COMPOUNDS, COMPOSITIONS, AND METHODS FOR REDUCING PRODUCTION OF TRIMETHYLAMINE CROSS-REFERENCE TO RELATED APPLICATIONS This application claims priority to and the benefit of U.S. Provisional Patent Application No.63/359,642, filed on July 8, 2022, which is incorporated herein by reference in its entirety. STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH This invention was made with government support under HL103866 awarded by the National Institutes of Health. The government has certain rights in the invention. FIELD Provided herein are compounds and compositions that inhibit production of trimethylamine (TMA), and methods of using the compounds, e.g., for inhibiting production of trimethylamine, and for treating disorders associated with conversion of choline to trimethylamine. BACKGROUND TMA and its derivative trimethylamine N-oxide (TMAO) are metabolites linked to disorders such as kidney disease, diabetes mellitus, obesity, trimethylaminuria, and cardiovascular disease (CVD). TMA is produced in the gut by bacteria that are capable of converting substrates, such as choline, to TMA. There is an unmet need for compounds that inhibit the production of TMA by bacteria. SUMMARY In one aspect, disclosed herein are compounds of formula (I): and pharmaceutically acceptable salts thereof, wherein: R ¹ is an amino acid side chain, -COOH, or a group ; R ² is hydrogen or a nitrogen protecting group; or R ¹ and R ² are taken together with the atoms to which they are attached to form a five-membered ring; Z is selected from a bond, -CH ₂ -, and -CH ₂ CH ₂ -; R ³ and R ⁴ are each independently selected from halomethyl and C ₃ -C ₆ cycloalkyl; and X ^– is an anion. In some embodiments, R ¹ is an amino acid side chain. In some embodiments, R ¹ is selected from hydrogen, -CH ₃ , -CH(CH ₃ ) ₂ , benzyl, -CH ₂ OH, -CH ₂ COOH, and - CH ₂ CH ₂ COOH. In some embodiments, R ¹ is -COOH. In some embodiments, R ² is hydrogen or -C(O)CH ₃ . In some embodiments, R ¹ and R ² are taken together with the atoms to which they are attached to form a five-membered ring. In some embodiments, R ³ is halomethyl. In some embodiments, R ³ is fluoromethyl. In some embodiments, Z is a bond. In some embodiments, Z is -CH ₂ - or -CH ₂ CH ₂ -. In some embodiments, X ^– is an anion selected from a halide and a carboxylate. In some embodiments, X ^– is selected from chloride and bromide. In some embodiments, the compound is selected from: and pharmaceutically acceptable salts thereof. In another aspect, disclosed herein is a pharmaceutical composition comprising a compound disclosed herein (e.g., a compound of formula (I)), or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier. In another aspect, disclosed herein is a method of treating a condition associated with conversion of choline to trimethylamine in a subject in need thereof, comprising administering to the subject an effective amount of a compound disclosed herein (e.g., a compound of formula (I)), or a pharmaceutically acceptable salt thereof. In some embodiments, the condition is selected from a cardiovascular disease, trimethylaminuria, reduced or impaired kidney function, kidney disease, diabetes mellitus, and obesity. In some embodiments, the condition is a cardiovascular disease selected from acute coronary syndrome, angina, arrhythmia, arterial aneurysm, atherosclerosis, cardiomyopathy, congestive heart failure, coronary artery disease, carotid artery disease, endocarditis, coronary thrombosis, myocardial infarction, high blood pressure/hypertension, hypercholesterolemia/hyperlipidemia, peripheral artery disease, and stroke. In some embodiments, the cardiovascular disease is due to oral biofilm formation and/or periodontal disease. In some embodiments, the condition is a kidney disease selected from chronic kidney disease and end-stage renal disease. In some embodiments, the condition is adverse ventricular remodeling, ventricular systolic dysfunction, ventricular diastolic dysfunction, cardiac dysfunction, or ventricular arrhythmia. In another aspect, disclosed herein is a method of improving or maintaining cardiovascular health in a subject in need thereof, comprising administering to the subject an effective amount of a compound disclosed herein (e.g., a compound of formula (I)), or a pharmaceutically acceptable salt thereof. In another aspect, disclosed herein is a method of inhibiting conversion of choline to trimethylamine in a subject in need thereof, comprising administering to the subject an effective amount of a compound disclosed herein (e.g., a compound of formula (I)), or a pharmaceutically acceptable salt thereof. In some embodiments, the subject has an elevated level of trimethylamine N-oxide (TMAO) in blood, plasma, serum, urine, or any combination thereof. In another aspect, disclosed herein is a method of reducing a trimethylamine N-oxide level in a subject in need thereof, comprising administering to the subject an effective amount of a compound disclosed herein (e.g., a compound of formula (I)), or a pharmaceutically acceptable salt thereof. In some embodiments, the subject has an elevated level of trimethylamine N-oxide (TMAO) in blood, plasma, serum, urine, or any combination thereof. In some embodiments, the methods disclosed herein further comprise administering a second therapeutic agent to the subject. In some embodiments, the second therapeutic agent is selected from Omega 3 oil, salicylic acid, dimethylbutanol, garlic oil, olive oil, krill oil, Co enzyme Q-10, a probiotic, a prebiotic, dietary fiber, psyllium husk, bismuth salts, phytosterols, grape seed oil, green tea extract, vitamin D, antioxidants, turmeric, curcumin, and resveratrol. Other aspects and embodiments will become apparent in light of the following description. BRIEF DESCRIPTION OF THE DRAWINGS FIG.1 shows data from an in vivo d ₉ -choline challenge model for certain compounds disclosed herein, as described in Example 3. FIG.2 shows data from an in vivo Q24 hour model, as described in Example 4. DETAILED DESCRIPTION The present disclosure is based, at least in part, on the discovery that compounds of formula (I) inhibit choline metabolism by gut microbiota, resulting in reduction of TMA formation. Accordingly, the disclosure provides compounds, compositions, and methods for, e.g., inhibiting conversion of choline to TMA in vitro and in vivo, for improving or maintaining cardiovascular, cerebrovascular, or peripherovascular health, and for treating disorders associated with conversion of choline to TMA. Definitions Unless otherwise defined herein, scientific and technical terms used in connection with the present disclosure shall have the meanings that are commonly understood by those of ordinary skill in the art. For example, any nomenclatures used in connection with, and techniques of, cell and tissue culture, molecular biology, immunology, microbiology, genetics, and protein and nucleic acid chemistry and hybridization described herein are those that are well known and commonly used in the art. The meaning and scope of the terms should be clear; in the event, however of any latent ambiguity, definitions provided herein take precedent over any dictionary or extrinsic definition. Further, unless otherwise required by context, singular terms shall include pluralities and plural terms shall include the singular. As used herein and in the appended claims, the singular forms “a,” “an,” and “the” include plural reference unless the context clearly dictates otherwise. As used herein, the term “and/or” includes any and all combinations of listed items, including any of the listed items individually. For example, “A, B, and/or C” encompasses A, B, C, AB, AC, BC, and ABC, each of which is to be considered separately described by the statement “A, B, and/or C.” For the recitation of numeric ranges herein, each intervening number there between with the same degree of precision is explicitly contemplated. For example, for the range of 6- 9, the numbers 7 and 8 are contemplated in addition to 6 and 9, and for the range 6.0-7.0, the number 6.0, 6.1, 6.2, 6.3, 6.4, 6.5, 6.6, 6.7, 6.8, 6.9, and 7.0 are explicitly contemplated. Definitions of specific functional groups and chemical terms are described in more detail below. For purposes of this disclosure, the chemical elements are identified in accordance with the Periodic Table of the Elements, CAS version, Handbook of Chemistry and Physics, 75 ^th Ed., inside cover, and specific functional groups are generally defined as described therein. Additionally, general principles of organic chemistry, as well as specific functional moieties and reactivity, are described in Sorrell, Organic Chemistry, 2 ^nd edition, University Science Books, Sausalito, 2006; Smith, March’s Advanced Organic Chemistry: Reactions, Mechanism, and Structure, 7 ^th Edition, John Wiley & Sons, Inc., New York, 2013; Larock, Comprehensive Organic Transformations, 3 ^rd Edition, John Wiley & Sons, Inc., New York, 2018; and Carruthers, Some Modern Methods of Organic Synthesis, 3 ^rd Edition, Cambridge University Press, Cambridge, 1987; the entire contents of each of which are incorporated herein by reference.

As used herein, the term “amino acid side chain” refers to a moiety attached to the a- carbon of an amino acid, preferably a naturally-occurring amino acid. For example, suitable amino acid side chains from naturally-occurring amino acids include hydrogen (as in glycine), -CH ₃ (as in alanine), -CH(CH ₃ ) ₂ (as in valine), -CH ₂ CH(CH ₃ ) ₂ (as in leucine), - CH(CH ₃ )CH ₂ CH ₃ (as in isoleucine), benzyl (as in phenylalanine), p-hydroxybenzyl (as in tyrosine), -CH ₂ -(1H-indol-3-yl) (as in tryptophan), -CH ₂ -(1H-imidazol-5-yl) (as in histidine),-CH2OH (as in serine), -CH(OH)CH3 (as in threonine), -CH2SH (as in cysteine), - CH2CH2SCH3 (as in methionine), -CH2COOH (as in aspartic acid), -CH2CH2COOH (as in glutamic acid), -CH2CONH2 (as in asparagine), -CH2CH2CONH2 (as in glutamine), - CH2CH2CH2CH2NH2 (as in lysine), -CH2CH2CH2NHC(NH)(NH2) (as in arginine), and - CH ₂ CH ₂ CH ₂ - (as in proline). Suitable amino acid side chains from non-naturally occurring amino acids include -CH ₂ CH ₂ CH ₂ COOH (as in aminoadipic acid) and - CH ₂ CH ₂ CH ₂ CH ₂ COOH (as in 2-aminopimelic acid). As used herein, the term “cycloalkyl” refers to a radical of a saturated carbocyclic ring system containing three to ten carbon atoms and zero heteroatoms. The cycloalkyl may be monocyclic, bicyclic, bridged, fused, or spirocyclic. Representative examples of cycloalkyl include, but are not limited to, cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, cyclooctyl, cyclononyl, cyclodecyl, adamantyl, bicyclo[2.2.1]heptanyl, bicyclo[3.2.1]octanyl, and bicyclo[5.2.0]nonanyl. As used herein, the term “halogen” or “halo” refers to F, Cl, Br, or I. As used herein, the term “nitrogen protecting group” refers to a group intended to protect an amino group against undesirable reactions during synthetic procedures. Common nitrogen protecting groups include acyl groups such as acetyl, benzoyl, 