹⁰ is hydrogen or CH ₃ ; R ¹¹ is hydrogen; and R ¹² is optionally substituted C1-C8 alkyl ; optionally C1-C4 alkyl; further optionally CH3. In another aspect, the invention includes a composition of any of the preceding aspects (e.g., a compound of formula (I), (II), or (III), or a pharmaceutically acceptable salt or zwitterion or prodrug thereof, and a pharmaceutically acceptable excipient. Such a pharmaceutical composition can be formulated, e.g., for oral, intranasal, subcutaneous, intramuscular, parenteral, topical, intraocular or pulmonary administration. Such a pharmaceutical composition may be formulated as an orally disintegrating tablet. Such a composition may comprise an amorphous or crystalline form of any of the compounds of any of the aspects and/or embodiments disclosed herein. In particular embodiments, the compound may be present as crystalline polymorphic form. In another aspect, provided herein is a method of treating 5-HT2 responsive conditions in a subject in need thereof, the method including administering to the subject a therapeutically effective amount of the compound or the pharmaceutical composition of any of the preceding aspects. In particular embodiments the 5-HT2 responsive condition is an inflammatory or neurological disorder. In some embodiments of any of the preceding embodiments or any of the methods described herein, the 5-HT2 responsive condition is an inflammatory disorder selected from asthma, chronic obstructive pulmonary disease, neuroinflammation, rheumatoid arthritis, atherosclerosis, psoriasis, type II diabetes, inflammatory bowel disease, Crohn’s disease, multiple sclerosis, septicemia, conjunctivitis, Alzheimer’s disease, or any inflammatory condition described herein. In another aspect, provided herein is a method of treating a psychological condition in a subject in need thereof, the method including administering to the subject a therapeutically effective amount of the compound or the pharmaceutical composition of any of the preceding aspects. In particular embodiments, the psychological condition is depression, anxiety, addiction, post-traumatic stress disorder, an eating disorder, compulsive behavior, autism spectrum disorders, or any psychological condition described herein. In another aspect, provided herein is a method of treating chronic pain in a subject in need thereof, the method including administering to the subject a therapeutically effective amount of the compound or the pharmaceutical composition of any of the preceding aspects. In another aspect, the described composition of matter embodies a new chemotype class of ligands targeting the 5-HT2 receptors that offers structural differentiation from previously known chemotype ligand classes for these receptors, namely substituted phenethylamines, lysergamides, and tryptamines non exhaustively. A different structural chemotype will likely not replicate the extended pharmacology at secondary and complementary targets known for these other ligand classes. Thus, any additional activities at secondary metabotropic, ionotropic, transporter, or enzyme targets for the molecules described in this application could contribute to an overall distinctive pharmacological profile compared to existing 5-HT2 receptor targeting medicines. In any of the methods provided herein, the compound can be administered by any suitable route of administration, e.g., orally, intranasally, or by inhalation. In some embodiments, the present compound or pharmaceutical composition thereof is administered by one or more of a variety of routes, including nasal, buccal, oral, by inhalation (e.g., as an oral spray, nebulizer, nasal spray, or aerosol), intravenous, intramuscular, intra-arterial, intramedullary, intrathecal, subcutaneous, intraventricular, transdermal, interdermal, rectal, intravaginal, intraperitoneal, topical (e.g., by powders, ointments, creams, gels, lotions, and/or drops), mucosal, enteral, vitreal, intratumoral, sublingual; by intratracheal instillation, bronchial instillation, and/or through a portal vein catheter. In some embodiments the composition is administered by systemic intravenous injection. In specific embodiments the composition is administered intravenously and/or orally. In another aspect, provided is a compound as described herein for use as a medicament; optionally wherein the medicament is for the treatment of a condition disclosed herein (e.g. treating 5-HT2 responsive conditions). In another aspect, provided is a compound as described herein for the manufacture of a medicament; optionally wherein the medicament is for the treatment of a condition disclosed herein (e.g. treating 5-HT2 responsive conditions). In an embodiment there is provided Compound C for use in a method of treatment which selectively activates the 5-HT2A receptor subtype. In an embodiment there is provided Compound F for use in a method of treatment which selectively activates the 5-HT2A receptor subtype. In an embodiment there is provided Compound G for use in a method of treatment which selectively activates the 5-HT2A receptor subtype. In an embodiment there is provided Compound O for use in a method of treatment which selectively activates the 5-HT2A receptor subtype. In an embodiment there is provided Compound Q for use in a method of treatment which selectively activates the 5-HT2A receptor subtype. Definitions To facilitate the understanding of this invention, a number of terms are defined below and throughout the disclosure. 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. The terminology herein is used to describe specific embodiments of the invention, but their usage does not limit the invention, except as outlined in the claims. At various places in the present specification, substituents of compounds of the present disclosure are disclosed in groups or in ranges. It is specifically intended that the present disclosure include each and every individual subcombination of the members of such groups and ranges. For example, the term “C1-8 alkyl” is specifically intended to individually disclose methyl, ethyl, C3 alkyl, C4 alkyl, C ₅ alkyl, C ₆ alkyl, C ₇ alkyl, and C ₈ alkyl. Herein a phrase of the form “optionally substituted X” (e.g., optionally substituted alkyl) is intended to be equivalent to “X, wherein X is optionally substituted” (e.g., “alkyl, wherein the alkyl is optionally substituted”). It is not intended to mean that the feature “X” (e.g., alkyl) per se is optional. As used herein, the terms “alkyl” and the prefix “alk-” are inclusive of both straight chain and branched chain groups and of cyclic groups, i.e., cycloalkyl, and combinations thereof. Cyclic groups can be monocyclic or polycyclic and preferably have from 3 to 6 ring carbon atoms, inclusive. Exemplary cyclic groups include cyclopropyl, cyclobutyl, cyclopentyl, and cyclohexyl groups. The C1-8 alkyl group may be substituted or unsubstituted. Exemplary substituents include alkoxy, aryloxy, sulfhydryl, alkylthio, arylthio, halide, hydroxyl, fluoroalkyl, perfluoralkyl, cyano, nitrilo, NH-acyl, amino, aminoalkyl, disubstituted amino, C _2-7 heterocyclyl, quaternary amino, hydroxyalkyl, carboxyalkyl, and carboxyl groups. C _1-8 alkyls include, without limitation, methyl; ethyl; n-propyl; isopropyl; cyclopropyl; cyclopropylmethyl; cyclopropylethyl; n-butyl; iso-butyl; sec-butyl; tert-butyl; cyclobutyl; cyclobutylmethyl; cyclobutylethyl; n- pentyl; cyclopentyl; cyclopentylmethyl; cyclopentylethyl; 1-methylbutyl; 2-methylbutyl; 3-methylbutyl; 2,2- dimethylpropyl; 1-ethylpropyl; 1,1-dimethylpropyl; 1,2-dimethylpropyl; 1-methylpentyl; 2-methylpentyl; 3- methylpentyl; 4-methylpentyl; 1,1-dimethylbutyl; 1,2-dimethylbutyl; 1,3-dimethylbutyl; 2,2-dimethylbutyl; 2,3-dimethylbutyl; 3,3-dimethylbutyl; 1-ethylbutyl; 2-ethylbutyl; 1,1,2-trimethylpropyl; 1,2,2-trimethylpropyl; 1-ethyl-1-methylpropyl; 1-ethyl-2-methylpropyl; and cyclohexyl. An alkylene is a divalent alkyl group. By “C _2-8 alkenyl” is meant a branched or unbranched hydrocarbon group containing one or more double bonds and having from 2 to 8 carbon atoms. A C2-8 alkenyl may optionally include monocyclic or polycyclic rings, in which each ring desirably has from three to six members. The C2-8 alkenyl group may be substituted or unsubstituted. Exemplary substituents include alkoxy, aryloxy, sulfhydryl, alkylthio, arylthio, halide, hydroxyl, fluoroalkyl, perfluoralkyl, cyano, nitrilo, NH-acyl, amino, aminoalkyl, disubstituted amino, quaternary amino, hydroxyalkyl, carboxyalkyl, and carboxyl groups. C2-8 alkenyls include, without limitation, vinyl; allyl; 2-cyclopropyl-1-ethenyl; 1-propenyl; 1-butenyl; 2-butenyl; 3-butenyl; 2-methyl-1- propenyl; 2-methyl-2-propenyl; 1-pentenyl; 2-pentenyl; 3-pentenyl; 4-pentenyl; 3-methyl-1-butenyl; 3- methyl-2-butenyl; 3-methyl-3-butenyl; 2-methyl-1-butenyl; 2-methyl-2-butenyl; 2-methyl-3-butenyl; 2-ethyl- 2-propenyl; 1-methyl-1-butenyl; 1-methyl-2-butenyl; 1-methyl-3-butenyl; 2-methyl-2-pentenyl; 3-methyl-2- pentenyl; 4-methyl-2-pentenyl; 2-methyl-3-pentenyl; 3-methyl-3-pentenyl; 4-methyl-3-pentenyl; 2-methyl- 4-pentenyl; 3-methyl-4-pentenyl; 1,2-dimethyl-1-propenyl; 1,2-dimethyl-1-butenyl; 1,3-dimethyl-1-butenyl; 1,2-dimethyl-2-butenyl; 1,1-dimethyl-2-butenyl; 2,3-dimethyl-2-butenyl; 2,3-dimethyl-3-butenyl; 1,3- dimethyl-3-butenyl; 1,1-dimethyl-3-butenyl and 2,2-dimethyl-3-butenyl. In particular embodiments the C2-8 alkenyl has a cis configuration around the double bond. By “C _2-7 heterocyclyl” is meant a stable 5- to 7-membered monocyclic or 7- to 14-membered bicyclic heterocyclic ring which is saturated, partially unsaturated, or unsaturated (aromatic), and which consists of 2 to 7 carbon atoms and 1, 2, 3, or 4 heteroatoms independently selected from the group consisting of N, O, and S, and including any bicyclic group in which any of the above-defined heterocyclic rings is fused to a benzene ring. The heterocyclyl group may be substituted or unsubstituted. Exemplary substituents include alkoxy, aryloxy, sulfhydryl, alkylthio, arylthio, halide, hydroxy, fluoroalkyl, perfluoralkyl, cyano, nitrilo, NH-acyl, amino, aminoalkyl, disubstituted amino, quaternary amino, hydroxyalkyl, carboxyalkyl, and carboxyl groups. The nitrogen and sulfur heteroatoms may optionally be oxidized. The heterocyclic ring may be covalently attached via any heteroatom or carbon atom which results in a stable structure, e.g., an imidazolinyl ring may be linked at either of the ring-carbon atom positions or at the nitrogen atom. A nitrogen atom in the heterocycle may optionally be quaternized. Preferably when the total number of S and O atoms in the heterocycle exceeds 1, then these heteroatoms are not adjacent to one another. Heterocycles include, without limitation, 1H-indazole, 2- pyrrolidonyl, 2H,6H-1,5,2-dithiazinyl, 2H-pyrrolyl, 3H-indolyl, 4-piperidonyl, 4aH-carbazole, 4H- quinolizinyl, 6H-1,2,5-thiadiazinyl, acridinyl, azocinyl, benzimidazolyl, benzofuranyl, benzothiofuranyl, benzothiophenyl, benzoxazolyl, benzthiazolyl, benztriazolyl, benztetrazolyl, benzisoxazolyl, benzisothiazolyl, benzimidazalonyl, carbazolyl, 4aH-carbazolyl, beta-carbolinyl, chromanyl, chromenyl, cinnolinyl, decahydroquinolinyl, 2H,6H-1,5,2-dithiazinyl, dihydrofuro[2,3-b]tetrahydrofuran, furanyl, furazanyl, imidazolidinyl, imidazolinyl, imidazolyl, 1H-indazolyl, indolenyl, indolinyl, indolizinyl, indolyl, isobenzofuranyl, isochromanyl, isoindazolyl, isoindolinyl, isoindolyl, isoquinolinyl, isothiazolyl, isoxazolyl, morpholinyl, naphthyridinyl, octahydroisoquinolinyl, oxadiazolyl, 1,2,3-oxadiazolyl, 1,2,4-oxadiazolyl, 1,2,5-oxadiazolyl, 1,3,4-oxadiazolyl, oxazolidinyl, oxazolyl, oxazolidinylperimidinyl, phenanthridinyl, phenanthrolinyl, phenarsazinyl, phenazinyl, phenothiazinyl, phenoxathiinyl, phenoxazinyl, phthalazinyl, piperazinyl, piperidinyl, pteridinyl, piperidonyl, 4-piperidonyl, pteridinyl, purinyl, pyranyl, pyrazinyl, pyrazolidinyl, pyrazolinyl, pyrazolyl, pyridazinyl, pyridooxazole, pyridoimidazole, pyridothiazole, pyridinyl, pyridyl, pyrimidinyl, pyrrolidinyl, pyrrolinyl, pyrrolyl, quinazolinyl, quinolinyl, 4H-quinolizinyl, quinoxalinyl, quinuclidinyl, carbolinyl, tetrahydrofuranyl, tetrahydroisoquinolinyl, tetrahydroquinolinyl, 