2-bromoacetyl, 4- bromobenzoyl, tert-butylacetyl, carboxaldehyde, 2-chloroacetyl, 4-chlorobenzoyl, a- chlorobutyryl, 4-nitrobenzoyl, o-nitrophenoxyacetyl, phthalyl, pivaloyl, propionyl, trichloroacetyl, and trifluoroacetyl; sulfonyl groups such as benzenesulfonyl and p- toluenesulfonyl; carbamate-forming groups such as benzyloxycarbonyl, benzyloxycarbonyl (Cbz), tert-butyloxycarbonyl (Boc), p-chlorobenzyloxycarbonyl, p- methoxybenzyloxycarbonyl, and the like. For compounds described herein, groups and substituents thereof may be selected in accordance with permitted valence of the atoms and the substituents, such that the selections and substitutions result in a stable compound, e.g., which does not spontaneously undergo transformation such as by rearrangement, cyclization, elimination, etc. As used herein, in chemical structures the indication: represents a point of attachment of one moiety to another moiety (e.g., a substituent group to the rest of the compound). When substituent groups are specified by their conventional chemical formulae, written from left to right, such indication also encompass substituent groups resulting from writing the structure from right to left. For example, if a bivalent group is shown as -CH ₂ O-, such indication also encompasses -OCH ₂ -; similarly, -OC(O)NH- also encompasses - NHC(O)O-. The terms “administer,” “administering,” or “administration,” as used herein refer to implanting, absorbing, ingesting, injecting, inhaling, or otherwise introducing a compound or a pharmaceutical composition. As used herein, the terms “condition,” “disease,” and “disorder” are used interchangeably. An “effective amount” of a compound or composition refers to an amount sufficient to elicit a desired biological response (e.g., treating a condition). As will be appreciated by those skilled in the art, the effective amount of a compound may vary depending on such factors as the desired biological endpoint, the pharmacokinetics of the compound, the condition being treated, the mode of administration, and the age and health of the subject. An effective amount encompasses therapeutic and prophylactic treatment. For example, in treating cancer, an effective amount of a compound or composition may reduce tumor burden or stop the growth or spread of a tumor. A “therapeutically effective amount” of a compound or composition is an amount sufficient to provide a therapeutic benefit in the treatment of a condition, or to delay or minimize one or more symptoms associated with the condition. In some embodiments, a therapeutically effective amount is an amount sufficient to provide a therapeutic benefit in the treatment of a condition or to minimize one or more symptoms associated with the condition. A therapeutically effective amount of a compound means an amount of therapeutic agent, alone or in combination with other therapies, that provides a therapeutic benefit in the treatment of the condition. The term “therapeutically effective amount” can encompass an amount that improves overall therapy, reduces or avoids symptoms or causes of the condition, or enhances the therapeutic efficacy of another therapeutic agent. A “subject” to which administration is contemplated includes, but is not limited to, a human (i.e., a male or female of any age group, e.g., a pediatric subject (e.g., infant, child, adolescent) or adult subject (e.g., young adult, middle-aged adult, or senior adult)) and/or other non-human animals, for example, mammals (e.g., primates (e.g., cynomolgus monkeys, rhesus monkeys); commercially relevant mammals such as cattle, pigs, horses, sheep, goats, cats, and/or dogs) and birds (e.g., commercially relevant birds such as chickens, ducks, geese, and/or turkeys). As used herein, the terms “treatment,” “treat,” and “treating” refer to reversing, alleviating, delaying the onset of or inhibiting the progress of a disease or condition, or one or more signs or symptoms thereof. In some embodiments, “treatment,” “treat,” and “treating” require that signs or symptoms of the disease disorder or condition have developed or have been observed. In other embodiments, treatment may be administered in the absence of signs or symptoms of the disease or condition. For example, treatment may be administered to a susceptible individual prior to the onset of symptoms (e.g., in light of a history of symptoms and/or in light of genetic or other susceptibility factors). Treatment may also be continued after symptoms have resolved, for example, to delay or prevent recurrence. Compounds Disclosed herein are compounds of formula (I): and pharmaceutically acceptable salts thereof, wherein: R ¹ is an amino acid side chain, -COOH, or a group ; R ² is hydrogen or a nitrogen protecting group; or R ¹ and R ² are taken together with the atoms to which they are attached to form a five-membered ring; Z is selected from a bond, -CH ₂ -, and -CH ₂ CH ₂ -; R ³ and R ⁴ are each independently selected from halomethyl and C ₃ -C ₆ cycloalkyl; and X ^– is an anion. In some embodiments, Z is a bond. In some embodiments, Z is -CH ₂ - or -CH ₂ CH ₂ -. In some embodiments, Z is -CH ₂ . In some embodiments, Z is -CH ₂ CH ₂ -. In some embodiments, R ¹ is an amino acid side chain. In some embodiments, R ¹ is a side chain from an amino acid selected from glycine, alanine, valine, leucine, isoleucine, phenylalanine, tyrosine, tryptophan, histidine, serine, threonine, cysteine, methionine, aspartic acid, glutamic acid, asparagine, glutamine, lysine, and arginine. For example, in some embodiments, R ¹ is selected from hydrogen, -CH ₃ , -CH(CH ₃ )2, -CH ₂ CH(CH ₃ )2, - CH(CH ₃ )CH ₂ CH ₃ , benzyl, p-hydroxybenzyl, -CH ₂ -(1H-indol-3-yl), -CH ₂ -(1H-imidazol-5- yl), -CH ₂ OH, -CH(OH)CH ₃ , -CH ₂ SH, -CH ₂ CH ₂ SCH ₃ , -CH ₂ COOH, -CH ₂ CH ₂ COOH, - CH ₂ CONH ₂ , -CH ₂ CH ₂ CONH ₂ , -CH ₂ CH ₂ CH ₂ CH ₂ NH ₂ , and -CH ₂ CH ₂ CH ₂ NHC(NH)(NH ₂ ). In some embodiments, R ¹ is selected from hydrogen, -CH ₃ , -CH(CH ₃ )2, benzyl, -CH ₂ OH, - CH ₂ COOH, and -CH ₂ CH ₂ COOH. In some embodiments, R ¹ is -COOH. In some embodiments, R ¹ is -COOCH ₂ CH ₂ N(CH ₂ R ^d )(CH ₂ R ^e )(CH ₂ R ^f ). The groups R ^d , R ^e , and R ^f are each independently selected from hydrogen and halo, wherein at least one of R ^d , R ^e , and R ^f is halo. In some embodiments, the halo is fluoro. In some embodiments, the halo is chloro. In some embodiments, the halo is bromo. In some embodiments, the halo is iodo. In some embodiments, R ^d is halo, and R ^b and R ^c are hydrogen. In some embodiments, R ^d is fluoro, and R ^e and R ^f are hydrogen. In some embodiments, R ^d is chloro, and R ^e and R ^f are hydrogen. In some embodiments, R ^d is bromo, and R ^e and R ^f are hydrogen. In some embodiments, R ^a is iodo, and R ^e and R ^f are hydrogen. In particular embodiments, Z is a bond, and R ¹ is an amino acid side chain (e.g., R ¹ is selected from hydrogen, -CH ₃ , -CH(CH ₃ )2, -CH ₂ CH(CH ₃ )2, -CH(CH ₃ )CH ₂ CH ₃ , benzyl, p- hydroxybenzyl, -CH ₂ -(1H-indol-3-yl), -CH ₂ -(1H-imidazol-5-yl), -CH ₂ OH, -CH(OH)CH ₃ , - CH ₂ SH, -CH ₂ CH ₂ SCH ₃ , -CH ₂ COOH, -CH ₂ CH ₂ COOH, -CH ₂ CONH ₂ , -CH ₂ CH ₂ CONH ₂ , - CH ₂ CH ₂ CH ₂ CH ₂ NH ₂ , and -CH ₂ CH ₂ CH ₂ NHC(NH)(NH ₂ ), or R ¹ is selected from hydrogen, - CH ₃ , -CH(CH ₃ ) ₂ , benzyl, -CH ₂ OH, -CH ₂ COOH, and -CH ₂ CH ₂ COOH. In other particular embodiments, Z is -CH ₂ - or -CH ₂ CH ₂ -, and R ¹ is -COOH. In other particular embodiments, Z is -CH ₂ - or -CH ₂ CH ₂ -, and R ¹ is - COOCH ₂ CH ₂ N(CH ₂ R ^d )(CH ₂ R ^e )(CH ₂ R ^f ). In some embodiments, R ² is hydrogen. In some embodiments, R ² is a nitrogen protecting group. In some embodiments, R ² is hydrogen or -C(O)CH ₃ . In some embodiments, R ¹ and R ² are taken together with the atoms to which they are attached to form a five-membered ring (e.g., a saturated five-membered ring). One skilled in the art will recognize that such embodiments encompass situations in which proline is used as the amino acid. In some embodiments, R ³ is halomethyl. In some embodiments, R ³ is fluoromethyl. In some embodiments, R ³ is chloromethyl. In some embodiments, R ³ is bromomethyl. In some embodiments, R ³ is iodomethyl. In some embodiments, R ³ is C ₃ -C ₆ cycloalkyl. In some embodiments, R ³ is cyclopropyl. In some embodiments, R ⁴ is halomethyl. In some embodiments, R ⁴ is fluoromethyl. In some embodiments, R ⁴ is chloromethyl. In some embodiments, R ⁴ is bromomethyl. In some embodiments, R ⁴ is iodomethyl. In some embodiments, R ⁴ is C ₃ -C ₆ cycloalkyl. In some embodiments, R ⁴ is cyclopropyl. In compounds of formula (I), X ^– is an anion. While any suitable anion can be used, in some embodiments, X ^– is selected from a halide and a carboxylate. In some embodiments, X ^– is a halide, such as chloride or bromide. In some embodiments, X ^– is a carboxylate, such as acetate or trifluoroacetate. In some embodiments, the compound is selected from: and pharmaceutically acceptable salts thereof. The compounds of the present disclosure have at least one asymmetric center. Additional asymmetric centers may be present depending upon the nature of the various substituent groups. Compounds with asymmetric centers give rise to enantiomers (optical isomers), diastereomers (configurational isomers) or both, and it is intended that all of the possible enantiomers and diastereomers, in mixtures and as pure or partially purified compounds, are included within the scope of this disclosure. The independent syntheses of the enantiomerically or diastereomerically enriched compounds, or their chromatographic separations, may be achieved as known in the art by appropriate modification of the methodology disclosed herein. The absolute stereochemistry of a compound may be determined by using X-ray crystallography to determine the crystal structure of crystalline products or crystalline intermediates that are derivatized, if necessary, with a reagent containing an asymmetric center of known absolute configuration. If desired, racemic mixtures of the compounds may be separated so that the individual enantiomers are isolated. The separation can be carried out by methods well known in the art, such as the coupling of a racemic mixture of compounds to an enantiomerically pure compound to form a diastereomeric mixture, followed by separation of the individual diastereomers by standard methods, such as fractional crystallization or chromatography. The coupling reaction is often the formation of salts using an enantiomerically pure acid or base. The diastereomeric derivatives may then be converted to the pure enantiomers by cleavage of the added chiral residue. The racemic mixture of the compounds can also be separated directly by chromatographic methods using chiral stationary phases, which methods are well known in the art. Alternatively, any enantiomer of a compound may be obtained by stereoselective synthesis using optically pure starting materials or reagents of known configuration by methods well known in the art. The compounds may possess tautomeric forms, and tautomers also constitute embodiments of