6H-1,2,5- thiadiazinyl, 1,2,3-thiadiazolyl, 1,2,4-thiadiazolyl, 1,2,5-thiadiazolyl, 1,3,4-thiadiazolyl, thianthrenyl, thiazolyl, thienyl, thienothiazolyl, thienooxazolyl, thienoimidazolyl, thiophenyl, triazinyl, 1,2,3-triazolyl, 1,2,4-triazolyl, 1,2,5-triazolyl, 1,3,4-triazolyl, xanthenyl. Preferred 5 to 10 membered heterocycles include, but are not limited to, pyridinyl, pyrimidinyl, triazinyl, furanyl, thienyl, thiazolyl, pyrrolyl, pyrazolyl, imidazolyl, oxazolyl, isoxazolyl, tetrazolyl, benzofuranyl, benzothiofuranyl, indolyl, benzimidazolyl, 1H- indazolyl, oxazolidinyl, isoxazolidinyl, benzotriazolyl, benzisoxazolyl, oxindolyl, benzoxazolinyl, quinolinyl, and isoquinolinyl. Preferred 5 to 6 membered heterocycles include, without limitation, pyridinyl, pyrimidinyl, triazinyl, furanyl, thienyl, thiazolyl, pyrrolyl, piperazinyl, piperidinyl, pyrazolyl, imidazolyl, oxazolyl, isoxazolyl, and tetrazolyl. By “C6-12 aryl” is meant an aromatic group having a ring system comprised of carbon atoms with conjugated π electrons (e.g., phenyl). The aryl group has from 6 to 12 carbon atoms. Aryl groups may optionally include monocyclic, bicyclic, or tricyclic rings, in which each ring desirably has five or six members. The aryl group may be substituted or unsubstituted. Exemplary subsituents include alkyl, hydroxy, alkoxy, aryloxy, sulfhydryl, alkylthio, arylthio, halide, fluoroalkyl, carboxyl, hydroxyalkyl, carboxyalkyl, amino, aminoalkyl, monosubstituted amino, disubstituted amino, and quaternary amino groups. By “C7-14 alkaryl” is meant an alkyl substituted by an aryl group (e.g., benzyl, phenethyl, or 3,4- dichlorophenethyl) having from 7 to 14 carbon atoms. By “C3-10 alkheterocyclyl” is meant an alkyl substituted heterocyclic group having from 7 to 14 carbon atoms in addition to one or more heteroatoms (e.g., 3-furanylmethyl, 2-furanylmethyl, 3- tetrahydrofuranylmethyl, or 2-tetrahydrofuranylmethyl). By “C1-8 heteroalkyl” is meant a branched or unbranched alkyl, alkenyl, or alkynyl group having from 1 to 8 carbon atoms in addition to1, 2, 3 or 4 heteroatoms independently selected from the group consisting of N, O, S, and P. Heteroalkyls include, without limitation, tertiary amines, secondary amines, ethers, thioethers, amides, thioamides, carbamates, thiocarbamates, hydrazones, imines, phosphodiesters, phosphoramidates, sulfonamides, and disulfides. A heteroalkyl may optionally include monocyclic, bicyclic, or tricyclic rings, in which each ring desirably has three to six members. The heteroalkyl group may be substituted or unsubstituted. Exemplary substituents include alkoxy, aryloxy, sulfhydryl, alkylthio, arylthio, halide, hydroxyl, fluoroalkyl, perfluoralkyl, cyano, nitrilo, NH-acyl, amino, aminoalkyl, disubstituted amino, quaternary amino, C2-7 heterocyclyl, hydroxyalkyl, hydroxyalkyl, carboxyalkyl, and carboxyl groups. Examples of C1-8 heteroalkyls include, without limitation, methoxymethyl and ethoxyethyl. By “halide” is meant bromine, chlorine, iodine, or fluorine. By “fluoroalkyl” is meant an alkyl group that is substituted with one or more fluorine atoms. By “carboxyalkyl” is meant a chemical moiety with the formula -(R)-COOH, wherein R is selected from C _1-8 alkyl, C _2-7 heterocyclyl, C _6-12 aryl, C _7-14 alkaryl, C _3-10 alkheterocyclyl, or C _1-8 heteroalkyl. By “hydroxyalkyl” is meant a chemical moiety with the formula -(R)-OH, wherein R is selected from C1-8 alkyl, C2-7 heterocyclyl, C6-12 aryl, C7-14 alkaryl, C3-10 alkheterocyclyl, or C1-8 heteroalkyl. By “alkoxy” is meant a chemical substituent of the formula -OR, wherein R is selected from C1-8 alkyl, C _2-7 heterocyclyl, C _6-12 aryl, C _7-14 alkaryl, C _3-10 alkheterocyclyl, or C _1-8 heteroalkyl. By “aryloxy” is meant a chemical substituent of the formula -OR, wherein R is a C _6-12 aryl group. By “alkylthio” is meant a chemical substituent of the formula -SR, wherein R is selected from C1-8 alkyl, C2-7 heterocyclyl, C6-12 aryl, C7-14 alkaryl, C3-10 alkheterocyclyl, or C1-8 heteroalkyl. By “arylthio” is meant a chemical substituent of the formula -SR, wherein R is a C _6-12 aryl group. By “quaternary amino” is meant a chemical substituent of the formula -(R)-N(R’)(R’’)(R’’’) ⁺ , wherein R, R’, R’’, and R’’’ are each independently an alkyl, alkenyl, alkynyl, or aryl group. R may be an alkyl group linking the quaternary amino nitrogen atom, as a substituent, to another moiety. The nitrogen atom, N, is covalently attached to four carbon atoms of alkyl and/or aryl groups, resulting in a positive charge at the nitrogen atom. By “acyl” is meant a chemical moiety with the formula R-C(O)-, wherein R is selected from C1-8 alkyl, C2-7 heterocyclyl, C6-12 aryl, C7-14 alkaryl, C3-10 alkheterocyclyl, or C1-8 heteroalkyl. The term “prodrug” means a compound (e.g., a drug precursor) that is transformed in vivo to yield a compound of the instant Formulas. The transformation may occur by various mechanisms (e.g., by metabolic or chemical processes), such as, for example, through hydrolysis in blood. A discussion of the use of prodrugs is provided by T. Higuchi and W. Stella, “Pro-drugs as Novel Delivery Systems,” Vol.14 of the A.C.S. Symposium Series, and in Bioreversible Carriers in Drug Design, ed. Edward B. Roche, American Pharmaceutical Association and Pergamon Press, 1987. For example, if a compound of the instant Formulas contains an alcohol functional group, a prodrug can be formed by the replacement of the hydrogen atom of the alcohol group with a group to form an ester or methylenedioxy-linked ester. Suitable prodrug esters can include, for example, phosphate esters or acyl esters. In particular embodiments, the prodrug ester is selected from phosphate esters of formula —P(O)(OH) ₂ , — P(O)(OH)(O)(C ₁ -C ₆ alkyl), —P(O)(O)(C ₁ -C ₆ alkyl) ₂ , either as directly linked phosphate esters or methyleneoxy-linked phosphate esters; C1-C6-alkanoyloxymethyl esters, dimethylamino acid esters, and C1-C6-alkanoyl esters (e.g., acetate esters), either as directly linked alkanoyl esters or methyleneoxy- linked alkanoyl esters. Terms such as "a", "an," and "the" are not intended to refer to only a singular entity but include the general class of which a specific example may be used for illustration. As used herein, the term “about” refers to a value that is within 10% above or below the value being described. As used herein, the terms “acute stress disorder” and “ASD” refer to a condition that arises as a response to a stressful event or situation of an exceptionally threatening or catastrophic nature, which is likely to cause pervasive distress in an individual (e.g., natural or man-made disaster, combat, serious accident, witnessing the violent death of others, or being the victim of torture, terrorism, rape, or other crime). Like PTSD, acute stress disorder is an anxiety disorder that involves a very specific reaction following exposure to a traumatic event or stressor. However, the duration of acute stress disorder is shorter than that for PTSD, such that the symptoms are present for at least one, two, or three days, but no more than four, five, or six weeks. For individuals exhibiting symptoms persisting for a longer period of time, a diagnosis of PTSD may be warranted. The term “administration” or “administering” refers to a method of giving a dosage of a compound or pharmaceutical composition to a subject. By "dysthymia" or "dysthymic disorder" is meant a chronically depressed mood that occurs for most of the day, more days than not, for at least two years. In children and adolescents, the mood may be irritable rather than depressed, and the required minimum duration is one year. During the two year period (one year for children or adolescents), any symptom-free intervals last no longer than 2 months. During periods of depressed mood, at least two of the following additional symptoms are present: poor appetite or overeating, insomnia or hypersomnia, low energy or fatigue, low self-esteem, poor concentration, or difficulty making decisions, and feelings of hopelessness. The symptoms cause clinically significant distress or impairment in social, occupational (or academic), or other important areas of functioning. The diagnosis of dysthymia is not made if: the individual has ever had a manic episode, a mixed episode, a hypomanic episode; has ever met the criteria for a cyclothymic disorder; the depressive symptoms occur exclusively during the course of a chronic psychotic disorder (e.g., schizophrenia); or if the disturbance is due to the direct physiological effects of a substance or a general medical condition. After the initial two-years of dysthymic disorder, major depressive episodes may be superimposed on the dysthymic disorder ("double depression"). Diagnostic and Statistical Manual of Mental Disorders (OSM IV), American Psychiatric Press, 4th Edition, I 994. Diagnostic guidance for psychological disorders can be found, for example, in the ICD-10 (The ICD-10 Classification of Mental and Behavioral Disorders: Diagnostic Criteria for Research, Geneva: World Health Organization, 1993) and the DSM-V (American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) Arlington, VA.; American Psychiatric Association, 2013). As used herein, the term “generalized anxiety disorder” refers to a condition characterized by excessive anxiety and worry (i.e., apprehensive expectation). Typically, the excessive anxiety and worry occur on more days than not for a period of time (e.g., one, two, three, or four months or more). The anxiety and worry can be associated with (i) restlessness, feeling keyed up, or on edge; and/or (ii) muscle tension. The anxiety and worry can be associated with (a) a marked avoidance of situations in which a negative outcome could occur; (b) a marked time and effort preparing for situations in which a negative outcome could occur; (c) a marked procrastination in behavior or decision-making due to worries; and (d) repeatedly seeking reassurance due to worries. The anxiety, worry, or physical symptoms can cause clinically significant distress or impairment in social, occupational, or other important areas of functioning in many, but not necessarily all individuals with GAD. As used herein, the terms “obsessive compulsive disorder,” “OCD,” and “anxiety and obsessive- compulsive spectrum disorders” refer to a condition characterized by obsessions and/or compulsions. Obsessions are recurrent and persistent thoughts, urges, or images that are experienced, at some time during the disturbance, as intrusive and unwanted and that usually cause marked anxiety or distress in which the obsessed individual attempts to ignore or suppress such thoughts, urges, or images, or to neutralize them with some other thought or action (i.e., by performing a compulsion). Compulsions are repetitive behaviors (e.g., hand washing, ordering, checking) or mental acts (e.g., praying, counting, repeating words silently) that the person feels driven to perform in response to an obsession, or according to rules that must be applied rigidly. The behaviors or mental acts are aimed at preventing or reducing anxiety or distress, or preventing some dreaded event or situation; however, these behaviors or mental acts either are not connected in a realistic way with what they are designed to neutralize or prevent or are clearly excessive. Typically, the obsessions or compulsions are time consuming (for example, take more than 1 hour a day), or cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. As used herein, the term “pharmaceutically acceptable salt” refers to those salts of the compounds described herein that are suitable for pharmaceutical use. Pharmaceutically acceptable salts are well known in the art. For example, pharmaceutically acceptable salts are described in: Berge et al., J. Pharmaceutical Sciences 66:1-19, 1977 and in Pharmaceutical Salts: Properties, Selection, and Use, (Eds. P.H. Stahl and C.G. Wermuth), Wiley-VCH, 2008. The salts can be prepared in situ during the final isolation and purification of the compounds described herein or separately, e.g., by reacting the free base of the compound with a suitable organic acid