the disclosure. The present disclosure also includes isotopically-labeled compounds, which are identical to those recited in formula (I) (including those compounds specifically exemplified herein), but for the fact that one or more atoms are replaced by an atom having an atomic mass or mass number different from the atomic mass or mass number usually found in nature. Examples of isotopes suitable for inclusion in the compounds of the disclosure are hydrogen, carbon, nitrogen, oxygen, phosphorus, sulfur, fluorine, and chlorine, such as, but not limited to ² H, ³ H, ¹³ C, ¹⁴ C, ¹⁵ N, ¹⁸ O, ³¹ P, ³⁵ S, ¹⁸ F, and ³⁶ Cl, respectively. Substitution with heavier isotopes such as deuterium, i.e. ² H, can afford certain therapeutic advantages resulting from greater metabolic stability, for example increased in vivo half-life or reduced dosage requirements and, hence, may be particularly useful in some circumstances. The compound may incorporate positron-emitting isotopes for medical imaging and positron-emitting tomography (PET) studies for determining the distribution of receptors. Suitable positron- emitting isotopes that can be incorporated into the compounds are ¹¹ C, ¹³ N, ¹⁵ O, and ¹⁸ F. Isotopically-labeled compounds can generally be prepared by conventional techniques known to those skilled in the art, or by processes analogous to those described herein using an appropriate isotopically-labeled reagent in place of a non-isotopically-labeled reagent. Compounds of formula (I) can be synthesized by a variety of methods, including those illustrated in the Examples. One approach is illustrated in Scheme 1, which involves reaction of fluorocholine chloride (which is commercially available from a variety of suppliers), with a suitably protected amino acid in the presence of a coupling agent, followed by appropriate deprotection steps. For example, the amino acid may include a protecting group on the alpha-amino moiety, and may optionally include a protecting group on the side chain when appropriate. As shown in Scheme 2, when aspartic acid and glutamic acid are used as the amino acids, they can be protected on the alpha carboxylic acid moiety rather than the side chain moiety, to produce compounds with different linkages. Scheme 1 Scheme 2 Compounds and intermediates may be isolated and purified by methods well-known to those skilled in the art of organic synthesis. Examples of conventional methods for isolating and purifying compounds can include but are not limited to chromatography on solid supports such as silica gel, alumina, or silica derivatized with alkylsilane groups, by recrystallization at high or low temperature with an optional pretreatment with activated carbon, thin-layer chromatography, distillation at various pressures, sublimation under vacuum, and trituration, as described for instance in “Vogel’s Textbook of Practical Organic Chemistry,” 5th edition (1989), by Furniss, Hannaford, Smith, and Tatchell, pub. Longman Scientific & Technical, Essex CM202JE, England. Reaction conditions and reaction times for each individual step can vary depending on the particular reactants employed and substituents present in the reactants used. Reactions can be worked up in a conventional manner, e.g., by eliminating the solvent from the residue and further purified according to methodologies generally known in the art such as, but not limited to, crystallization, distillation, extraction, trituration and chromatography. Unless otherwise described, the starting materials and reagents are either commercially available or can be prepared by one skilled in the art from commercially available materials using methods described in the chemical literature. Standard experimentation, including appropriate manipulation of the reaction conditions, reagents and sequence of the synthetic route, protection of any chemical functionality that cannot be compatible with the reaction conditions, and deprotection at a suitable point in the reaction sequence of the method are included in the scope of the disclosure. Suitable protecting groups and the methods for protecting and deprotecting different substituents using such suitable protecting groups are well known to those skilled in the art; examples of which can be found in PGM Wuts and TW Greene, in Greene’s book titled Protective Groups in Organic Synthesis (4 ^th ed.), John Wiley & Sons, NY (2006). When an optically active form of a disclosed compound is required, it can be obtained by carrying out one of the procedures described herein using an optically active starting material (prepared, for example, by asymmetric induction of a suitable reaction step), or by resolution of a mixture of the stereoisomers of the compound or intermediates using a standard procedure (such as chromatographic separation, recrystallization or enzymatic resolution). Similarly, when a pure geometric isomer of a compound is required, it can be obtained by carrying out one of the procedures described herein using a pure geometric isomer as a starting material, or by resolution of a mixture of the geometric isomers of the compound or intermediates using a standard procedure such as chromatographic separation. The synthetic schemes and specific examples as described are illustrative and are not to be read as limiting the scope of the disclosure or the claims. Alternatives, modifications, and equivalents of the synthetic methods and specific examples are contemplated. The disclosed compounds may exist as pharmaceutically acceptable salts. Compounds of formula (I) are already in salt form (with a positive charge on the nitrogen atom and an associated anion X ^– ). Nevertheless, the compound may bear one or more additional charges ( e.g., on the -NHR ² moiety, or on an amino acid side chain), and thus the compound may be prepared as an additional salt form. The term “pharmaceutically acceptable salt” refers to salts or zwitterions of the compounds which are water or oil-soluble or dispersible, suitable for treatment of disorders without undue toxicity, irritation, or allergic response, commensurate with a reasonable benefit/risk ratio and effective for their intended use. The salts may be prepared during the final isolation and purification of the compounds or separately by reacting an amino group of the compounds with a suitable acid. For example, a compound may be dissolved in a suitable solvent, such as but not limited to methanol and water, and treated with at least one equivalent of an acid, such as hydrochloric acid. The resulting salt may precipitate out and be isolated by filtration and dried under reduced pressure. Alternatively, the solvent and excess acid may be removed under reduced pressure to provide a salt. Representative salts include acetate, adipate, alginate, citrate, aspartate, benzoate, benzenesulfonate, bisulfate, butyrate, camphorate, camphorsulfonate, digluconate, glycerophosphate, hemisulfate, heptanoate, hexanoate, formate, isethionate, fumarate, lactate, maleate, methanesulfonate, naphthylenesulfonate, nicotinate, oxalate, pamoate, pectinate, persulfate, 3-phenylpropionate, picrate, oxalate, maleate, pivalate, propionate, succinate, tartrate, trichloroacetate, trifluoroacetate, glutamate, para-toluenesulfonate, undecanoate, hydrochloric, hydrobromic, sulfuric, phosphoric and the like. The amino groups of the compounds may also be quaternized with alkyl chlorides, bromides and iodides such as methyl, ethyl, propyl, isopropyl, butyl, lauryl, myristyl, stearyl, and the like. In one embodiment, the compound is in the form of a halide salt, such as a chloride or bromide salt. Basic addition salts may be prepared during the final isolation and purification of the disclosed compounds by reaction of a carboxyl group with a suitable base such as the hydroxide, carbonate, or bicarbonate of a metal cation such as lithium, sodium, potassium, calcium, magnesium, or aluminum, or an organic primary, secondary, or tertiary amine. Quaternary amine salts can be prepared, such as those derived from methylamine, dimethylamine, trimethylamine, triethylamine, diethylamine, ethylamine, tributylamine, pyridine, N,N-dimethylaniline N-methylpiperidine N-methylmorpholine dicyclohexylamine, procaine, dibenzylamine, N,N-dibenzylphenethylamine, 1-ephenamine and N,N’- dibenzylethylenediamine, ethylenediamine, ethanolamine, diethanolamine, piperidine, piperazine, and the like. Compounds disclosed herein can exist in unsolvated forms as well as solvated forms, including hydrated forms. In general, the solvated forms are equivalent to unsolvated forms and are encompassed within the scope of the present disclosure. Certain compounds of the disclosure may also exist in multiple crystalline or amorphous forms. In general, all physical forms are equivalent for the uses contemplated by the present disclosure and are intended to be within the scope of the present disclosure. Pharmaceutical Compositions The disclosed compounds may be incorporated into pharmaceutical compositions suitable for administration to a subject (such as a patient, which may be a human or non- human). The pharmaceutical compositions may include a “therapeutically effective amount” or a “prophylactically effective amount” of the agent. A “therapeutically effective amount” refers to an amount effective, at dosages and for periods of time necessary, to achieve the desired therapeutic result. A therapeutically effective amount of the composition may be determined by a person skilled in the art and may vary according to factors such as the disease state, age, sex, and weight of the individual, and the ability of the composition to elicit a desired response in the individual. A therapeutically effective amount is also one in which any toxic or detrimental effects of a compound of the disclosure are outweighed by the therapeutically beneficial effects. A “prophylactically effective amount” refers to an amount effective, at dosages and for periods of time necessary, to achieve the desired prophylactic result. Typically, since a prophylactic dose is used in subjects prior to or at an earlier stage of disease or condition, the prophylactically effective amount will be less than the therapeutically effective amount. The pharmaceutical compositions may include pharmaceutically acceptable carriers. The term “pharmaceutically acceptable carrier,” as used herein, means a non-toxic, inert solid, semi-solid or liquid filler, diluent, encapsulating material or formulation auxiliary of any type. Some examples of materials which can serve as pharmaceutically acceptable carriers are sugars such as, but not limited to, lactose, glucose and sucrose; starches such as, but not limited to, corn starch and potato starch; cellulose and its derivatives such as, but not limited to, sodium carboxymethyl cellulose, ethyl cellulose and cellulose acetate; powdered tragacanth; malt; gelatin; talc; excipients such as, but not limited to, cocoa butter and suppository waxes; oils such as, but not limited to, peanut oil, cottonseed oil, safflower oil, sesame oil, olive oil, corn oil and soybean oil; glycols; such as propylene glycol; esters such as, but not limited to, ethyl oleate and ethyl laurate; agar; buffering agents such as, but not limited to, magnesium hydroxide and aluminum hydroxide; alginic acid; pyrogen-free water; isotonic saline; Ringer’s solution; ethyl alcohol, and phosphate buffer solutions, as well as other non-toxic compatible lubricants such as, but not limited to, sodium lauryl sulfate and magnesium stearate, as well as coloring agents, releasing agents, coating agents, sweetening, flavoring and perfuming agents, preservatives and antioxidants can also be present in the composition, according to the judgment of the formulator. Thus, the compounds and their pharmaceutically acceptable salts may be formulated for administration by, for example, solid dosing, eye drop, in a topical oil-based formulation, injection, inhalation (either through the mouth or the nose), implants, or oral, buccal, parenteral, or rectal administration. Techniques and formulations may generally be found in “Remington’s Pharmaceutical Sciences,” (Meade Publishing Co., Easton, Pa.). Therapeutic compositions must typically be sterile and stable under the conditions of manufacture and storage. The route by which the disclosed compounds are administered and the form of the composition will dictate the type of carrier to be used. The composition may be in a variety of forms, suitable, for example, for systemic administration (e.g., oral, rectal, nasal, sublingual, buccal, implants, or parenteral) or topical administration (e.g., dermal, pulmonary, nasal, aural, ocular, liposome delivery systems, or iontophoresis). Carriers for systemic administration typically include at least one of diluents, lubricants, binders, disintegrants, colorants, flavors, sweeteners, antioxidants, preservatives, glidants, solvents, suspending agents, wetting agents, surfactants, combinations thereof, and others. All carriers are optional in the compositions. Suitable diluents include sugars such as glucose, lactose, dextrose, and sucrose; diols such as propylene glycol; calcium carbonate; sodium carbonate; sugar alcohols, such as glycerin; mannitol; and sorbitol. The amount of diluent(s) in a systemic or topical composition is typically about 50 to about 90% by weight of the composition. Suitable lubricants include silica, talc, stearic acid and its magnesium salts and calcium salts, calcium sulfate; and liquid lubricants such as polyethylene glycol and vegetable oils such as peanut oil, cottonseed oil, sesame oil, olive oil, corn oil and oil of theobroma. The amount of lubricant(s) in a systemic or topical composition is typically about 5 to about 10% by weight of the composition Suitable binders include polyvinyl pyrrolidone; magnesium aluminum silicate; starches such as corn starch and potato starch; gelatin; tragacanth; and cellulose and its derivatives, such as sodium carboxymethylcellulose, ethyl cellulose, methylcellulose, microcrystalline cellulose, and sodium carboxymethylcellulose. The amount of binder(s) in a systemic composition is typically about 5 to about 50% by weight of the composition. Suitable disintegrants include agar, alginic acid and the sodium salt thereof, effervescent mixtures, croscarmellose, crospovidone, sodium carboxymethyl starch, sodium starch glycolate, clays, and ion exchange resins. The amount of disintegrant(s) in a systemic or topical composition is typically about 0.1 to about 10% by weight of the composition. Suitable colorants include a colorant such as an FD&C dye. When used, the amount of colorant in a systemic or topical composition is typically about 0.005 to about 0.1% by weight of the composition. Suitable flavors include menthol, peppermint, and fruit flavors. The amount of flavor(s), when used, in a systemic or topical composition is typically about 0.1 to about 1.0%. Suitable sweeteners include aspartame and saccharin. The amount of sweetener(s), when used, in a systemic or topical composition is typically about 0.001 to about 1% by weight of the composition. Suitable antioxidants include butylated hydroxyanisole (“BHA”), butylated hydroxytoluene (“BHT”), and vitamin E. The amount of antioxidant(s) in a systemic or topical composition is typically about 0.1 to about 5% by weight of the composition. Suitable preservatives include benzalkonium chloride, methyl paraben, and sodium benzoate. The amount of preservative(s) in a systemic or topical composition is typically about 0.01 to about 5% by weight of the composition. Suitable glidants include silicon dioxide. The amount of glidant(s) in a systemic or topical composition is typically about 1 to about 5% by weight of the composition. Suitable solvents include water, isotonic saline, ethyl oleate, glycerin, hydroxylated castor oils, alcohols such as ethanol, and phosphate buffer solutions. The amount of solvent(s) in a systemic or topical composition is typically from about 0 to about 100% by weight of the composition. Suitable suspending agents include AVICEL RC-591 (from FMC Corporation of Philadelphia, PA) and sodium alginate. The amount of suspending agent(s) in a systemic or topical composition is typically about 1 to about 8% by weight of the composition. Suitable surfactants include lecithin, Polysorbate 80, and sodium lauryl sulfate, and the TWEENS from Atlas Powder Company of Wilmington, Delaware. Suitable surfactants include those disclosed in the C.T.F.A. Cosmetic Ingredient Handbook, 1992, pp.587-592; Remington’s Pharmaceutical Sciences, 15th Ed.1975, pp.335-337; and McCutcheon’s Volume 1, Emulsifiers & Detergents, 1994, North American Edition, pp.236-239. The amount of surfactant(s) in the systemic or topical composition is typically about 0.1% to about 5% by weight of the composition. Although the amounts of components in the systemic compositions may vary depending on the type of systemic composition prepared, in general, systemic compositions include 0.01% to 50% by weight of an active compound and 50% to 99.99% by weight of one or more carriers. Compositions for parenteral administration typically include 0.1% to 10% by weight of actives and 90% to 99.9% by weight of a carrier including a diluent and a solvent. Compositions for oral administration can have various dosage forms. For example, solid forms include tablets, capsules, granules, and bulk powders. These oral dosage forms include a safe and effective amount, usually at least about 5% by weight, and more particularly from about 25% to about 50% by weight of actives. The oral dosage compositions include about 50% to about 95% by weight of carriers, and more particularly, from about 50% to about 75% by weight. Tablets can be compressed, tablet triturates, enteric-coated, sugar-coated, film-coated, or multiple-compressed. Tablets typically include an active component, and a carrier comprising ingredients selected from diluents, lubricants, binders, disintegrants, colorants, flavors, sweeteners, glidants, and combinations thereof. Specific diluents include calcium carbonate, sodium carbonate, mannitol, lactose and cellulose. Specific binders include starch, gelatin, and sucrose. Specific disintegrants include alginic acid and croscarmellose. Specific lubricants include magnesium stearate, stearic acid, and talc. Specific colorants are the FD&C dyes, which can be added for appearance. Chewable tablets preferably contain sweeteners such as aspartame and saccharin, or flavors such as menthol, peppermint, fruit flavors, or a combination thereof. Capsules (including implants, time release and sustained release formulations) typically include an active compound (e.g., a compound of formula (I)), and a carrier including one or more diluents disclosed above in a capsule comprising gelatin. Granules typically comprise a disclosed compound, and preferably glidants such as silicon dioxide to improve flow characteristics. Implants can be of the biodegradable or the non-biodegradable type. The selection of ingredients in the carrier for oral compositions depends on secondary considerations like taste, cost, and shelf stability, which are not critical for the purposes of this disclosure. Solid compositions may be coated by conventional methods, typically with pH or time-dependent coatings, such that a disclosed compound is released in the gastrointestinal tract in the vicinity of the desired application, or at various points and times to extend the desired action. The coatings typically include one or more components selected from the group consisting of cellulose acetate phthalate, polyvinyl acetate phthalate, hydroxypropyl methyl cellulose phthalate, ethyl cellulose, EUDRAGIT® coatings (available from Evonik Industries of Essen, Germany), waxes and shellac. Compositions for oral administration can have liquid forms. For example, suitable liquid forms include aqueous solutions, emulsions, suspensions, solutions reconstituted from non-effervescent granules, suspensions reconstituted from non-effervescent granules, effervescent preparations reconstituted from effervescent granules, elixirs, tinctures, syrups, and the like. Liquid orally administered compositions typically include a disclosed compound and a carrier, namely, a carrier selected from diluents, colorants, flavors, sweeteners, preservatives, solvents, suspending agents, and surfactants. Peroral liquid compositions preferably include one or more ingredients selected from colorants, flavors, and sweeteners. Other compositions useful for attaining systemic delivery of the subject compounds include sublingual, buccal and nasal dosage forms. Such compositions typically include one or more of soluble filler substances such as diluents including sucrose, sorbitol and mannitol; and binders such as acacia, microcrystalline cellulose, carboxymethyl cellulose, and hydroxypropyl methylcellulose. Such compositions may further include lubricants, colorants, flavors, sweeteners, antioxidants, and glidants. The disclosed compounds can be topically administered. Topical compositions that can be applied locally to the skin may be in any form including solids, solutions, oils, creams, ointments, gels, lotions, shampoos, leave-on and rinse-out hair conditioners, milks, cleansers, moisturizers, sprays, skin patches, and the like. Topical compositions include: a disclosed compound (e.g., a compound of formula (I)), or a pharmaceutically acceptable salt thereof), and a carrier. The carrier of the topical composition preferably aids penetration of the compounds into the skin. The carrier may further include one or more optional components. The amount of the carrier employed in conjunction with a disclosed compound is sufficient to provide a practical quantity of composition for administration per unit dose of the compound. Techniques and compositions for making dosage forms useful in the methods of this disclosure are described in the following references: Modern Pharmaceutics, Chapters 9 and 10, Banker & Rhodes, eds. (1979); Lieberman et al., Pharmaceutical Dosage Forms: Tablets (1981); and Ansel, Introduction