or inorganic acid. Pharmaceutically acceptable salts may include, for example, chloride, bromide, malate, fumarate, succinate, benzoate, phosphate, diphosphate, sodium, sulfate, acetate, potassium citrate, mesylate, nitrate, tartrate and gluconate salts. Pharmaceutically acceptable salts may include, for example, chloride, bromide, malate, fumarate, succinate, benzoate, phosphate, diphosphate, sulfate, acetate, citrate, mesylate, nitrate, tartrate and gluconate salts. As used herein, the term “panic disorder” refers to a condition characterized by recurrent and unexpected panic attacks. Panic disorder includes both panic disorder with agoraphobia and panic disorder without agoraphobia. Subjects with this condition can exhibit one or both of the following: (i) a persistent concern or worry about additional panic attacks or their consequences (e.g., losing control, having a heart attack, going crazy); and/or (ii) significant maladaptive change in behavior related to the attacks (e.g., behaviors designed to avoid having panic attacks), which may include agoraphobic avoidance. As used herein, the terms “post traumatic stress disorder” and “PTSD” refer to a condition that arises as a delayed and/or protracted response to a stressful event or situation (either short- or long- lasting) of an exceptionally threatening or catastrophic nature, which is likely to cause pervasive distress in an individual (e.g., natural or man-made disaster, combat, serious accident, witnessing the violent death of others, or being the victim of torture, terrorism, rape, or other crime). Predisposing factors such as personality traits (e.g., compulsive, asthenic) or previous history of neurotic illness may lower the threshold for the development of the condition or aggravate its course, but they are neither necessary nor sufficient to explain its occurrence. PTSD is a less frequent and more enduring consequence of psychological trauma than the more frequently seen acute stress response. PTSD has been recognized in the past as railway spine, stress syndrome, shell shock, battle fatigue, traumatic war neurosis, and post-traumatic stress syndrome. Diagnostic symptoms include re-experiencing original trauma(s), by means of flashbacks or nightmares; avoidance of stimuli associated with the trauma; and increased arousal, such as difficulty falling or staying asleep, anger, and hypervigilance. Formal diagnostic criteria (DSM-V, DSM-IV, and/or ICD-9) require that the symptoms last more than one month and cause significant impairment in social, occupational, or other important areas of functioning (e.g., problems with work and/or relationships). Formal diagnostic criteria can include: (i) intrusion symptoms that are associated with the traumatic event (e.g., (a) spontaneous or cued recurrent, involuntary, and intrusive distressing memories of the traumatic event; (b) recurrent distressing dreams in which the content and/or affect of the dream is related to the event; (c) dissociative reactions (e.g., flashbacks) in which the individual feels or acts as if the traumatic event were recurring (such reactions may occur on a continuum, with the most extreme expression being a complete loss of awareness of present surroundings; (d) intense or prolonged psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event; and/or (e) marked physiological reactions to reminders of the traumatic event); (ii) persistent avoidance of stimuli associated with the traumatic event (e.g., (a) thoughts, feelings, or physical sensations that arouse recollections of the traumatic event; (b) activities, places, physical reminders, or times (e.g., anniversary reactions) that arouse recollections of the traumatic event; and/or (c) people, conversations, or interpersonal situations that arouse recollections of the traumatic event); (iii) negative alterations in cognitions and mood that are associated with the traumatic event (e.g., (a) inability to remember an important aspect of the traumatic event (typically dissociative amnesia); (b) persistent and exaggerated negative expectations about one’s self, others, or the world; (c) persistent distorted blame of self or others about the cause or consequences of the traumatic event; (d) pervasive negative emotional state (e.g., fear, horror, anger, guilt, or shame); (e) markedly diminished interest or participation in significant activities; (f) feeling of detachment or estrangement from others; and/or (g) persistent inability to experience positive emotions (e.g., unable to have loving feelings, psychic numbing); and (iv) alterations in arousal (i.e., hyperarousal) and reactivity that are associated with the traumatic event (e.g., (a) irritable, angry, or aggressive behavior; (b) reckless or self-destructive behavior; (c) hypervigilance; (d) exaggerated startle response; (e) problems with concentration; and/or (f) sleep disturbance (e.g., difficulty falling or staying asleep, or restless sleep)). Formal diagnostic criteria can further include that the duration of disturbance is more than a certain period of time (e.g., one month, three months, or six months) and that the disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning. In a small proportion of patients, the condition may show a chronic course over many years and a transition to an enduring personality change. The three main symptoms associated with PTSD are (1) “reliving” the traumatic event, such as flashbacks, nightmares, intrusive thoughts, and recollections, (2) avoidance behaviors and emotional numbing, and (3) hypersensitivity such as an inability to sleep, anxious feelings, overactive startle response, hyperarousal, hypervigilance, irritability, and outbursts of anger. As used herein, the terms “psychological disorder” and “psychological condition” refer to a condition characterized by a disturbance in one’s emotional or behavioral regulation that reflects a dysfunction in the psychological, biological, or developmental processes underlying mental function. Psychological disorders include, but are not limited to depressive disorders (major depression, treatment resistant depression, melancholic depression, atypical depression, or dysthymia), anxiety disorders (end of life anxiety, generalized anxiety disorder, panic disorder, social anxiety, post-traumatic stress disorder, acute stress disorder, obsessive compulsive disorder, or social phobia), addictions (e.g., substance abuse, e.g., alcoholism, tobacco abuse, or drug abuse)), eating disorders (e.g., anorexia nervosa, bulimia nervosa, and binge eating disorder) and compulsive behavior disorders (e.g., primary impulse-control disorders or obsessive-compulsive disorder). Psychological disorders can be any psychological condition associated with one or more symptoms, e.g., somatic symptoms (e.g., chronic pain, anxiety disproportionate to severity of physical complaints, pain disorder, body dysmorphia, conversion (i.e., loss of bodily function due to anxiety), hysteria, or neurological conditions without identifiable cause), or psychosomatic symptoms (e.g., back pain, fibromyalgia, migraines, and chronic fatigue syndrome). Psychological disorders also include repetitive body-focused behaviors, such as tic disorders (e.g., Tourette's Syndrome, trichotillomania, nail-biting, temporomandibular disorder, thumb-sucking, repetitive oral-digital, lip-biting, fingernail biting, eye-rubbing, skin-picking, or a chronic motor tic disorder). In some cases, development of a psychological disorder is associated with or characterized by a prodromal symptom, such as depressed mood, decreased appetite, weight loss, increased appetite, weight gain, initial insomnia, middle insomnia, early waking, hypersomnia, decreased energy, decreased interest or pleasure, self-blame, decreased concentration, indecision, suicidality, psychomotor agitation, psychomotor retardation, crying more frequently, inability to cry, hopelessness, worrying/brooding, decreased self-esteem, irritability, dependency, self-pity, somatic complaints, decreased effectiveness, helplessness, and decreased initiation of voluntary responses. As used herein, the terms “social phobia” and “social anxiety disorder” refer to a condition characterized by fear or anxiety associated with one or more social situations. Subjects with this condition typically exhibit a marked fear or anxiety about one or more social situations in which the person is exposed to possible scrutiny by others. Examples include social interactions (e.g., having a conversation), being observed (e.g., eating or drinking), or performance in front of others (e.g., giving a speech). Typically, an individual with this condition (i) fears that he or she will act in a way, or show anxiety symptoms that will be negatively evaluated (i.e., be humiliating, embarrassing, lead to rejection, or offend others); (ii) the social situations almost invariably provoke immediate fear or anxiety; (iii) the social situations are avoided or endured with intense fear or anxiety; and (iv) the fear or anxiety is out of proportion to the danger posed by the social situation. In children, the fear or anxiety may be expressed by crying, tantrums, freezing, clinging, shrinking or refusal to speak in social situations. The fear, anxiety, and avoidance can cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. The term “therapeutically effective amount,” as used herein, refers to an amount, e.g., pharmaceutical dose, effective in inducing a desired effect in a subject or in treating a subject having a condition or disorder described herein (e.g., an inflammatory disorder). It is also to be understood herein that a “therapeutically effective amount” may be interpreted as an amount giving a desired therapeutic and/or preventative effect, taken in one or more doses or in any dosage or route, and/or taken alone or in combination with other therapeutic agents. For example, in the context of administering a composition described herein that is used for the treatment of a disorder or condition, an effective amount of a compound is, for example, an amount sufficient to prevent, slow down, or reverse the progression of the disorder or condition as compared to the response obtained without administration of the compound. As used herein, the terms “treat,” “treating,” or “treatment” refer to administration of a compound or pharmaceutical composition for a therapeutic purpose. To “treat a disorder” or use for “therapeutic treatment” refers to administering treatment to a patient already suffering from a disease to ameliorate the disease or one or more symptoms thereof to improve the patient’s condition (e.g., by reducing one or more symptoms of a 5-HT2 responsive condition, such as inflammation, depression, anxiety, Alzheimer’s disease, etc.). The term “therapeutic” includes the effect of mitigating deleterious clinical effects of certain inflammatory processes (i.e., consequences of the inflammation, rather than the symptoms of inflammation). The methods of the invention can be used as a primary prevention measure, i.e., to prevent a condition or to reduce the risk of developing a condition. Prevention refers to prophylactic treatment of a patient who may not have fully developed a condition or disorder, but who is susceptible to, or otherwise at risk of, the condition. Thus, in the claims and embodiments, the methods of the invention can be used either for therapeutic or prophylactic purposes. By "unipolar depression" or "major depressive disorder" is meant a clinical course that is characterized by one or more major depressive episodes in an individual without a history of manic, mixed, or hypomanic episodes. The diagnosis of unipolar depression is not made if: manic, mixed, or hypomanic episodes develop during the course of depression; if the depression is due to the direct physiological effects of a substance; if the depression is due to the direct physiological effects of a general medical condition; if the depression is due to a bereavement or other significant loss ("reactive depression"); or if the episodes are better accounted for by schizoaffective disorder and are not superimposed on schizophrenia, schizophreniform disorder, delusional disorder, or psychotic disorder. If manic, mixed, or hypomanic episodes develop, then the diagnosis is changed to a bipolar disorder. Depression may be associated with chronic general medical conditions (e.g., diabetes, myocardial infarction, carcinoma, and stroke). Generally, unipolar depression is more severe than dysthymia. The essential feature of a major depressive episode is a period of at least two15 weeks during which there is either depressed mood or loss of interest or pleasure in nearly all activities. In children and adolescents, the mood may be irritable rather than sad. The episode may be a single episode or may be recurrent. The individual also experiences at least four additional symptoms drawn from a list that includes changes in appetite or weight, sleep, and psychomotor activity; decreased energy; feelings of worthlessness or guilt; difficulty thinking, concentrating, or making decisions; or recurrent thoughts of death or suicidal ideation, plans, or attempts. Each symptom must be newly present or must have clearly worsened compared with the person's pre-episode status. The symptoms must persist for most of the day, nearly every day, for at least two consecutive weeks, and the episode must be accompanied by clinically significant distress or impairment in social, occupational (or academic), or other important areas of functioning (Diagnostic and Statistical Manual of Mental Disorders (OSM IV), American Psychiatric Press, 4th Edition, 1994). Diagnostic guidance for psychological disorders can be found, for example, in the ICD-10 (The ICD-10 Classification of Mental and Behavioral Disorders: Diagnostic Criteria for Research, Geneva: World Health Organization, 1993) and the DSM-V (American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) Arlington, VA.; American Psychiatric Association, 2013). Other features and advantages of the invention will be apparent from the following Detailed Description, Examples, and Claims. DETAILED DESCRIPTION OF THE INVENTION The invention features compounds of formula (I), (II), or (III). The compounds are useful for treating 5-HT2 responsive conditions (e.g., inflammation, pain, depression, anxiety, PTSD, and Alzheimer’s disease). The compounds can be resistant to metabolism (e.g., by monoamineoxidase degradation in vivo), and can exhibit a longer in-vivo half-life and hence longer lasting pharmacological effect. Serotonin (also referred to as 5-hydroxytryptamine or 5-HT) is a neurotransmitter that has been strongly implicated in the pathophysiology and treatment of a wide variety of neuropsychiatric disorders. Serotonin exerts its effects through a diverse family of serotonin receptor molecules or serotonin reuptake sites (referred to herein as “5-HT receptors,” “5-HTRs,” or the SERT). Classically, members of the serotonin receptor family have been grouped into seven (7) subtypes pharmacologically, i.e., according to their specificity of various serotonin antagonists. Thus, although all the 5-HT receptors specifically bind with serotonin, they are pharmacologically distinct and are encoded by separate genes. To date, fourteen (14) mammalian serotonin receptors have been identified and sequenced. More particularly, these fourteen separate 5-HT receptors have been grouped into seven (7) pharmacological subtypes, designated 5-HT1, 5-HT2, 5-HT3, 5-HT4, 5-HT5, 5-HT6, and 5-HT7. Several of the subtypes are further subdivided such that the receptors are grouped pharmacologically as follows: 5-HT1A, 5-HT1B, 5-HT1D, 5-HT1E, 5-HT1F, 5-HT2A, 5-HT2B, 5-HT2C, 5-HT3A, 5-HT3B, 5-HT4, 5-HT5A, 5-HT6, 5-HT7. Of the fourteen different mammalian serotonin receptors that have been cloned, all but one are members of the G-protein coupled receptor superfamily. Serotonin receptors 5-HT1A, 5-HT1B, and 5- HT1D inhibit adenylate cyclase, and 5-HT2 receptors activate phospholipase C pathways, stimulating breakdown of polyphosphoinositides. The 5-HT2 receptor belongs to the family of rhodopsin-like signal transducers that are distinguished by a seven-transmembrane configuration and functional linkage to G- proteins. The 5-HT3 receptor family includes ligand-gated ion channel receptors that have four putative TMDs. Serotonin regulates a wide variety of sensory, motor, and behavioral functions in the mammalian CNS, including behaviors such as learning and memory, sleep, thermoregulation, motor activity, pain, sexual and aggressive behaviors, appetite, neuroendocrine regulation, and biological rhythms. Serotonin has also been linked to pathophysiological conditions such as anxiety, depression, obsessive-compulsive disorders, schizophrenia, suicide, autism, migraine, emesis, alcoholism and neurodegenerative disorders. This biogenic amine neurotransmitter is synthesized by neurons of the brain stem that project throughout the CNS, with highest density in basal ganglia and limbic structures (Steinbusch, 1984, In: Handbook of Chemical Neuroanatomy 3:68-125, Bjorklund et al., Eds., Elsevier Science Publishers, B. V.). Studies have suggested that serotonin may play a role in the immune system since data demonstrate that serotonin receptors are present on various cells of the immune system. There have been reports in the literature about the immunomodulatory effects of adding serotonin exogenously to mitogenically stimulated lymphocyte cultures. Under some circumstances, serotonin has been shown to stimulate the activated T cells (Foon et al., 1976, J. Immunol. 117:1545-1552; Kut et al., 1992, Immunopharmacol. Immunotoxicol. 14:783-796; Young et al., 1993, Immunology 80:395-400), whereas other laboratories report that high concentrations of added serotonin inhibit the proliferation (Slauson et al., 1984, Cell. Immunol. 84:240-252; Khan et al., 1986, Int. Arch. Allergy Appl. Immunol. 81:378-380; Mossner & Lesch, 1998, Brain, Behavior, and Immunity 12:249-271). Of the fourteen known pharmacologically distinct serotonin receptors, lymphocytes express type 2A, type 2B, type 2C, type 6 and type 7 on resting cells (Ameisen et al., 1989, J. Immunol. 142:3171- 3179; Stefulj et al., 2000, Brain, Behavior, and Immunity 14:219-224) and that the type 1A and type 3 receptors are up-regulated upon activation (Aune et al., 1993, J. Immunol. 151:1175-1183; Meyniel et al., 1997, Immunol. Lett. 55:151-160; Stefulj et al., 2000, Brain, Behavior, and Immunity 14:219-224). The involvement of the 5-HT1A receptors in human and murine T cells has also been demonstrated (Aune et al., 1990, J. Immunol. 145:1826-1831; Aune et al., 1993, J. Immunol. 151:1175- 1183; Aune et al., 1994, J. Immunol. 153:1826-1831). These studies established that IL-2-stimulated human T cell proliferation could be inhibited by a blockade of tryptophan hydroxylase, i.e., the first enzyme involved in the conversion of tryptophan to serotonin, and that the inhibition could be reversed by the addition of 5-hydroxy tryptophan. Furthermore, human T cell proliferation was blocked in vitro with a 5-HT1A-specific receptor antagonist. In a murine model, a type 1A receptor antagonist, but not a type 2 receptor antagonist, was able to inhibit the in vivo contact sensitivity response, but not antibody responses, to oxazalone. PCT Publication No. WO 03/106660 discloses the use of fluphenazine, an antagonist of 5- HT(1B/1D) and 5-HT(2C) receptors, for inhibiting proliferation and inducing cell death in lymphocytes. The new chemotypes of the invention may be screened for activity at the various 5-HT subtypes or monoamine transporters as described in Example 2. Compounds The invention features compounds of formula (I), (II), or (III). In particular embodiments, the compound of formula (I) is selected from: , , and pharma In particular embodiments, the compound of formula (I) is selected from: , and In particular embodiments, the compound of formula (II) is selected from: , , and In , and The compounds of formula (I), (II), or (III) can be synthesized using methods analogous to those described, e.g., in Matsuzono et al Tet. Lett., 2001, 42 (43), 7621-7623; Billote. Syn. Lett., 1998, (4), 379- 380; and the synthetic methods described in the Examples. Pharmaceutical Compositions Pharmaceutical compositions of any of the aforementioned compounds include tablets for oral use containing the compound in a mixture with non-toxic pharmaceutically acceptable excipients. These excipients may be, for example, inert diluents or fillers (e.g., sucrose, sorbitol, sugar, mannitol, microcrystalline cellulose, starches including potato starch, sodium chloride, or lactose); granulating and disintegrating agents (e.g., cellulose derivatives including microcrystalline cellulose, starches including potato starch, croscarmellose sodium, alginates, or alginic acid); binding agents (e.g., sucrose, glucose, sorbitol, acacia, alginic acid, sodium alginate, gelatin, starch, pregelatinized starch, microcrystalline cellulose, magnesium aluminum silicate, carboxymethylcellulose sodium, methylcellulose, hydroxypropyl methylcellulose, ethylcellulose, polyvinylpyrrolidone, or polyethylene glycol); and lubricating agents, glidants, and antiadhesives (e.g., magnesium stearate, zinc stearate, stearic acid, silicas, hydrogenated vegetable oils, or talc). Other pharmaceutically acceptable excipients can be colorants, flavoring agents, plasticizers, humectants, buffering agents, and the like. In some embodiments, a pharmaceutically acceptable excipient is at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100% pure. In some embodiments, an excipient is approved for use in humans and for veterinary use. In some embodiments, an excipient is approved by United States Food and Drug Administration. In some embodiments, an excipient is pharmaceutical grade. In some embodiments, an excipient meets the standards of the United States Pharmacopoeia (USP), the European Pharmacopoeia (EP), the British Pharmacopoeia, and/or the International Pharmacopoeia. In some embodiments, the pharmaceutical composition is prepared, packaged, and/or sold in a formulation suitable for pulmonary administration, e.g., via a nebulizer. Such a formulation may include dry particles that include the active ingredient in the form of dry powders for administration using a device including a dry powder reservoir to which a stream of propellant may be directed to disperse the powder and/or using a self-propelling solvent/powder dispensing container such as a device including the active ingredient dissolved and/or suspended in a low-boiling propellant in a sealed container. Pharmaceutical compositions may be in the form of tablets and/or lozenges made using conventional methods, and may contain from 0.1% to 60% (w/w) active ingredient, the balance including an orally dissolvable and/or degradable composition and, optionally, one or more of the additional ingredients described herein. Pharmaceutical compositions for oral use may also be presented as chewable tablets, or as hard gelatin capsules in which the compound is mixed with an inert solid diluent (e.g., potato starch, lactose, microcrystalline cellulose, calcium phosphate, or kaolin), or as soft gelatin capsules wherein the compound is mixed with water or an oil medium, for example, peanut oil, liquid paraffin, or olive oil. Powders and granulates may be prepared using the ingredients mentioned above under tablets and capsules in a conventional manner using, e.g., a mixer, a fluid bed apparatus or a spray drying equipment. The pharmaceutical composition may also be administered parenterally by injection, infusion or implantation (intravenous, intramuscular, subcutaneous, or the like) in dosage forms, formulations, or via suitable delivery devices or implants containing conventional, non-toxic pharmaceutically acceptable carriers, and adjuvants. The formulation and preparation of such compositions are well known to those skilled in the art of pharmaceutical formulation. Formulations can be found in Hayes (Remington: The Science and Practice of Pharmacy, volume I and volume II. Twenty-second edition. Philadelphia, 2012). Methods Provided herein are methods of using a compound or pharmaceutical composition described herein to treat 5-HT2 responsive conditions