to Pharmaceutical Dosage Forms, 2nd Ed., (1976). A carrier may include a single ingredient or a combination of two or more ingredients. In the topical compositions, the carrier includes a topical carrier. Suitable topical carriers include one or more ingredients selected from phosphate buffered saline, isotonic water, deionized water, monofunctional alcohols, symmetrical alcohols, aloe vera gel, allantoin, glycerin, vitamin A and E oils, minerafl oil, propylene glycol, PPG-2 myristyl propionate, dimethyl isosorbide, castor oil, combinations thereof, and the like. More particularly, carriers for skin applications include propylene glycol, dimethyl isosorbide, and water, and even more particularly, phosphate buffered saline, isotonic water, deionized water, monofunctional alcohols, and symmetrical alcohols. The carrier of a topical composition may further include one or more ingredients selected from emollients, propellants, solvents, humectants, thickeners, powders, fragrances, pigments, and preservatives, all of which are optional. Suitable emollients include stearyl alcohol, glyceryl monoricinoleate, glyceryl monostearate, propane-1,2-diol, butane-1,3-diol, mink oil, cetyl alcohol, isopropyl isostearate, stearic acid, isobutyl palmitate, isocetyl stearate, oleyl alcohol, isopropyl laurate, hexyl laurate, decyl oleate, octadecan-2-ol, isocetyl alcohol, cetyl palmitate, di-n-butyl sebacate, isopropyl myristate, isopropyl palmitate, isopropyl stearate, butyl stearate, polyethylene glycol, triethylene glycol, lanolin, sesame oil, coconut oil, arachis oil, castor oil, acetylated lanolin alcohols, petroleum, mineral oil, butyl myristate, isostearic acid, palmitic acid, isopropyl linoleate, lauryl lactate, myristyl lactate, decyl oleate, myristyl myristate, and combinations thereof. Specific emollients for skin include stearyl alcohol and polydimethylsiloxane. The amount of emollient(s) in a skin-based topical composition is typically about 5% to about 95% by weight of the composition. Suitable propellants include propane, butane, isobutane, dimethyl ether, carbon dioxide, nitrous oxide, and combinations thereof. The amount of propellant(s) in a topical composition is typically about 0% to about 95% by weight of the composition. Suitable solvents include water, ethyl alcohol, methylene chloride, isopropanol, castor oil, ethylene glycol monoethyl ether diethylene glycol monobutyl ether diethylene glycol monoethyl ether, dimethylsulfoxide, dimethyl formamide, tetrahydrofuran, and combinations thereof. Specific solvents include ethyl alcohol and homotopic alcohols. The amount of solvent(s) in a topical composition is typically about 0% to about 95% by weight of the composition. Suitable humectants include glycerin, sorbitol, sodium 2-pyrrolidone-5-carboxylate, soluble collagen, dibutyl phthalate, gelatin, and combinations thereof. Specific humectants include glycerin. The amount of humectant(s) in a topical composition is typically 0% to 95% by weight of the composition. The amount of thickener(s) in a topical composition is typically about 0% to about 95% by weight of the composition. Suitable powders include beta-cyclodextrins, hydroxypropyl cyclodextrins, chalk, talc, fullers earth, kaolin, starch, gums, colloidal silicon dioxide, sodium polyacrylate, tetra alkyl ammonium smectites, trialkyl aryl ammonium smectites, chemically-modified magnesium aluminum silicate, organically-modified montmorillonite clay, hydrated aluminum silicate, fumed silica, carboxyvinyl polymer, sodium carboxymethyl cellulose, ethylene glycol monostearate, and combinations thereof. The amount of powder(s) in a topical composition is typically 0% to 95% by weight of the composition. The amount of fragrance in a topical composition is typically about 0% to about 0.5%, particularly, about 0.001% to about 0.1% by weight of the composition. Suitable pH adjusting additives include HCl or NaOH in amounts sufficient to adjust the pH of a topical pharmaceutical composition. Methods of Use Disclosed herein are methods of reducing the production of TMA (including inhibiting the conversion of choline to TMA by a bacterium), methods of treating a condition associated with conversion of choline to TMA, methods of improving or maintaining cardiovascular health, and the like, using compounds of formula (I) (or pharmaceutically acceptable salts thereof), or compositions comprising compounds of formula (I) (or pharmaceutically acceptable salts thereof). TMA synthesized by bacteria resident in the gut of mammals is oxidized in the liver to trimethylamine N-oxide (TMAO, TMANO). Exemplary precursors of TMA include choline, betaine, phosphatidylcholine, phosphocholine, glycerophosphocholine, carnitine (such as L-carnitine), TMAO, sphingomyelin, and lecithin, many of which are derived from dietary sources such as whole eggs and beef liver. Without wishing to be bound to a particular mechanism or biochemical pathway, the anaerobic conversion of choline to TMA is facilitated by a glycyl radical enzyme homologue, choline trimethylamine-lyase (CutC). Craciun et al., Proc. Natl. Acad. Sci. (2012), 109: 21307-21312. The reduction of choline conversion to TMA by bacteria in the gut of an individual leads to a reduction in TMA absorption from the gut, leading to a subsequent reduction in plasma TMAO following oxidation of TMA to TMAO by the flavin monooxygenase 3 (FM03) enzyme in the liver. Wang et al., Nature (2011), 472: 57-63. Lower plasma TMAO levels are related to a lower incidence of major cardiovascular events in humans. Tang et al., NEJM (2013) 368: 1575- 1584. The conversion of choline to TMA may be mediated by one species of bacteria or may comprise a multi-step process involving two, three or more species of bacteria. As described previously, the present disclosure is based, at least in part, on the discovery that compounds of formula (I) interfere with choline metabolism by gut microbiota, resulting in reduction in the formation of TMA and TMAO. Accordingly, the disclosed compounds and compositions can be used in methods that, for example, inhibit the conversion of choline to TMA in vitro and in vivo, improve or maintain cardiovascular, cerebrovascular, and peripherovascular health, and treat or improve a condition associated with increased TMA and TMAO. Disclosed herein is a method of inhibiting conversion of choline to TMA in a subject in need thereof, comprising administering to the subject an effective amount of a compound of formula (I) or a pharmaceutically acceptable salt thereof, or a composition comprising a compound of formula (I) or a pharmaceutically acceptable salt thereof. Similarly, also disclosed herein is a method of reducing a TMAO level in a subject in need thereof, comprising administering to the subject an effective amount of a compound of formula (I) or a pharmaceutically acceptable salt thereof, or a composition comprising a compound of formula (I) or a pharmaceutically acceptable salt thereof. In certain embodiments, the subject may be in need of reduced TMA levels, improvement of cardiovascular health, and the like. An individual may exhibit an elevated level of TMA or a metabolite thereof (e.g., TMAO, dimethylamine (DMA), or monomethylamine (MMA)) prior to administration, e.g., in blood, plasma, serum, urine, or the like, or any combination thereof. In various embodiments, the individual suffers from cardiovascular disease (CVD), ingests a diet high in choline, or exhibits one or more CVD risk factors (e.g., smoking, stress, high total cholesterol, high LDL cholesterol, low HDL cholesterol, age, hypertension, family history of CVD, obesity, prediabetes, diabetes, or the like). Also disclosed herein is a method of inhibiting conversion of choline to TMA in vitro. For example, in some embodiments, the method comprises contacting a bacterium, such as a bacterium that is represented in the gut microflora, or a bacterial lysate that metabolizes choline to produce TMA, with a compound of formula (I) or a pharmaceutically acceptable salt thereof, or a composition comprising a compound of formula (I) or a pharmaceutically acceptable salt thereof. In various embodiments, the bacterium may be selected from Proteus mirabilis, Desulfovibrio alaskensis, Clostridium ljungdahlii, Clostridium scindens, Clostridium aldenense, Clostridium aminobutyricum, Collinsella tanakaei, Anaerococcus vaginalis, Streptococcus dysgalactiae, Desultitobacterium hafniense, Klebsiella variicola, Klebsiella pneumoniae, Proteus penneri, Eggerthella lenta, Edwardsiella tarda, Escherichia coli, and Escherichia fergussonii, or any combination thereof. In certain embodiments, the bacterium expresses the cutC/D gene cluster. The disclosure further provides a method of identifying a compound that inhibits TMA production. The method comprises contacting a bacterium, such as a bacterium that is part of the gut microflora, or a bacterial lysate that metabolizes choline to produce TMA with a candidate compound, such as a compound of formula (I) or a pharmaceutically acceptable salt thereof, and detecting TMA (or a metabolite thereof). In certain embodiments, the level of TMA (or metabolite thereof) produced by the bacterium in contact with the candidate compound is compared to (a) the level of TMA produced by a bacterium or lysate not contacted with a candidate compound or known TMA inhibitor or (b) the level of TMA produced by the bacterium prior to contact with the candidate compound. A reduction in the level of TMA produced by the bacterium or lysate indicates that the candidate compound inhibits conversion of choline to TMA. It will be appreciated that “inhibiting conversion of choline to TMA” does not require complete elimination of TMA production via choline metabolism. Any reduction in TMA formation from choline or a choline-related metabolite as a precursor is contemplated, e.g., at least 1%, at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, or 100% reduction; and also including from about 1% to about 100%, from about 10% to about 90%, from about 20% to about 80%, from about 30% to about 70%, from about 40% to about 60%, and any combinations thereof. In certain embodiments, the inhibition of conversion of choline to TMA by the compounds of formula (I) (or pharmaceutically acceptable salts thereof) is not brought about by an antibiotic mechanism of action for example it is not brought about by an antibacterial mechanism of action, or by a mechanism of action which reduces cell viability to 10% or lower, when compared to vehicle control. In certain embodiments, the amount of compound needed to provide 50% inhibition of conversion of choline to TMA is less than the amount of compound that reduces cell viability to 10% or lower, when compared to vehicle control. Any suitable method for measuring TMA in vitro or in vivo can be used in the context of the methods disclosed herein. TMA, metabolites of TMA (including TMAO, DMA, or MMA), stable isotopes of TMA (such as deuterium labeled TMA, such as d ₃ -, d ₆ -, or d ₉ - TMA), stable isotopes of TMAO (such as deuterium labeled TMAO, such as d ₃ -, d ₆ -, or d ₉ - TMAO), stable isotopes of DMA (such as deuterium labeled DMA, such as d3-, or d6-DMA), stable isotopes of MMA (such as deuterium labeled MMA, such as d3-MMA), or choline (including stable isotopes of choline, for example d9-choline) can be assessed quantitatively or qualitatively. Exemplary methods of detecting and quantifying TMA are described in, for example U.S. Pub. No.2010/00285517, the disclosure of which is incorporated herein by reference in its entirety. For example, levels of TMA (or trimethylamine N-oxide (TMAO), DMA, or MMA) or choline are optionally measured via mass spectrometry, ultraviolet spectroscopy, or nuclear magnetic resonance spectroscopy. Mass spectrometers include an ionizing source (such as electrospray ionization), an analyzer to separate the ions formed in the ionization source according to their mass-to-charge (m/z) ratios, and a detector for the charged ions. In tandem mass spectrometry, two or more analyzers are included. Such methods are standard in the art and include, for example, HPLC with on-line electrospray ionization (ESI) and tandem mass spectrometry. In various embodiments, TMA or TMAO is measured in a biological sample from an individual. Biological samples include, but are not limited to, whole blood, plasma, serum, urine, feces, saliva, sweat, vaginal fluid, gingival crevicular fluid, or tissue. The sample may be collected using any clinically-acceptable practice and, if desired, diluted in an appropriate buffer solution, heparinized, concentrated, or fractionated. Any of a number of aqueous buffer solutions at physiological pH, such as phosphate, Tris, or the like, can be used. Acidified buffers also may be used. For example, the final pH after adding buffer to sample may optionally be between pH 1 and pH 6, or between pH 1.5 and pH 3.0. In addition, levels of TMA (or a metabolite or stable isotope thereof) or choline in the biological sample may be compared to a control value. The control value utilized will depend on the embodiment of the invention. In certain embodiments, the control value may be the level of TMA or TMAO produced in the individual (or by the bacterium) prior to administration or exposure to a compound of formula (I) (or a pharmaceutically acceptable salt thereof). In addition, the control value may be based on levels measured in comparable samples obtained from a reference group, such as a group of individuals from the general population, individuals diagnosed with a CVD or other TMA-associated condition, individuals not previously diagnosed with a TMA-associated condition, nonsmokers, and the like, who have not been exposed to a compound of formula (I) (or a pharmaceutically acceptable salt thereof). Levels of TMA or TMAO or choline may be compared to a single control value or to a range of control values. An individual is optionally identified as having an enhanced level of TMA prior to administration by comparing the amount of TMA in a biological sample from the individual with a control value. Also disclosed herein are methods of improving cardiovascular health of in a subject in need thereof, comprising administering to the subject an effective amount of a compound of formula (I) (or a pharmaceutically acceptable salt thereof), or a composition comprising a compound of formula (I) (or a pharmaceutically acceptable salt thereof). In some embodiments, cardiovascular health is assessed by testing arterial elasticity, blood pressure, ankle/brachial index, electrocardiogram, ventricular ultrasound, platelet function (for example platelet aggregation), and/or blood/urine tests to measure, e.g., cholesterol, albumin excretion, C-reactive protein, and/or plasma B-type peptide (BNP) concentration. In various embodiments, administration of the compound of formula (I) (or pharmaceutically acceptable salt thereof), improves or maintains one or more of the assay outcomes within normal ranges. Normal ranges of outcomes of each test are known in the art. Improvement in cardiovascular health is, in some embodiments, marked by a reduction in circulating total cholesterol levels, reduction in circulating low density lipoproteins (LDLs), reduction in circulating triglycerides, or reduction in blood pressure. In some embodiments, the subject has an elevated level of TMAO, e.g., in blood, plasma, serum, urine, or any combination thereof. Also disclosed herein are methods of treating a condition associated with conversion of choline to TMA in a subject in need thereof, comprising administering to the subject an effective amount of a compound of formula (I) or a pharmaceutically acceptable salt thereof, or a composition comprising a compound of formula (I) or a pharmaceutically acceptable salt thereof. In some embodiments, the condition associated with the conversion of choline to TMA is a cardiovascular disease, trimethylaminuria, reduced or impaired kidney function, kidney disease (e.g., chronic kidney disease or end-stage renal disease), trimethylaminuria, obesity, or diabetes mellitus. In some embodiments, the condition is cardiovascular disease. The term “cardiovascular disease” (CVD) is used in the art in reference to conditions affecting the heart, heart valves, and vasculature (such as arteries and veins) of the body and encompasses diseases and conditions including, but not limited to, angina, arrhythmia, arteriosclerosis, atherosclerosis, myocardial infarction, acute coronary syndrome, cardiomyopathy, congestive heart failure, coronary thrombosis, arterial aneurysm (e.g., aortic aneurysm, iliac aneurysm, or femoral aneurysm), aortic dissection, pulmonary embolism, high blood pressure/hypertension (e.g., primary hypertension), hypercholesterolemia/hyperlipidemia, atrial fibrillation, stroke, transient ischemic attack, systolic dysfunction, diastolic dysfunction, myocarditis, atrial tachycardia, ventricular fibrillation, endocarditis, arteriopathy, vasculitis, atherosclerotic plaque, vulnerable plaque, acute coronary syndrome, acute ischemic attack, sudden cardiac death, peripheral vascular disease, coronary artery disease (CAD), carotid artery disease, peripheral artery disease (PAD), cerebrovascular disease, adverse ventricular remodeling, ventricular systolic dysfunction, ventricular diastolic dysfunction, cardiac dysfunction, ventricular arrhythmia, stroke, and the like. In some embodiments, the cardiovascular disease is due to oral biofilm formation and/or periodontal disease. In some embodiments, the condition is atherosclerosis. Atherosclerosis involves the formation of atheromatous plaques that lead to narrowing ("stenosis") of the vasculature, which can ultimately lead to partial or complete occlusion or rupture (aneurism) of the vessel, heart failure, aortic dissection, and ischemic events such as myocardial infarction and stroke. In various non-limiting embodiments, an inventive method inhibits, reduces, or reverses (in whole or in part) the onset or progression of atherosclerosis (for example reducing or preventing hardening or thickening of the arteries, plaque formation, endothelium damage, or arterial inflammation). In some embodiments, the condition is trimethylaminurina. Trimethylaminuria (TMAU) is a condition characterized by an inability of individuals to convert TMA to TMAO, wherein affected individuals may have a fish-like body odor present in their urine, sweat or breath. (Yamazaki et al. Life Sciences (2004) 74: 2739-2747). Such individuals may benefit from a reduction in metabolism of substrates including but not limited to choline, to TMA by bacteria in the gut. Individuals with TMAU or those wishing to reduce their levels of TMA and TMAO, may also consume activated charcoal or copper chlorophyllin, which act as sequestering agents, for example to make TMA unavailable to transfer into the blood stream of an individual. Such sequestering agents may adsorb TMA, which is then excreted from the digestive tract along with the sequestering agent Other conditions associated with increased levels of TMA may include production of TMA by bacteria in the vagina leading to vaginal odor, or production of TMA by bacteria on the body leading to body odor, or production of TMA by bacteria in the mouth leading to bad breath or oral care biofilm development. Furthermore, during pregnancy where the third trimester and post-partum period are associated with an increased risk of thrombosis, lowering TMA and TMAO levels may reduce this risk. Also disclosed herein are methods of improving a condition associated with conversion of choline to TMA in a subject in need thereof, comprising administering to the subject an effective amount of a compound of formula (I) or a pharmaceutically acceptable salt thereof, or a composition comprising a compound of formula (I) or a pharmaceutically acceptable salt thereof. As used herein, “improving a condition” refers to any reduction in the severity or onset of symptoms associated with a disorder caused, at least in part, by TMA. One of ordinary skill in the art will appreciate that any degree of protection from, or amelioration of, a TMA-related disorder or symptom associated therewith is beneficial to an individual, such as a human. The quality of life of an individual is improved by reducing to any degree the severity of symptoms in an individual or delaying the appearance of symptoms. Accordingly, a method in one aspect is performed as soon as possible after it has been determined that an individual is at risk for developing a TMA-related disorder or as soon as possible after a TMA-related disorder is detected. In various embodiments, administration of the compound formula (I) (or a pharmaceutically acceptable salt thereof) results in reduced TMA or TMAO levels, reduced total cholesterol levels, reduced LDL levels, increased HDL levels, reduced triglyceride levels, or normalized levels of other biomarkers associated with CVD (for example excreted albumin, C-reactive protein, or plasma B-type peptide (BNP)). In some embodiments, the compound of formula (I) (or a pharmaceutically acceptable salt thereof) reduces the risk of cardiovascular disease, trimethylaminuria, reduced or impaired kidney function, kidney disease (e.g., chronic kidney disease or end-stage renal disease), trimethylaminuria, obesity, or diabetes mellitus, when administered to a subject. In some embodiments, the amount of compound or composition administered to the individual is sufficient to inhibit (in whole or in part) formation of TMA from choline. In various aspects of the disclosure, the amount improves cardiovascular health or achieves a beneficial biological response with respect to an unwanted condition associated with TMA (for instance the amount is sufficient to ameliorate, slow the progression, or prevent a condition (such as CVD)) The effect can be detected by for example an improvement in clinical condition, reduction in symptoms, or by any of the assays or clinical diagnostic tests described herein. The precise effective amount for an individual can depend upon the