in a subject. Methods of treating 5-HT2 responsive conditions include administering to a subject in need thereof a therapeutically effective amount of a compound or pharmaceutical composition of the invention. The exact amount of the compound or composition required for therapeutic effect can vary from subject to subject, depending on the species, age, weight, and general condition of the subject, the severity of the disease, the particular composition, its mode of administration, its mode of activity, and the like. Pharmaceutical compositions in accordance with the present disclosure are typically formulated in dosage unit form for ease of administration and uniformity of dosage. It will be understood, however, that the total daily usage of the compositions of the present disclosure will be decided by the attending physician within the scope of sound medical judgment. The specific therapeutically effective level for any particular subject will depend upon a variety of factors including the particular inflammatory disorder being treated and the severity thereof; the activity of the specific compound employed; the specific composition employed; the age, body weight, general health, sex and diet of the subject; the time of administration, route of administration, and rate of excretion of the specific compound employed; the duration of the treatment; drugs used in combination or coincidental with the specific compound employed; and like factors well known in the medical arts. Compositions described herein may be administered to subjects, such as human patients or, alternatively, to other mammals, such as domesticated animals, cats, dogs, mice, or rats. Compositions described herein may be administered by any route. In some embodiments, the present compound or pharmaceutical composition thereof is administered by one or more of a variety of routes, including nasal, buccal, oral, by inhalation (e.g., as an oral spray, nasal spray, or aerosol), intravenous, intramuscular, intra-arterial, intramedullary, intrathecal, subcutaneous, intraventricular, transdermal, interdermal, rectal, intravaginal, intraperitoneal, topical (e.g., by powders, ointments, creams, gels, lotions, and/or drops), mucosal, enteral, vitreal, intratumoral, sublingual; by intratracheal instillation, bronchial instillation, and/or through a portal vein catheter. In some embodiments the composition is administered by systemic intravenous injection. In specific embodiments the composition is administered intravenously and/or orally. A compound of the invention can be administered in a therapeutically effective amount (e.g., an amount that results in the desired therapeutic effect, e.g., within the therapeutic window between a dose sufficient to reduce inflammation and a dose that elicits a psychoactive effect (about a ten-fold difference)). In some embodiments, the compound is administered in an amount resulting in circulating drug plasma levels of less than 200 ng/mL (e.g., 0.5 to 200 ng/mL, e.g., 1 to 150 ng/mL, .5 to 100 ng/mL, or 10 to 50 ng/mL, e.g., 0.5 to 1 ng/mL, 1 to 2 ng/mL, 2 to 3 ng/mL, 3 to 4 ng/mL, 4 to 5 ng/mL, 5 to 10 ng/mL, 10 to 50 ng/mL, 50 to 100 ng/mL, 100 to 150 ng/mL, or 150 to 200 ng/mL, e.g., about 0.5 ng/mL, 1 ng/mL, 2 ng/mL, 5 ng/mL, 10 ng/mL, 20 ng/mL, 25 ng/mL, 50 ng/mL, 75 ng/mL, 100 ng/mL, 120 ng/mL, 150 ng/mL, or 200 ng/mL), e.g., in a human subject. In some embodiments, the circulating drug plasma level of the compound is below the limit of detection (e.g., 0.1 ng/mL or less). In some embodiments, a therapeutically effective amount of the compound can be less than about 2000 µg/kg body weight (e.g., less than 1000 µg/kg, less than 500 µg/kg, less than 100 µg/kg, or less than 50 µg/kg body weight, e.g., from 100 to 2000 µg/kg body weight, e.g., from 100 to 500 µg/kg, from 500 to 1000 µg/kg, from 1000 to 1500 µg/kg, or from 1500 to 1000 µg/kg, e.g., about 500 µg/kg, about 1000 µg/kg, about 1500 µg/kg, or about 2000 µg/kg). In certain embodiments, compositions in accordance with the present disclosure may be administered at dosage levels sufficient to deliver from about 0.0001 µg/kg to about 2 mg/kg, from about 0.01 µg/kg to about 500 µg/kg, from about 0.1 µg/kg to about 400 µg/kg, from about 0.5 µg/kg to about 30 µg/kg, from about 0.01 µg/kg to about 10 µg/kg, from about 0.1 µg/kg to about 10 µg/kg, from about 1 µg/kg to about 25 µg/kg, from about 25 µg/kg to about 0.5 mg/kg, from about 0.5 mg/kg to about 1.5 mg/kg, from about 1 mg/kg to about 2 mg/kg, or from about 1.5 mg/kg to about 2 mg/kg of subject body weight per day, one or more times a day, to obtain the desired therapeutic effect. The desired dosage may be delivered, e.g., once a day. Psychological Conditions In particular embodiments, the 5-HT2 responsive condition to be treated is a psychological condition. Disclosed herein are methods of treating psychological conditions. The psychological condition may be any psychological condition described herein. In some embodiments the psychological condition is depression, anxiety, addiction, post-traumatic stress disorder (PTSD), an eating disorder, or compulsive behavior. In some embodiments, the psychological condition may be depression. The psychological condition may also be anxiety. The anxiety may be experienced by a subject who is receiving palliative care or is enrolled in a hospice program. In certain embodiments, the subject who is experiencing anxiety has symptoms such as hypervigilance, fatigue, racing thoughts, irritability, excessive worry, and/or fear. A subject with a psychological condition may be diagnosed by a clinician, a physician, or a therapist. The subject may be diagnosed with a psychological condition by evaluation of the subject’s symptoms by a physician, clinician, or therapist based on a physical examination. For example, a blood test may be used to evaluate blood concentration levels of certain biomarkers such as hormones, calcium, vitamin D, electrolytes, and iron in diagnosing depression. Additionally or alternatively, for patients with a possible depression condition a depression screening test may be performed by the physician, clinician, or therapist to aid in the diagnosis of depression. The depression screening test may be the Patient Health Questionnaire-9 (PHQ-9), the Beck Depression Inventory (BDI), the Zung Self- Rating Depression Scale, the Center for Epidemiological Studies Depression Scale (CES-D), the Hamilton Rating Scale for Depression (HRSD), or the Montgomery-Asberg Depression Rating Scale (MADRS-C). In some embodiments, the methods described herein may be used to treat psychosomatic pain conditions. In some embodiments, the psychosomatic pain condition may be fibromyalgia, chronic fatigue, migraines, or back pain. In some embodiments, the patient is being treated for depression with a compound of formula (I), (II), or (III). The patient may have their symptoms of depression evaluated using a depression screening test. The symptoms of depression may be evaluated by a clinician using the Clinical Global Impression (CGI) rating. The depression screening test may be the Patient Health Questionnaire-9 (PHQ-9), the Beck Depression Inventory (BDI), the Zung Self-Rating Depression Scale, the Center for Epidemiological Studies Depression Scale (CES-D), the Hamilton Rating Scale for Depression (HRSD), and/or the Montgomery-Asberg Depression Rating Scale (MADRS). The patient being treated for depression with a compound of formula (I) or (II) may have their symptoms of depression evaluated using the Montgomery- Asberg Depression Rating Scale (MADRS-C). In some embodiments, the patient evaluated using the MADRS-C by a clinician, physician, or third-party rater. In certain embodiments, the patient may self- evaluate using the MADRS. The patient’s score obtained using the MADRS-C may be decreased compared to the score before treatment. The patient’s score may be decreased by at least 50% compared to the score before treatment. The patient’s score obtained using the MADRS-C may be less than 10. In some embodiments, the decrease in the patient’s score using the MADRS-C is decreased for 1 week after treatment. In certain embodiments, the decrease in the patient’s score using the MADRS-C is decreased for 4 weeks after treatment. In particular embodiments, the patient’s score using the MADRS-C is decreased for more than 4 weeks after treatment. In certain embodiments, the patient is being treated for anxiety with a compound of formula (I), (II), or (III). The patient may have their symptoms of anxiety evaluated using an anxiety screening test. The anxiety screening test may be the Zung Self-Rating Anxiety Scale, the Hamilton Anxiety Scale, the Beck Anxiety Inventory, the Social Phobia Inventory, the Penn State Worry Questionnaire, the Yale- Brown Obsessive-Compulsive Scale, or the - General Anxiety Disorder-7. In some embodiments, the patient’s anxiety score using any one of these screening tests decreases in comparison to the patient’s score before receiving treatment. In certain embodiments, the patient’s anxiety score using any one of the above screening tests decreases by 50% in comparison to the patient’s score before receiving treatment. In particular embodiments, the patient meets fewer criteria for anxiety as described by the Diagnostic and Statistical Manual of Mental Disorders in comparison before receiving treatment. In one embodiment, the methods of the invention are used to treat psychological conditions, e.g., depression, anxiety, PTSD, an eating disorder, and compulsive behavior, by administering a compound of formula (I) or (II) as needed to treat the symptoms associated with the psychological condition. Neurological Injuries In particular embodiments, the 5-HT2 responsive condition to be treated is a neurological injury. Also disclosed herein are methods of treating a neurological injury. The neurological injury may be any neurological injury. In some embodiments, the neurological injury is a stroke, a traumatic brain injury, or a spinal cord injury. The methods of treating a neurological injury described herein may reduce acute inflammation. In certain embodiments, hippocampal hyperactivity is reduced. Also, the methods described herein for treating a neurological injury may be administered in combination with a behavioral, physical, or speech therapy. In particular embodiments, the methods of the invention are used to treat a neurological injury, e.g., stroke, traumatic brain injury, and spinal cord injury , by administering a compound of formula (I) or (II) as needed to pain, inflammation, and/or other symptoms associated with the neurological injury. Inflammatory Conditions In particular embodiments, the 5-HT2 responsive condition to be treated is an inflammatory condition. An inflammatory condition in a subject can be treated with a compound of formula (I), (II), (III) using the methods of the invention. The inflammatory condition to be treated can be a lung inflammation (e.g., chronic obstructive pulmonary disease (COPD)), neuroinflammation (e.g., Alzheimer’s disease), chronic inflammation, rheumatoid arthritis, atherosclerosis, psoriasis, type II diabetes, inflammatory bowel disease, Crohn’s disease, conjunctivitis, multiple sclerosis, and/or septicemia. In one embodiment, inflammation is treated by administering a compound of formula (I), (II), or (III) as needed to treat (i) acute attacks of inflammation (e.g., inflammatory bowel disease), or (ii) chronic inflammatory conditions (e.g., arthritis). Chronic Pain In particular embodiments, the 5-HT2 responsive condition to be treated is chronic pain. A disorder of condition associated with chronic pain can be treated with a compound of formula (I), (II), or (III) using the methods of the invention. The chronic pain may result from post-operative pain, tension headaches, chronic lower back pain, fibromyalgia, nephropathy, multiple sclerosis, shingles, complex regional pain syndrome, cephalic pain, or sciatica. The chronic pain may arise from an operation. The chronic pain may also be pain associated with a particular disease or condition such as nephropathy, multiple sclerosis, shingles, or complex