individual's body weight, size, and health; the nature and extent of the condition; and the compound or combination of agents selected for administration. In various aspects, the amount of compound administered to an individual is about 0.001 mg/kg to about 1000 mg/kg. Specific ranges of doses in mg/kg include about 0.1 mg/kg to about 500 mg/kg, about 0.5 mg/kg to about 200 mg/kg, about 1 mg/kg to about 100 mg/kg, about 2 mg/kg to about 50 mg/kg, and about 5 mg/kg to about 30 mg/kg. An effective amount may be administered to an individual as a single deployment of compound or as a divided dose (such as a single dose administered in multiple subunits contemporaneously or close in time). An amount of compound may be delivered one, two, or three times a day; one, two, or three times a week; or one, two, three, or four times a month. The compound may be delivered as a prodrug, which is converted to an active drug in vitro or in vivo. A compound or composition can be administered by any route that allows inhibition of choline conversion to TMA. The compound or composition is, in various aspects of the invention, delivered to an individual parenterally (for example intravenously, intraperitoneally, intrapulmonary, subcutaneously or intramuscularly), intrathecally, topically, transdermally, rectally, orally, sublingually, nasally or by inhalation. In various embodiments, a compound or a composition is administered to the gastrointestinal tract, such as by ingestion. Sustained release formulations may also be employed to achieve a controlled release of the compound when in contact with body fluids in the gastrointestinal tract. Sustained release formulations are known in the art, and typically include a polymer matrix of a biological degradable polymer, a water-soluble polymer, or a mixture of both, optionally with suitable surfactants. In some embodiments, the compounds described herein may be provided in a delayed release composition and are optionally released in a specific region of the digestive tract of an individual. For example, the composition may be provided such that the compounds are released from an orally dosed composition in the distal portion of the digestive tract such as the ileum or the colon. In certain embodiments, the delayed release composition releases the compounds at a specific pH, or at a range of pH for targeted delivery within the digestive tract of an individual. The compounds may be released, for example, between pH 6.0 and pH 9.0, between pH 6.5 and pH 8.0, between pH 6.5 and pH 7.5, between pH 7.0 and pH 7.5, or between pH 7.0 and pH 8.0. Methods described herein may comprise administering a second agent to an individual. The term “second agent,” as used herein, serves to distinguish the agent from the compound of formula (I) (or pharmaceutically acceptable salt thereof) and is not meant to limit the number of additional agents used in a method or denote an order of administration. One or more second agents are optionally incorporated in a composition with the compound of formula (I) (or pharmaceutically acceptable salt thereof), administered concurrently but in separate dosage forms, or administered separately in time. Exemplary second agents include, but are not limited to, antimicrobials (such as antibiotics that kill bacteria in the gut); agents that improve intestinal motility (such as fiber or psyllium); agents that further reduce TMA levels in the gut including sequestering agents (such as activated charcoal, or copper chlorophyllin); agents that further reduce TMA levels or production of TMA metabolites; agents that improve one or more aspects of cardiovascular health, such as agents that normalize blood pressure, decrease vascular inflammation, reduce platelet activation, normalize lipid abnormalities; agents that promote the excretion of TMA from the body; or agents that bind TMA so that it cannot be converted to TMAO. In various embodiments, the second agent is selected from the group consisting of an omega-3 oil, salicylic acid (aspirin), dimethylbutanol, garlic oil, garlic extract, olive oil, krill oil, coenzyme Q10, a probiotic, a prebiotic, a dietary fiber, psyllium husk, bismuth salts, phytosterols, grape seed oil, green tea extract, vitamin D, an antioxidant (such as vitamin C and vitamin E), turmeric, curcumin, resveratrol, activated charcoal, or copper chlorophyllin. In certain embodiments, the second agent is dimethylbutanol or inhibitors of the formation of TMA from precursors other than choline (for example betaine, phosphatidylcholine, crotonobetaine, or carnitine). Additional exemplary second agents are described in US 2017/0151208, US 2017/0151250, US 2017/0152222, or US 2018/0000754, which are incorporated here by reference. Methods disclosed herein may further comprise administration of one or more cardiovascular disease therapies. Examples of therapies include, but are not limited to, statins (e.g., Lipitor™ (atorvastatin), Pravachol™ (pravastatin), Zocor™ (simvastatin), Mevacor™ (lovastatin), and Lescol™ (fluvastatin)) or other agents that interfere with the activity of HMGCoA reductase, nicotinic acid (niacin, which lowers LDL cholesterol levels), fibrates (which lower blood triglyceride levels and include, for example Bezafibrate (such as Bezalip®), Ciprofibrate (such as Modalim®), Clofibrate, Gemfibrozil (such as Lopid®) and Fenofibrate (such as TriCor®)), bile acid resins (such as Cholestyramine, Colestipol (Colestid), and Cholsevelam (Welchol)) cholesterol absorption inhibitors (such as Ezetimibe (Zetia®, Ezetrol®, Ezemibe®)), phytosterols such as sitosterol (Take Control (Lipton)), sitostanol (Benechol), or stigmastanol), alginates and pectins, lecithin, and nutraceuticals (such as extract of green tea and other extracts that include polyphenols, particularly epigallocatechin gallate (EGCG), Cholest-Arrest™ (500 mg garlic and 200 mg lecithin). 8OVSLZ[H^H`b #0)) TN 8HSJP\T JHYIVUH[L% *0) TN THNULZP\T V_PKLT .) mN JOYVTP\T picolinate), Cholest-Off™ (900 mg of plant sterols/stanols), Guggul Bolic (750 mg gugulipid (Commiphora mukul gum resin), and Kyolic® (600 mg aged garlic extract and 380 mg lecithin)). Kits For use in the methods described herein, kits and articles of manufacture are also provided, which include a compound or pharmaceutical composition described herein (e.g., a compound of formula (I) or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound of formula (I) or a pharmaceutically acceptable salt thereof ). In some embodiments, such kits comprise a carrier, package, or container that is compartmentalized to receive one or more containers such as vials, tubes, and the like, each of the container(s) comprising one of the separate elements to be used in a method described herein. Suitable containers include, for example, bottles, vials, syringes, and test tubes. The containers are formed from a variety of materials such as glass or plastic. The articles of manufacture provided herein contain packaging materials. Packaging materials for use in packaging pharmaceutical products include those found in, e.g., U.S. Patent Nos.5,323,907, 5,052,558 and 5,033,252. Examples of pharmaceutical packaging materials include, but are not limited to, blister packs, bottles, tubes, inhalers, pumps, bags, vials, containers, syringes, bottles, and any packaging material suitable for a selected formulation and intended mode of administration and treatment. For example, in some embodiments the container(s) includes a compound of formula (I), or a pharmaceutically acceptable salt thereof, optionally in a composition or in combination with another agent as disclosed herein. The container(s) optionally have a sterile access port (for example the container is an intravenous solution bag or a vial having a stopper pierceable by a hypodermic injection needle). Such kits optionally comprisie a compound with an identifying description or label or instructions relating to its use in one or more methods described herein. For example, a kit typically includes one or more additional containers, each with one or more of various materials (such as reagents, optionally in concentrated form, and/or devices) desirable from a commercial and user standpoint for use of a compound described herein. Non-limiting examples of such materials include, but not limited to, buffers, diluents, filters, needles, syringes; carrier, package, container, vial and/or tube labels listing contents and/or instructions for use, and package inserts with instructions for use. A set of instructions will also typically be included. A label is optionally on or associated with the container. For example, a label is on a container when letters, numbers or other characters forming the label are attached, molded or etched into the container itself, a label is associated with a container when it is present within a receptacle or carrier that also holds the container, e.g., as a package insert. In addition, a label is used to indicate that the contents are to be used for a specific therapeutic application. In addition, the label indicates directions for use of the contents, such as in the methods described herein. In certain embodiments, the pharmaceutical composition is presented in a pack or dispenser device which contains one or more unit dosage forms containing a compound provided herein. The pack, for example, contains metal or plastic foil, such as a blister pack. Or, the pack or dispenser device is accompanied by instructions for administration. Or, the pack or dispenser is accompanied with a notice associated with the container in form prescribed by a governmental agency regulating the manufacture, use, or sale of pharmaceuticals, which notice is reflective of approval by the agency of the form of the drug for human or veterinary administration. Such notice, for example, is the labeling approved by the U.S. Food and Drug Administration for prescription drugs, or the approved product insert. In some embodiments, compositions containing a compound provided herein formulated in a compatible pharmaceutical carrier are prepared, placed in an appropriate container, and labeled for treatment of an indicated condition. Examples Abbreviations used in the Examples include the following: Boc is tert- butyloxycarbonyl; DMF is N,N-dimethylformamide; DMSO is dimethylsulfoxide; EtOAc is ethyl acetate; HRMS is high resolution mass spectrometry; LCMS is liquid chromatography mass spectrometry; MeOH is methanol; NMR is nuclear magnetic resonance; TBS is tert- butyldimethylsilyl; and THF is tetrahydrofuran; Example 1: Compound Syntheses Compound 1: 2-(2-Aminoacetoxy)-N-(fluoromethyl)-N,N-dimethylethanaminium dibromide Step 1: 2-(Dimethylamino)ethyl 2-((tert-butoxycarbonyl)amino)acetate. To a solution of 2-((tert-butoxycarbonyl)amino)acetic acid (590 mg, 3.36 mmol) in THF (15 mL) was added 1,1’-carbonyldiimidazole (818 mg, 5.04 mmol, 1.5 equiv) at room temperature. The 5 mixture was stirred for 2 h and then 2-(dimethylamino) ethanol (300 mg, 3.36 mmol, 1.0 equiv) was added. The resulting mixture stirred for 16 h and then concentrated. The residue was purified using flash chromatography eluting with 0-10 percent methanol- dichloromethane to afford the product (80 mg, 9.7%) as colorless oil. LCMS (API-ES): m/z 247.3 [M + H] <sup>+</sup> . Step 2.2-(2-Aminoacetoxy)-N-(fluoromethyl)-N,N-dimethylethanamini um dibromide. To a solution of 2-(dimethylamino)ethyl 2-((tert-butoxycarbonyl)amino)acetate (80 mg, 0.325 mmol) in acetonitrile (2 mL) was added bromofluoromethane (44 mg, 0.390 mmol, 1.2 equiv). The resulting mixture was stirred at room temperature for 48 h and then concentrated under reduced pressure to dryness. The crude material was dissolved into 48% HBr (2 mL) and stirred for 2 h and then concentrated. The resulting crude material was triturated with 10:1 petroleum ether-methanol (10 mL) to give the product (25.2 mg, 23.1%) as a white solid. <sup>1</sup> H-NMR (400 MHz, DMSO-d <sub>6</sub> $3 k 1'))&1',) #IYVHK ZPUNSL[% ,<$% .'