regional pain syndrome. One particular disorder or condition associated with cephalic pain can be treated with a compound of formula (I), (II), or (III) using the methods of the invention. As used herein, a disorder or condition associated with cephalic pain is a disorder or condition which has as one of its symptoms cephalic/head pain (e.g., headache). Examples of such disorders or conditions include trigeminal autonomic cephalalgias such as episodic and chronic cluster headache (CH), episodic and chronic paroxysmal hemicrania (PH), and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT). Other examples of disorders or conditions which can be treated according to the present invention include vascular headaches (e.g., migraine headaches), tension headaches, headaches associated with the use of a substance (e.g., triptans such as sumatriptan, benzodiazepines such as alprazolam, analgesics such as ibuprofen, ergots such as ergotamine, opioids such as morphine, recreational drugs such as caffeine, nicotine, alcohol, and hormone replacement therapy containing, for example, estrogen) or its withdrawal. Yet additional examples of disorders or conditions associated with cephalic pain include miscellaneous headache unassociated with a structural lesion, headache associated with a nonvascular intracranial disorder, headache associated with a non-cephalic infection, headache associated with a metabolic disorder, headache associated with a disorder of the cranium, neck, eyes, nose, sinuses, teeth, mouth, or other facial or cranial structure, nerve trunk pain and deafferentiation pain. EXAMPLES The following examples are put forth so as to provide those of ordinary skill in the art with a description of how the compositions and methods claimed herein can be performed, made, and evaluated, and are intended to be purely exemplary of the invention and are not intended to limit the scope of what the inventor regards as his or her invention. Example 1. Synthesis and characterization of Compounds (A)-(B). Compounds (A)-(B) can be synthesized according to Scheme 1 (details below). (B)

Scheme 1. Synthesis of 6-(Methoxymethoxy)-1H-indazole (1) MOM-Br (746 mg, 6.0 mmol) was added to a mixture of 1H-indazol-6-ol (1.0 g, 7.5 mmol) and K2CO3 (1.5 g, 11.2 mmol) in DMF (20 mL) at 0 °C. The mixture was stirred at room temperature for 2 h. The mixture was quenched with water (60 mL), and extracted with EtOAc (3 x 50 mL). The combined organic phases were washed with brine (2 x 100 mL), and dried (Na ₂ SO ₄ ), filtered and concentrated to dryness. The residue was purified by silica gel chromatography (EtOAc/hexane =1:2) to afford compound 1 (600 mg, 45% yield). Synthesis of tert-Butyl-3-(6-(methoxymethoxy)-1H-indazol-1-yl)azetidine-1 -carboxylate (2) NaH (60%, 108 mg, 2.7 mmol) was added portionwise to a solution of compound 1 of Scheme 1 (370 mg, 2.1 mmol) in THF (10 mL) at 0 ºC. The mixture was stirred at 0 ºC for 1 h, and then a solution of Boc-3-iodoazetidine (647 mg, 2.3 mmol) in THF (5 mL) was added dropwise over 10 min. The mixture was allowed to warm to room temperature and stirred overnight. The mixture was quenched with ice water (30 mL), and extracted with EtOAc (3 x 30 mL). The combined organic phases were washed with brine (50 mL), dried, filtered and concentrated to dryness. The residue was purified by silica gel chromatography (EtOAc/hexane =1:1) to afford compound 2 (550 mg, 79% yield). Synthesis of Compound (A) Trifluoroacetic acid (6 ml) was added to a solution of compound 2 of Scheme 1 (600 mg, 1.8 mmol) in DCM (6 mL) at 0 °C. The mixture was allowed to warm to room temperature and stirred for 2 h. The solvent was concentrated to afford the TFA salt. This salt was dissolved in DCM, alkalinized with aqueous 5% NaHCO3, extracted with DCM, dried and concentrated to dryness. The residue was purified by silica gel chromatography (DCM/MeOH=10:1) and the product fraction acidified with HCl-dioxane (1 mL) to afford compound (A) HCl salt (390 mg, 96% yield) as white solid. ¹ H-NMR (400 MHz, DMSO-d6): δ 9.30~9.50 (bs, 2H), 7.95~8.00 (d, J = 0.4Hz, 1H), 7.65~7.75 (dd, J = 0.4 and 8.8 Hz, 1H), 6.70~6.80 (m, 2H), 5.10~5.20 (m, 1H), 4.40~4.50 (m, 2H), 3.95~4.05 (m, 2H). LC-MS: m/z 190.0 [M+H] ⁺ . Synthesis of Compound (B) Lithium aluminum hydride (300 mg, 7.9 mmol) was added portionwise to a solution of compound 2 of Scheme 1 (300 mg, 0.9 mmol) in THF (10 mL). The mixture was heated at reflux and stirred for 18 h. After cooling to 0 °C, the reaction mixture was quenched with water (0.3 mL), followed by 15% sodium hydroxide (0.3 mL), and finally water (0.9 mL). The mixture was filtered, and the cake was washed with EtOAc (20 mL). The combined filtrate was washed with brine (2 x 20 mL), dried (Na ₂ SO ₄ ) and filtered. The filtrate was concentrated, and the residue was purified by prep-HPLC to afford the TFA salt. The TFA salt was dissolved in DCM, alkalinized with aqueous 5% NaHCO3, extracted with DCM, dried, concentrated and acidified with HCl-dioxane (1 mL) to afford compound (B) HCl salt (71 mg, 39% yield) as white solid. ¹ H-NMR (400 MHz, DMSO-d6): δ 12.95 (bs, 1H), 9.80~10.50 (bs, 1H), 7.99 (s, 1H), 7.65~7.75 (d, J = 9.2 Hz, 1H), 6.70~6.85 (m, 2H), 5.00~5.20 (m, 1H), 4.70~4.80 (m, 1H), 4.20~4.50 (m, 3H), 2.94 (s, 3H). LC-MS: m/z 203.9 [M+H] ⁺ . Example 2. Synthesis and characterization of Compounds (C)-(G). Compounds (C)-(G) can be synthesized according to Scheme 2 (details below). (E) Scheme 2. Synthesis of 1-(Benzyloxy)-2-bromo-3-fluorobenzene (1) Benzyl bromide (4.9 g, 28.7 mmol) and K ₂ CO ₃ (4.7 g, 34.0 mmol) were added to a solution of 2- bromo-3-fluorophenol (5.0 g, 26.2 mmol) in acetone (70 mL). The resulting mixture was stirred for 16 h at 60 °C. After cooling to room temperature, the mixture was quenched with water (200 mL) and extracted with EtOAc (2x 200 mL). The combined organic phases were washed with saturated aqueous NaHCO3 (200 mL), brine (2 x 200 mL), and dried (Na ₂ SO ₄ ), filtered and concentrated to dryness. The residue was purified by silica gel chromatography (EtOAc/hexane =1:50) to afford compound 1 (6.5 g, 88% yield). Synthesis of tert-Butyl-3-(methoxy(methyl)carbamoyl)azetidine-1-carboxyla te (2) HATU (62.4 g, 164.2 mmol) and DIPEA (48.1 g, 373.1 mmol) were added to a suspension of Boc- azetidine-3-carboxylic acid (30.0 g, 149.2 mmol) and N,O-Dimethylhydroxylamine hydrochloride (21.8 g, 224.0 mmol) in DMF (500 mL) at 0 °C. The mixture was stirred overnight at room temperature. The reaction was quenched with water (1 L) and extracted with EtOAc (3 x 1 L). The combined organic phases were washed with 1N aq HCl (1 L), and brine (2 x 1 L), dried (Na2SO4), filtered and concentrated to dryness. The residue was purified by silica gel chromatography (EtOAc/hexane =1:2) to afford compound 2 (20.6 g, 56% yield). Synthesis of tert-Butyl 3-(2-(benzyloxy)-6-fluorobenzoyl)azetidine-1-carboxylate (3a) Isopropylmagnesium chloride (2.0 M solution in THF, 10.7 mL) was added dropwise over 5 min to a solution of compound 1 of Scheme 2 (5 g, 17.8 mmol) in THF (50 mL) at -78 °C. The mixture was stirred for 0.5 h at -78 °C. A solution of compound 2 of Scheme 2 (5.21 g, 21.4 mmol) in THF (15 mL) was added dropwise over 20 min. The mixture was allowed to warm to room temperature and stirred overnight. The mixture was quenched with aqueous 10% NH4Cl (200 mL) and extracted with EtOAc (2 x 200 mL). The combined organic phases were washed with water (2 x 200 mL), saturated aqueous NaHCO ₃ (2 x 200 mL), brine (200 mL), and dried (Na ₂ SO ₄ ), filtered and concentrated to dryness. The residue was purified by silica gel chromatography (EtOAc/hexane =1:5) to afford compound 3a of Scheme 2 (3.1 g, 45% yield). Synthesis of tert-Butyl-3-(2-fluoro-6-methoxybenzoyl)azetidine-1-carboxyl ate (3b) n-BuLi (1.6 M solution in hexane, 1.9 mL, 3.07 mmol) was added dropwise over 5 min to a solution of 2-bromo-1-fluoro-3-methoxybenzene (500 mg, 2.05 mmol) in THF (15 mL) at -78 ºC. The mixture was stirred for 0.5 h at -78 ºC and then a solution of compound 2 of Scheme 2 (504 mg, 2.46 mmol) in THF (5 mL) was added dropwise over 5 min. The mixture was further stirred for 0.5 h at -78 ºC, and then quenched with aqueous 10% NH ₄ Cl (50 mL), extracted with EtOAc (2 x 50 mL). The combined organic phases were washed with saturated aqueous NaHCO ₃ (2 x 50 mL), and brine (50 mL) then dried (Na2SO4), filtered and concentrated to dryness. The residue was purified by silica gel chromatography (EtOAc/hexane =1:5) to afford compound 3b of Scheme 2 (420 mg, 66% yield). Synthesis of tert-Butyl-3-(4-(benzyloxy)-1H-indazol-3-yl)azetidine-1-carb oxylate (4a) Hydrazine hydrate (80%, 4.87 g, 77.9 mmol) was added to a solution of compound 3a of Scheme 2 (3.0 g, 7.9 mmol) in NMP (30 mL) at room temperature. The mixture was stirred at 120 °C for 4 h. After cooling to room temperature, the mixture was quenched with water (90 mL), and extracted with EtOAc (2 x 100 mL). The combined organic phases were washed with brine (2 x 100 mL), dried (Na ₂ SO ₄ ), filtered and concentrated to dryness. The crude was purified by silica gel chromatography (EtOAc/hexane =1:1) to afford compound 4a of Scheme 2 (2.5 g, 85% yield). Synthesis of tert-Butyl-3-(4-methoxy-1H-indazol-3-yl)azetidine-1-carboxyl ate (4b) This compound was synthesized from compound 3b of Scheme 2 (400 mg, 1.3 mmol) and hydrazine hydrate (80%, 340 g, 6.8 mmol) with a procedure similar to that used for compound 4a of Scheme 2 to give the title compound as a yellow solid (210 mg, 54% yield). Synthesis of Compound (C) & Compound (D) Lithium aluminum hydride (300 mg, 7.9 mmol) was added portion-wise over 10 min to a solution of compound 4a of Scheme 2 (300 mg, 0.79 mmol) in THF (10 mL) at 0 °C. The mixture was then heated at reflux and stirred for 18 h. After cooling to 0 °C, the mixture was quenched with water (0.3 mL), followed by 15% sodium hydroxide (0.3 mL), and finally water (0.9 mL). The mixture was filtered, and the cake washed with EtOAc (50 mL). The filtrate was washed with brine (2 x 50 mL), dried (Na ₂ SO ₄ ), filtered and concentrated. The residue was purified by silica gel chromatography (DCM/MeOH =50:1 to 20:1) to afford compound (C) (65 mg, 41% yield) and compound (D) (52 mg, 22% yield). Compound (C) free base, white solid ¹ H-NMR (400 MHz, DMSO-d6): δ 12.60 (bs, 1H), 7.05~7.15 (dd, J = 7.6 and 8.0 Hz, 1H), 6.78~7.85 (d, J = 8.0 Hz, 1H), 6.30~6.35 (d, J = 7.6 Hz, 1H), 3.95~4.05 (m, 1H), 3.75~3.85 (t, J = 8.0 Hz, 2H), 3.50~3.60 (m, 2H), 2.45 (s, 3H). LC-MS: m/z 204.1[M+H] ⁺ . Compound (D) free base, off-white solid ¹ H-NMR (400 MHz, DMSO-d6): δ 12.73 (bs, 1H), 7.50~7.55 (d, J = 6.8 Hz, 2H), 7.30~7.60 (m, 4H), 7.15~7.25 (m. 2H), 7.00~7.05 (d, J = 8.0 Hz, 1H), 6.50~6.60 (d, J = 7.6 Hz, 1H), 5.20 (s, 2H), 4.00~4.10 (t, J = 8.0 Hz, 1H), 3.60~3.65 (t, J = 7.6 Hz, 2H), 3.50~3.60 (m, 2H), 2.25 (s, 3H). LC-MS: m/z 294.3[M+H] ⁺ . Synthesis of Compound (E) Toluene sulfonic acid (226 mg, 1.19 mmol) was added to a solution of compound 4a of Scheme 2 (150 mg, 0.40 mmol) in acetonitrile (10 mL). The mixture was stirred at room temperature for 4 h. The solvent was removed in vacuo, and the residue was triturated with ACN (5 mL), filtered and dried to afford compound (E) as the tosylate salt (1:2) (104 mg, 42 % yield). ¹ H-NMR (400 MHz, DMSO-d6): δ 13.01 (bs, 1H), 8.60~8.80 (bs, 2H), 7.40~7.60 (m, 9H), 7.20~7.30 (t, J = 8.0 Hz, 1H), 7.05~7.15 (m, 5H), 6.60~6.65 (d, J = 8.0 Hz, 1H), 5.22 (s, 2H), 4.40~4.50 (m, 1H), 4.20~4.30 (m, 2H), 4.10~4.20 (m, 2H), 2.29 (s, 3H). LC-MS: m/z 280.1[M+H] ⁺ Synthesis of Compound (F) Pd/C (10% on carbon, 200 mg, 0.19 mmol) was added to a solution of compound (E) (200 mg, 0.72 mmol) in MeOH (10 mL). The mixture was stirred at room temperature under 1 atmosphere of hydrogen for 5 h. Pd/C was removed by filtration, and the filtrate was concentrated to dryness. The crude was dissolved in EtOAc (3 mL) and 5N HCl/EtOAc (6 mL) was added at 0 °C. The mixture was stirred at 0 °C for 10 min and concentrated to dryness in vacuo. The crude was triturated with EtOAc/hexane (3 mL/6 mL), and filtered to afford compound (F) (30 mg, 20% yield) as the HCl salt as a brown solid. ¹ H-NMR (400 MHz, DMSO-d6): δ 8.56 (bs, 1H), 6.58 (s, 1H), 6.54 (s, 1H), 3.70 (s, 3H), 2.65~2.75 (m, 2H), 2.50~2.55 (m, 2H), 2.30~2.35 (d, J = 7.2 Hz, 2H), 1.85~1.95 (m, 1H), 0.80~0.90 (d, J = 6.8 Hz, 6H). LC-MS: m/z 223.9[M+H] ⁺ . Synthesis of Compound (G) This compound was synthesized from compound 4b of Scheme 2 (100 mg, 0.33 mmol) with LAH (100 mg. 2.63 mmol) with a procedure similar to that used for compound (E) to give title compound (G) as an off-white solid (40 mg, 56% yield). ¹ H-NMR (400 MHz, DMSO-d6): δ 12.73 (bs, 1H), 7.15~7.25 (dd, J = 7.6 and 8.4Hz, 1H), 6.95~7.05 (d, J = 8.4 Hz, 1H), 6.45~6.50 (d, J = 7.6 Hz, 1H), 4.05~4.12 (t, J = 8.0 Hz, 1H), 3.88 (s, 3H), 3.75~3.85 (m, 2H), 3.30~3.45 (m, 2H), 2.35 (s, 3H). LC-MS: m/z 218.0[M+H] ⁺ Example 3. Synthesis and characterization of Compounds (H)-(N). Compounds (H)-(N) can be synthesized according to Scheme 3 (details below). , (N)

Scheme 3. Procedures Synthesis of Compound (K) K ₂ CO ₃ (340 mg, 2.46 mmol) and 3-(chloromethyl)pyridazine hydrochloride (162 mg, 1 mmol) were added to a solution of compound (C) (200 mg, 1 mmol, prepared according to the procedure for compound (C)) in DMF (5 mL) at 0ºC. The mixture was stirred at 45ºC overnight. The mixture was quenched with ice water (20 mL), and then extracted with EtOAc (3 x 30 mL). The combined organic phases were washed with brine (2 x 30 mL), dried (Na ₂ SO ₄ ), filtered, and concentrated to dryness. The residue was purified by silica gel chromatography (DCM/MeOH =10:1) to afford compound (K) as the free base. This was treated with HCl/dioxane to afford compound (K) HCl salt (77mg, 26% yield) as an off- white solid. ¹ H-NMR (400 MHz, DMSO-d6): δ12.96 (bs, 1H), 10.81 (bs, 1H), 9.33 (s, 1H), 8.00~8.05 (m, 1H), 7.85~7.95 (m, 1H), 7.20~7.30 (m, 1H), 7.00~7.05 (d, J = 8.4 Hz, 1H), 6.45~6.50 (d, J = 7.6 Hz, 1H), 4.88 (s, 2H), 4.60~4.70 (m, 1H), 4.30~4.40 (m, 1H), 4.05~4.15 (m, 1H), 3.60~3.70 (m, 2H), 3.03 (s, 3H).LC-MS: m/z 296.1[M+H] ⁺ . Synthesis of Compound (H) This compound was synthesized from compound (C) (200 mg, 1 mmol) using a procedure similar to that for compound (K) with 2-(chloromethyl)pyrazine (HCl salt, 162 mg, 1 mmol) to give compound (H) (124 mg, 42% yield) as HCl salt, as an off-white solid. ¹ H-NMR (400 MHz, DMSO-d6): δ12.96 (bs, 1H), 10.76 (bs, 1H), 8.92 (s, 1H), 8.75 (s, 2H), 7.25~7.30 (d, J = 8.0 Hz, 1H), 7.00~7.05 (d, J = 8.0 Hz, 1H), 6.45~6.50 (d, J = 7.6 Hz, 1H), 4.70~4.80 (m. 2H), 4.40~4.50 (m, 1H), 4.00~4.10 (m, 2H), 3.55~3.65 (m, 2H), 3.01 (s, 3H).LC-MS: m/z 296.1[M+H] ⁺ . Synthesis of Compound (I) This compound was synthesized from compound (C) (200 mg, 1 mmol) and 2- (chloromethyl)pyrimidine (HCl salt, 162 mg, 1 mmol) using a procedure similar to used for compound (K) to give compound (I) (101 mg, 34% yield) as the free base, an off-white solid. ¹ H-NMR (400 MHz, DMSO- d6): δ12.63 (bs, 1H), 8.79 (s, 1H), 7.40~7.45 (m, 1H), 7.15~7.20 (m, 1H), 6.90~6.95 (d, J = 8.0 Hz, 1H), 6.35~6.40 (d, J = 7.2 Hz, 1H), 4.45~4.50 (m, 1H), 4.35~4.45 (m, 1H), 3.95~4.05 (m, 1H), 3.75~3.85 (m, 1H), 3.55~3.60 (m, 1H), 2.85~2.95 (m, 1H), 2.70~2.80 (m, 1H), 2.33 (s, 3H).LC-MS: m/z 296.1[M+H] ⁺ . Synthesis of Compound (J) This compound was synthesized from compound (C) (200 mg, 1 mmol) and 5- (chloromethyl)pyrimidine (HCl salt, 162 mg, 1 mmol) using a procedure similar to that used for compound (K) to provide compound (J) oxalate salt(86 mg, 29% yield) as an off-white solid. ¹ H-NMR (400 MHz, DMSO-d6): δ12.72 (bs, 1H), 9.18 (s, 1H), 8.80 (s, 2H), 7.15~7.25 (m, 1H), 6.90~7.00 (d, J = 8.0 Hz, 1H), 6.35~6.40 (d, J = 7.2 Hz, 1H), 4.50~4.55 (m, 1H), 4.35~4.45 (m, 1H), 3.70~3.90 (m, 3H), 2.70~2.90 (m, 2H), 2.36 (s, 3H).LC-MS: m/z 296.1[M+H] ⁺ . Synthesis of Compound (M) K ₂ CO ₃ (354 mg, 2.56 mmol) and 3-(chloromethyl)pyridine (HCl salt, 210 mg, 1.3 mmol) were added to a solution of compound (C) (200 mg, 1 mmol) in MeOH (15 mL) at 0ºC. The mixture was stirred overnight at 45ºC then quenched with ice water (20 mL), and extracted with EtOAc (3 x 30 mL). The combined organic phases were washed with brine (2 x 30 mL), dried (Na ₂ SO ₄ ), filtered, and concentrated to dryness. The residue was purified by silica gel chromatography (DCM/MeOH =10:1) to afford compound (M) as the free base. Subsequent treatment with oxalic acid afforded compound (M) oxalate salt (139mg, 48% yield) as an off-white solid. ¹ H-NMR (400 MHz, DMSO-d6): δ12.80 (bs, 1H), 8.55~8.60 (d, J = 1.6 Hz, 1H), 8.50~8.55 (m, 1H), 7.80~7.90 (d, J = 8.0 Hz, 1H), 7.35~7.45 (m, 1H), 7.20~7.30 (m 1H), 6.95~7.00 (d, J = 8.0 Hz, 1H), 6.40~6.45 (d, J = 7.2 Hz, 1H), 4.50~4.55 (m, 1H), 4.35~4.40 (m, 1H), 3.80~3.95 (m, 2H), 3.75~3.80 (m, 1H), 2.85~2.95 (m, 2H), 2.44 (s, 3H).LC-MS: m/z 295.1[M+H] ⁺ . Synthesis of Compound (L) This compound was synthesized from compound (C) (200 mg, 1 mmol) and 4- (chloromethyl)pyridine (HCl salt, 162 mg, 1 mmol) using a procedure similar to that used for compound (M) to give compound (L) (free base,118 mg, 41% yield) as an off-white solid. ¹ H-NMR (400 MHz, DMSO- d6): δ12.65 (bs, 1H), 8.45~8.50 (d, J = 4.4 Hz, 2H), 7.30~7.35 (d, J = 4.4 Hz, 2H), 7.15~7.20 (m, 1H), 6.90~6.95 (d, J = 8.4 Hz, 1H), 6.35~6.40 (d, J = 7.6 Hz, 1H), 4.55~4.60 (m, 1H), 4.40~4.45 (m, 1H), 3.70~3.75 (d, J = 14 Hz, 1H), 7.60~7.70 (m, 1H), 7.55~7.60 (d, J = 14 Hz, 1H), 2.60~2.80 (m, 1H), 2.26 (s, 3H).LC-MS: m/z 295.1[M+H] ⁺ . Synthesis of Compound (N) This compound was synthesized from compound (C) (200 mg, 1 mmol) with 2- (chloromethyl)pyridine (HCl salt, 162 mg, 1 mmol) using a procedure similar to that used for compound (M) to give compound (N) HCl salt (150 mg, 52% yield) as an off-white solid. ¹ H-NMR (400 MHz, DMSO- d6): δ12.95 (bs, 1H), 10.18 (bs, 1H), 8.65~8.70 (d, J = 4.4 Hz, 1H), 7.90~8.00 (m, 1H), 7.55~7.65 (d, J = 8.0 Hz, 1H), 7.45~7.50 (m, 1H), 7.20~7.30 (m, 1H), 7.00~7.05 (d, J = 8.0 Hz, 1H), 6.45~6.50 (d, J = 7.6 Hz, 1H), 4.66 (s, 2H), 4.60~4.65 (m, 1H), 4.30~4.40 (m, 1H), 4.05~4.15 (m, 1H), 3.60~3.70 (m, 2H), 2.99 (s, 3H).LC-MS: m/z 295.2[M+H] ⁺ . Example 4. Synthesis and characterization of Compounds (O)-(Q). Compounds (O)-(Q) can be synthesized according to Scheme 4 (details below).

Scheme 4. Synthesis of tert-Butyl-3-(methoxy(methyl)amino)-3-oxopropyl(methyl)carba mate (1) NaH (60%, 2.6 g, 66.1 mmol) was added portion-wise to a solution of 3-(tert- butoxycarbonylamino)propanoic acid (5.0 g, 26.4 mmol) in THF (50 mL) at 0 ºC. The mixture was stirred at 0 ºC for 1 h then a solution of MeI (9.4 g, 66.1 mmol) in THF (10 mL) was added dropwise over 5 min. The mixture was allowed to warm to room temperature and stirred overnight. The mixture was quenched with ice water (100 mL), and extracted with EtOAc (3 x 100 mL). The combined organic phases were washed with brine (200 mL), dried (Na2SO4), filtered and concentrated to dryness. The residue was purified by silica gel chromatography (EtOAc/hexane =1:1) to afford 3-(tert- butoxycarbonyl(methyl)amino)propanoic acid (4.5 g, 84% yield). HATU (9.3 g, 24.4 mmol) was added to a mixture of 3-(tert-butoxycarbonyl(methyl) amino)propanoic acid (4.5 g, 22.2 mmol), N,O-Dimethylhydroxylamine hydrochloride (3.2 g, 33.2 mmol) and DIPEA (7.14 g, 55.4 mmol) in DMF (50 mL) at 0 °C. The mixture was stirred for 12 h at room temperature. The reaction mixture was quenched with water (100 mL) and extracted with EtOAc (3 x 100 mL). The combined organic phases were washed with 1N aq HCl (100 mL), brine (2 x 100 mL), dried (Na2SO4), filtered and concentrated to dryness. The residue was purified by silica gel chromatography (EtOAc/hexane =1:2) to afford compound 1 of Scheme 4 (4.2 g, 77% yield). Synthesis of tert-Butyl-3-(2-(benzyloxy)-6-fluorophenyl)-3-oxopropyl(meth yl)carbamate (2a) Isopropylmagnesium chloride (2.0 M solution in THF, 2.6 mL, 5.2 mmol) was added dropwise over 5 min to a solution of 1-(benzyloxy)-2-bromo-3-fluorobenzene (1.0 g, 3.6 mmol) in THF (20 mL) at - 78 °C. The mixture was stirred for 0.5 h at -78 °C. A solution of compound 1 (1.06 g, 4.3 mmol) in THF (10 mL) was then added. The mixture was allowed to warm to room temperature and stirred overnight. The mixture was quenched with aqueous 10% NH ₄ Cl (200 mL) and extracted with EtOAc (2 x 200 mL). The combined organic phases were collected and washed with brine (200 mL), dried (Na2SO4), filtered and concentrated to dryness. The residue was purified by silica gel chromatography (EtOAc/hexane =1:4) to afford compound 2a (700 mg, 51% yield). Synthesis of tert-Butyl-3-(2-fluoro-6-methoxyphenyl)-3-oxopropyl(methyl)c arbamate (2b) This compound was synthesized from compound 1 of Scheme 4 (1.4 g, 5.8mmol) with 2-bromo- 1-fluoro-3-methoxybenzene (1.0 g, 4.9 mmol) with a procedure similar to that used for compound 2a of Scheme 4 to give title compound 2b of Scheme 4 (700 mg, 47% yield). Synthesis of tert-Butyl-2-(4-(benzyloxy)-1H-indazol-3-yl)ethyl(methyl)car bamate (3a) Hydrazine hydrate (80%, 969 mg, 15.5 mmol) was added to a solution of compound 2a of Scheme 4 (1.2 g, 3.1 mmol) in NMP (20 mL) at room temperature. The mixture was heated to 120 °C and stirred for 4 h. After cooling to room temperature, the mixture was quenched with water (60 mL) and extracted with EtOAc (2 x 60 mL). The combined organic phases were washed with brine (2 x 60 mL), dried (Na2SO4), filtered and concentrated to dryness. The crude was purified by silica gel chromatography (EtOAc/hexane =1:2) to afford compound 3a of Scheme 4 (600 mg, 51% yield). Synthesis of tert-Butyl-2-(4-methoxy-1H-indazol-3-yl)ethyl(methyl)carbama te (3b) This compound was synthesized from compound 2b of Scheme 4 (250 mg, 0.80 mmol) with hydrazine hydrate (80%, 502 mg, 8.0 mmol) using a procedure similar to that used for compound 3a of Scheme 4 to give the title compound (170 mg, 69% yield). Synthesis of Compound (O) and Compound (P) Lithium aluminum hydride (600 mg, 15.8 mmol) was added portion-wise over 10 min to a solution of compound 3a of Scheme 4 (200 mg, 1.6 mmol) in THF (10 mL) at 0 °C. The mixture was heated under reflux and stirred for 16 h. After cooling to 0 °C, the reaction mixture was quenched with water (0.6 mL), followed by 15% sodium hydroxide (0.6 mL), and finally water (1.8 mL). The mixture was filtered, and the cake was washed with EtOAc (50 mL). The filtrate was washed with brine (2 x 50 mL), dried (Na ₂ SO ₄ ), filtered and concentrated. The residue was purified by silica gel chromatography (DCM/MeOH =30:1 to 20:1) to afford compound (O) (49 mg, 45% yield) and compound (P) (44 mg, 27% yield). Compound (O): free base, white solid. ¹ H-NMR (400 MHz, DMSO-d6): δ 12.45 (bs, 1H), 11.50 (bs, 1H), 7.00~7.10 (dd, J = 7.6 and 8.0 Hz, 1H), 6.75~6.85 (d, J = 8.0 Hz, 1H), 6.25~6.35 (d, J = 7.6 Hz, 1H), 3.05~3.10 (t, J = 6.8Hz, 2H), 2.60~6.70 (t, J = 6.8Hz, 2H), 2.26 (s, 6H). LC-MS: m/z 206.5 [M] ⁺ . Compound (P): free base, white solid. ¹ H-NMR (400 MHz, DMSO-d6): δ 12.64 (bs, 1H), 7.50~7.60 (d, J = 7.2 Hz, 2H), 7.30~7.50 (m, 3H), 7.15~7.25 (dd, J = 7.6 and 8.0 Hz, 1H), 6.95~7.05 (d, J = 8.0 Hz, 1H), 6.55~6.65 (d, J = 7.6 Hz, 1H), 5.22 (s, 2H), 3.05~3.10 (m, 2H), 2.60~6.70 (m, 2H), 2.08 (s, 6H). LC-MS: m/z 296.3 [M] ⁺ . Synthesis of Compound (Q) Lithium aluminum hydride (170 mg, 4.47 mmol) was added by portion-wise over 30 min to a solution of compound 3b of Scheme 4 (170 mg, 0.56 mmol) in THF (10 mL) at 0 °C. The mixture was heated at reflux overnight. After cooling to 0 °C, the reaction mixture was quenched with water (0.17 mL), followed by 15% sodium hydroxide (0.17 mL), and finally water (0.51 mL). The mixture was filtered, and the cake was washed with EtOAc (20 mL). The combined organic filtrate was washed with brine (2 x 20 mL), dried (Na2SO4), filtered and concentrated. The residue was purified by silica gel chromatography (DCM/MeOH =30:1) and acidified with oxalic acid (140 mg, 1.11 mmol) in EtOH (10 mL) to afford synthesis (Q) as the oxalate salt (69 mg, 31 % yield). ¹ H-NMR (400 MHz, DMSO-d6): δ 7.23~7.28 (dd, J = 8.0 and 8.4 Hz, 1H), 7.02~7.05 (d, J = 8.4 Hz, 1H), 6.51~6.54 (d, J = 8.0 Hz, 1H), 3.92 (s, 3H), 3.35~3.45 (m, 4H), 2.86 (s, 6H). LC-MS: m/z 220.1 [M] ⁺ . Example 5. Synthesis and characterization of Compounds (R)-(S). Compounds (R)-(S) can be synthesized according to Scheme 5 (details below).

Scheme 5. Synthesis of tert-Butyl 2-(4-(benzyloxy)-1H-indazol-3-yl)ethyl(methyl)carbamate (1) Hydrazine hydrate (80%, 1.94 g, 30 mmol) was added to a solution of compound A of Scheme 5 (2.4 g, 6mmol, prepared according to the procedure for compounds (O), (P), and (Q) in NMP (40 mL) at room temperature. The mixture was heated to 120°C and stirred for 4 h. After cooling to room temperature, the mixture was quenched with water (100 mL), and extracted with EtOAc (3 x 100 mL). The combined organic phases were washed with brine (2 x 100 mL), dried (Na ₂ SO ₄ ), filtered, and then concentrated to dryness. The crude product was purified by silica gel chromatography (EtOAc/hexane =1:2) to afford compound 1 of Scheme 5 (1.3 g, 55% yield). Synthesis of Compound (R) p-Toluenesulfonic acid (1.20 g, 6.3mmol) was added to a solution of compound 1 of Scheme 5 (600 mg, 1.6mmol) in acetonitrile (10 mL). The mixture was stirred at room temperature for 4 h. The mixture was quenched with water (30 mL) and extracted with EtOAc (3 x 30 mL). The combined organic phases were washed with brine (2 x 30 mL), then dried (Na ₂ SO ₄ ), filtered, and concentrated to dryness. The residue was triturated with EtOAc/hexane (10 mL, 1:1) to afford compound (R) free base as a white solid (48 mg, 10% yield). ¹ H-NMR (400 MHz, DMSO-d6): δ12.63 (bs, 1H), 7.50~7.60 (m, 2H), 7.30~7.45 (m, 3H), 7.10~7.20 (dd, J = 7.6 and 8.0Hz, 1H), 6.95~7.05 (d, J = 7.6Hz, 1H), 6.50~6.60 (d, J = 8.0Hz, 1H), 5.24 (s, 2H), 3.05~3.15 (t, J = 7.2Hz, 2H), 2.08~2.85 ((t, J = 7.2Hz, 2H), 2.22 (s, sH). LC-MS: m/z 282.1 [M+H] ⁺ . Synthesis of tert-Butyl 2-(4-hydroxy-1H-indazol-3-yl)ethyl(methyl)carbamate (2) Pd/C (10%, 100 mg) was added to a solution of compound 1 of Scheme 5 (600 mg, 1.6 mmol) in MeOH (20 mL). The reaction was stirredunder1 atmosphere of hydrogen at room temperature for 5 h. The Pd/C was removed by filtration, and the filtrate was concentrated to dryness. The crude was purified by silica gel chromatography (DCM/MeOH = 9:1) to afford compound 2 of Scheme 5 (410 mg, 89% yield). Synthesis of Compound (S) p-Toluenesulfonic acid (784 mg, 4mmol) was added to a solution of compound 2 of Scheme 5 (300 mg, 1mmol) in acetonitrile (10 mL). The reaction was stirred at room temperature for 4 h. The solvent was removed in vacuo, and the residue triturated with ACN (5 mL), filtered, then dried to afford compound (S) PTSA salt (336 mg, 63% yield) as a white solid. ¹ H-NMR (400 MHz, DMSO-d6): δ12.67 (bs, 1H), 10.16 (bs, 1H), 8.40 (bs, 2H), 7.45~7.50 (d, J = 8.4 Hz, 4H), 7.00~7.20 (m, 5H), 6.80~6.90 (d, J = 8.4 Hz, 1H), 6.35~7.40 (d, J = 7.2 Hz, 1H), 6.00~6.20 (bs, 3H), 3.25~3.40 (m, 4H), 2.60~2.65 (t, J = 4.6 Hz, 3H), 2.30 (s, 6H). LC-MS: m/z 192.0 [M+H] ⁺ . Example 6. 5-HT Binding Studies. Compounds can be evaluated in binding assays of various 5-HT2A, B, C and 5-HT1A receptors and potential adrenergic receptor off targets adrenergic 2a and adrenergic 2B. Radioligand binding can be assessed at equilibrium, using the ligands indicated in Table 1, at recombinantly expressed human receptors from membrane preparations using standard conditions at Cerep Eurofins Discovery and gold standard filtration methods, in accordance with generally accepted methodologies as described in Auld et al. (Receptor Binding Assays for HTS and Drug Discovery. 2012. In: Sittampalam et al., editors. Assay Guidance Manual [Internet], Bethesda (MD): Eli Lilly & Company and the National Center for Advancing Translational Sciences; 2004). Table 1. ASSAY h5 HT1A i t di li d ³ H8 OH DPAT Table 2 shows the apparent IC50 of the endogenous agonist serotonin in radioligand binding assays. Serotonin was used as a reference ligand for each 5-HT2 receptor tested under generally similar experimental conditions. Generally, the IC50 values of tested compounds (Table 2) indicate that these ligands have comparable to lower apparent affinities, along with differentiated specificity profile, for the 5- HT2 targets in comparison to the endogenous ligand serotonin. Compounds (T) is: Compound Binding HT2A Binding HT2C Binding HT2C IC50 (M) Emax % IC50 (M) Emax % Table 3 shows EC50 results. Table 3. Binding HT2A Binding HT2A COMPOUND EC50 (M) Emax % G 5.7E-07 44.1 H >1E-05 0 IC50 and EC50 Cerep (Hill software) and validated by comparison with data generated by the commercial software SigmaPlot ® 4.0 for Windows ® (© 1997 by SPSS Inc.). Example 7. 5-HT2A Receptor In Vitro Functional Studies. Gαq-mediated calcium flux downstream of 5-HT2A receptor activation can be determined using HEK293 cells stably expressing the human 5-HT2A receptor. Cells are seeded in DMEM supplemented with 10% fetal bovine serum, 100 units/mL penicillin, 100 mg/mL streptomycin, and 100 mg/mL Zeocin™ onto 96-well poly-D-lysine plates with clear bottoms (12,000 cells/well) and cultured at 37˚C. The following day, media is aspirated and replaced with serum-free DMEM for 12 h. On the day of the experiment, the cells are washed once with HBSS supplemented with 20 mM HEPES, loaded with 75 μL of 3 μM Fluo-2 AM HA (Ion Indicators, LLC) diluted in HBSS-HEPES buffer, incubated for 1 h at 37˚C, washed again with HBSS-HEPES, and maintained in 50 μL HBSS-HEPES at 25˚C. The plate of dye- loaded cells are placed into a FlexStation 3 microplate reader (Molecular Devices, LLC) to monitor fluorescence (excitation, 485 nm; emission, 525 nm; cutoff, 515 nm). The plate is read for 20 s (2-second interval) to establish baseline fluorescence and then challenged with compound diluted in a range of 10 pM to 10 μM or buffer and read for an additional 80 s. After obtaining a calcium mobilization trace for each sample, the mean baseline fluorescence is subtracted from peak fluorescence in each well. EMAX value is determined by normalization to the maximum 5-HT response (100%) on the same plate. The data are analyzed using non-linear regression curve-fitting routines in Graph-Pad Prism 8.0 (GraphPad Software, Inc.) to generate EC ₅₀ values. Example 8. 5-HT2A and 5-HT2C In Vitro Receptor Binding Study. This example describes testing of compounds in assays of 5-HT2A and 5-HT2C agonism and antagonism. Cell Culture Procedure Frozen adherent/epithelial HEK293 cells were thawed at 37°C water bath with a continuous agitation. Cells were gently added, drop by drop to a 15 ml centrifuge tube containing 5 ml of fresh pre- warmed complete DMEM medium. The cells were centrifuged at 1000 rpm for 10 minutes. Supernatant medium was discarded, and the cell pellet was resuspended in 5 ml of fresh pre-warmed complete DMEM medium. Cells were transferred to a T25 flask and incubated at 37°C with 5% CO2 until the cells reached >90% confluence. The recovery rate for frozen cells is usually 70% or above. When the cells reached 90% confluence, the cells were split. Media was carefully aspirated off, the cell layer gently rinsed with the appropriate amount of 0.2% trypsin-EDTA, and the media aspirated off again. A minute passed, and the cells were dislodged by gently tapping of the sides of the flask. The cells were resuspended with the appropriate amount of cell culture medium. Media was changed every other day. Following a reiteration of the subculture, the cells were centrifuged at 1000 rpm for 10 minutes, the supernatant aspirated, the cells resuspended in 90% FBS and 10% DMSO at a density of 2- 3 x 10 ⁶ cells/ml, and frozen at -80 °C overnight, before being transferred into cryogenic storage in liquid nitrogen at -196 °C. 5-HT2A, 5-HT2B, 5-HT2B Agonism and Antagonism In Vitro Studies Test compounds were serially diluted with DMSO to 400X stock solution (top dose=4mM, 3-fold dilution, 11 points) in a LDV plate. Following the dilution, 250 nL of the compound solution was spotted and dispensed in a 20 µL/well assay buffer to make 5X working solutions in a 384-well compound plate by MultiDrop. The cells were cultured with DMEM medium (10% FBS). When the cells reached 80% confluence, the cells were dissociated with 0.25% Trypsin-EDTA. The cell density was measured and the cells diluted to 6.6 x10e5 cells/mL with DMEM (10% FBS). Following the dilution, 30μl of cells was dispensed into each well (20000 cells per well) of a 384-well plate (corning 3764#, pre-coated with Matrigel) with multidrop and cultured at 37℃, 5% CO2 for 20-24hrs. 10ul was added per well of 4X loading dye into cell plate. The cells were incubated at 37°C, 5% CO2 in the dark for 1h. Following 1 hour the Flipr program was loaded. The tips, cell plate and compound plates were placed into the machine and the program run. Per the Flipr program, 10 µl to 40 µl was added to the cell plate to obtain an agonist mode signal. The program was run repeatedly until all plates were tested, with fresh tips for each new cell plate. The plate was incubated at 25℃ in the dark for 15 min before antagonist mode signal readout. Following incubation, 20 µl/well in 384-well assay plate was prepared (Greiner 784075#) of working solution (6X) of agonist (Serotonin) in 1X HBSS+20mM HEPES+0.1% BSA. The concentration of Serotonin used in this assay was determined by dose response in previous agonist mode. EC80 was used in the assay as final agonist concentration. Following 15 minutes elapsed, the Flipr program was loaded. The tips, cell plate and compound plates were placed into the machine, and the program run. Per the Flipr program, 10 µl to 50ul was added to the cell plate to obtain an antagonist mode signal. FLIPR results were read at room temperature using the specified settings. Data was analyzed by using XL-fit and is shown in Table 4 below. Compound (U) is: U) FLIPR IC50 5-HT2A FLIPR 5-HT2A FLIPR 5-HT2C FLIPR 5-HT2C FLIPR (uM) [5-HT2A COMPOUND agonist EC50 agonist Emax agonist EC50 agonist Emax (h)] OTHER EMBODIMENTS All publications, patents, and patent applications mentioned in this specification are herein incorporated by reference to the same extent as if each independent publication or patent application was specifically and individually indicated to be incorporated by reference. Although the invention has been described in connection with specific embodiments thereof, it will be understood that it is capable of further modifications and this application is intended to cover any variations, uses, or adaptations of the invention following, in general, the principles of the invention and including such departures from the present disclosure that come within known or customary practice within the art to which the invention pertains and may be applied to the essential features hereinbefore set forth, and follows in the scope of the claims. Other embodiments are within the claims.