./ #K% =<%; 5 --'1 Hz, 2H), 4.52-4.70 (m, 2H), 3.71-3.93 (m, 4H), 3.21 (s, 6H) LCMS (API-ES): C <sub>7</sub> H <sub>17</sub> FN <sub>2</sub> O <sub>2</sub> + m/z = 180.0. High resolution mass spec: Calculated for C <sub>7</sub> H <sub>16</sub> FN <sub>2</sub> O <sub>2</sub> <sup>+</sup> , 179.1190; found, 179.1190. Compound 2: (S)-2-((2-Amino-3-methylbutanoyl)oxy)-N-(fluoromethyl)-N,N- dimethylethanaminium dibromide Step 1: (S)-2-(Dimethylamino)ethyl 2-((tert-butoxycarbonyl)amino)-3- methylbutanoate. To a solution of (S)-2-((tert-butoxycarbonyl)amino)-3-methylbutanoic acid (732 mg, 3.36 mmol) in THF (10 mL) was added 1,1’-carbonyldiimidazole (818 mg, 5.04 mmol, 1.5 equiv) at room temperature. The mixture was stirred for 2 h.2-(dimethylamino) ethanol (300 mg, 3.36 mmol, 1.0 equiv) was then added and the resulting mixture stirred at room temperature for 16 h. After the reaction was complete, the solvent was removed under reduced pressure. The residue was purified by flash chromatography eluting with 0-10 percent MeOH-dichloromethane to afford the product (80 mg, 8.2%) as colorless oil. LCMS (API-ES): m/z 289.0 [M + H] <sup>+</sup> . Step 2. (S)-2-((2-Amino-3-methylbutanoyl)oxy)-N-(fluoromethyl)-N,N- dimethylethanaminium dibromide. To a solution of (S)-2-(dimethylamino)ethyl 2-((tert- butoxycarbonyl)amino)-3-methylbutanoate (80 mg, 0.272 mmol) in acetonitrile (3 mL) was added bromofluoromethane (38 mg, 0.332 mmol, 1.2 equiv). The mixture was stirred at room temperature for 48 h. The reaction solution was concentrated under reduced pressure to dryness and the residue dissolved into 48% HBr (2 mL) and the resulting mixture stirred for 2 h. The reaction mixture was concentrated and triturated with 50:1 petroleum ether-MeOH (10 mL) to give the product (35.8 mg, 58.6%) as a pale solid. <sup>1</sup> H-NMR (400 MHz, DMSO-d6$3 k 8.44 (broad singlet, 3H), 5.57 (d, JH,F = 44.8 Hz, 2H), 4.66 (t, J = 4.4 Hz, 2H), 4.00-4.12 (m, 1H), 3.85-3.93 (m, 2H), 3.22 (s, 6H), 2.14-2.28 (m, 1H), 1.01 (d, J = 5.2 Hz, 3H), 0.99 (d, J = 5.6 Hz, 3H). LCMS (API-ES): C10H <sub>2</sub> 3FN2O2 <sup>+</sup> m/z = 222.0. Compound 3: (S)-2-((2-Aminopropanoyl)oxy)-N-(fluoromethyl)-N,N- dimethylethanaminium dibromide Step 1: (S)-2-(Dimethylamino)ethyl 2-((tert-butoxycarbonyl)amino)propanoate. To a solution of (S)-2-((tert-butoxycarbonyl)amino)propanoic acid (762 mg, 4.03 mmol, 1.2 equiv) in THF (10 mL) was added 1,1’-carbonyldiimidazole (656 mg, 4.03 mmol, 1.2 equiv) at room temperature. The mixture was stirred at 50 ºC for 2 h.2-(dimethylamino)ethanol (300 mg, 3.36 mmol, 1.0 equiv) was then added and stirred at 50 ºC for 16 h. After the reaction was complete, the solvent was removed under reduced pressure. The residue was purified by flash chromatography eluting with 0-10 percent methanol-dichloromethane to afford the product (500 mg, 57.1%) as colorless oil. LCMS (API-ES): m/z 261.3 [M + H] <sup>+</sup> . Step 2. (S)-2-((2-Aminopropanoyl)oxy)-N-(fluoromethyl)-N,N-dimethyle thanaminium dibromide. To a solution of (S)-2-(dimethylamino)ethyl 2-((tert- butoxycarbonyl)amino)propanoate (500 mg, 1.92 mmol) in acetonitrile (5 mL) was added bromofluoromethane (260 mg, 2.30 mmol, 1.2 equiv) at room temperature. The mixture was stirred at room temperature for 48 h and then concentrated under reduced pressure to dryness. The residue was dissolved into 48% HBr (4 mL) and the resulting mixture stirred at room temperature for 0.5 h. The reaction mixture was concentrated and the residue was lyophilized to give product (200 mg 541%) as a white solid <sup>1</sup> H-NMR (400 MHz DMSO-d <sub>6</sub> $3 k$8.41 (broad singlet, 3H), 5.58 (d, JH,F = 44.8 Hz, 2H), 4.47-4.74 (m, 2H), 4.18 (q, J = 7.2 Hz, 1H), 3.85 (broad singlet, 2H), 3.22 (s, 6H), 1.44 (d, J = 7.2 Hz, 3H). LCMS (API-ES): C8H19FN2O2 <sup>+</sup> m/z = 194.0. High resolution mass spec: Calculated for C8H18FN2O2 <sup>+</sup> , 193.1345; found, 193.1347. Compound 4: N-(fluoromethyl)-N,N-dimethyl-2-(prolyloxy)ethan-1-aminium chloride hydrochloride Step 1: 2-(((tert-butoxycarbonyl)prolyl)oxy)-N-(fluoromethyl)-N,N-di methylethan-1- aminium chloride. To a stirred solution of BOC-proline (2.05 g, 9.55 mmol) in DMF (7.50 mL) was added N,N’-diisopropylcarbodiimide (802 mg, 6.36 mmol), OxymaPure® (ethyl cyano(hydroxyimino)acetate, 904 mg, 6.36 mmol), and fluoromethylcholine chloride (500 mg, 3.18 mmol) under a nitrogen atmosphere and the resulting mixture stirred at room temperature for 16 h. Thereafter, the reaction mixture was quenched with water (10.0 mL) and extracted with ethyl acetate (3 × 50.0 mL). The aqueous layer was concentrated under reduced pressure to obtain the crude product. The crude product was purified by C-18 column chromatography using water as eluent to afford 2-(((tert-butoxycarbonyl)prolyl)oxy)-N- (fluoromethyl)-N,N-dimethylethan-1-aminium chloride (250 mg, 22%) as a colourless syrup. Step 2. N-(fluoromethyl)-N,N-dimethyl-2-(prolyloxy)ethan-1-aminium chloride hydrochloride. To a solution of 2-(((tert-butoxycarbonyl)prolyl)oxy)-N-(fluoromethyl)-N,N- dimethylethan-1-aminium chloride (250 mg, 0.783 mmol) in trifluoroethanol (2.00 mL) was added chlorotrimethylsilane (0.20 mL) at 0 °C. The reaction mixture was stirred at room temperature for 1 h. Thereafter, the reaction mixture was concentrated and lyophilized for 24 h to afford N-(fluoromethyl)-N,N-dimethyl-2-(prolyloxy)ethan-1-aminium chloride hydrochloride (140 mg, 50%) as a colourless solid. <sup>1</sup> H NMR (400 MHz, DMSO-d6$3 k 2',.& 11.14 (m, 2H), 5.66-5.72 (m, 1H), 5.54-5.60 (m, 1H), 4.63 (t, J = 4.0 Hz, 2H), 4.39 (t, J = 8.0 Hz, 1H), 3.92 (d, J = 4.8 Hz, 2H), 3.15-3.29 (m, 8H), 2.1812.29 (m, 1H), 2.0312.14 (m, 1H), 1.88-1.99 (m, 2H). ESI MS: m/z = 219 [M] <sup>+</sup> . HPLC: 95.9% (CAD analysis). High resolution mass spec: Calculated for C10H <sub>2</sub> 0FN2O2 <sup>+</sup> , 219.1503; found, 219.1502 Compound 5: N-(fluoromethyl)-N,N-dimethyl-2-(prolyloxy)ethan-1-aminium chloride hydrochloride Prepared in a similar manner to Compound 4. <sup>1</sup> H-NMR (400 MHz, D2A$3 k .',1 #K% JH,F = 44.8 Hz, 2H), 4.64-4.70 (m, 2H), 4.52 (t, J = 7.6 Hz, 1H), 3.82-3.92 (m, 2H), 3.32-3.42 (m, 2H), 3.23 (s, 6H), 2.36-2.48 (m, 1H), 2.08-2.18 (m, 1H), 2.02 (quintet, J = 7.2 Hz, 2H). 5 Mass: Calculated for C10H <sub>2</sub> 0FN2O2 <sup>+</sup> , 219; found, 219. Compound 6: 2-((L-phenylalanyl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1 -aminium dibromide Step 1: 2-(dimethylamino)ethyl (tert-butoxycarbonyl)-L-phenylalaninate. To a solution of (tert-butoxycarbonyl)-L-phenylalanine (1.07 g, 4.04 mmol, 1.2 equiv) in 5 mL dry-THF was added 1,1’-carbonyldiimidazole (654 mg, 4.04 mmol, 1.2 equiv). The resulting mixture was stirred at 50 ºC for 2 h under nitrogen. A solution of 2-(dimethylamino)ethan-1- ol (300 mg, 3.37 mmol, 1.0 equiv) in dry-THF (2 mL) was added. The mixture was stirred at 50 ºC overnight. After cooling, the mixture was concentrated to give the crude product which was purified using silica gel column chromatography eluting with 0-10% methanol- dichloromethane gradient to give the product (503 mg, 44.4%) as a colorless oil. LC-MS (API-ES): >95% (214, 254 nm), m/z = 337.2 [M+H] <sup>+</sup> . Step 2.2-(((tert-butoxycarbonyl)-L-phenylalanyl)oxy)-N-(fluoromet hyl)-N,N- dimethylethan-1-aminium bromide. To a solution of 2-(dimethylamino)ethyl (tert- butoxycarbonyl)-L-phenylalaninate (100 mg, 0.30 mmol, 1.0 equiv) in acetonitrile (1.5 mL) was added bromofluoromethane (50.5 mg, 0.45 mmol, 1.5 equiv). The mixture was stirred at room temperature for 48 h. The mixture was concentrated to give the crude product. The mixture was washed with EtOAc (3 x 5 mL). The product was dried in vacuo to give the product (85 mg, 77.4%) as a colorless oil. LC-MS (API-ES): >95% (214, 254 nm), m/z = 369.2 [M-Br] <sup>+</sup> . Step 3: 2-((L-phenylalanyl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1 -aminium dibromide.2-(((tert-butoxycarbonyl)-L-phenylalanyl)oxy)-N-(f luoromethyl)-N,N- dimethylethan-1-aminium bromide (85 mg, 0.23 mmol, 1.0 equiv) was dissolved in 48% HBr (1 mL). The mixture was stirred at room temperature for 18 h. The mixture was concentrated to give the product (25 mg, 40.3%) as a white solid. <sup>1</sup> H-NMR (400 MHz, D2A$ k 0',/&0'+- (m, 5H), 5.19 (dd, J = 5.6, 10.8Hz, 1H), 5.08 (dd, J = 5.6, 10.8 Hz, 1H), 4.63 (dd, J = 7.6, 14.8 Hz, 1H), 4.51 (dd, J = 6.0, 14.0 Hz, 1H), 4.46 (t, J = 7.6 Hz, 1H), 3.71 (dd, J = 6.4, 14.4 Hz, 1H), 3.56 (dd, J = 6.4, 14.4 Hz, 1H), 3.24-3.19 (m, 2H), 2.97 (s, 6H). LC-MS (API-ES): >95% (214, 254 nm), C <sub>14</sub> H <sub>23</sub> FN <sub>2</sub> O <sub>2</sub> <sup>+</sup> m/z = 270.2. Compound 7: 2-((L-phenylalanyl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1 -aminium dichloride Step 1: 2-(((tert-butoxycarbonyl)-L-phenylalanyl)oxy)-N-(fluoromethy l)-N,N- dimethylethan-1-aminium chloride. To a stirred solution of (tert-butoxycarbonyl)-L- phenylalanine (2.53 g, 6.36 mmol) in DMF (7.50 mL) was added N,N’- diisopropylcarbodiimide (802 mg, 6.36 mmol), OxymaPure® (ethyl cyano(hydroxyimino)acetate, 904 mg, 6.36 mmol), and fluoromethylcholine chloride (500 mg, 3.18 mmol) under a nitrogen atmosphere and the resulting mixture stirred at room temperature for 16 h. Thereafter, the reaction mixture was quenched with water (10.0 mL) and extracted with ethyl acetate (3 × 50.0 mL). The aqueous layer was concentrated under reduced pressure to obtain the crude product. The crude product was purified by C-18 column chromatography using water as eluent to afford 2-(((tert-butoxycarbonyl)-L- phenylalanyl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1-amini um chloride (230 mg, 18%) as a colourless syrup. <sup>1</sup> H NMR (400 MHz, DMSO-d <sub>6</sub> $3 k 0'-, #K% J = 8.0 Hz, 1H), 7.20-7.34 (m, 5H), 5.47 (d, J = 44.9 Hz, 2H), 4.41-4.59 (m, 2H), 4.20-4.30 (m, 1H), 3.67-3.80 (m, 2H), 3.13 (s, 6H), 3.04 (dd, J = 5.2 and 14.0 Hz, 1H), 2.87 (dd, J = 4.0 and 14.0 Hz, 1H),1.32 (s, 9H). ESI MS: m/z = 369 [M] <sup>+</sup> . Step 2: 2-((L-phenylalanyl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1 -aminium chloride hydrochloride. To a solution of 2-(((tert-butoxycarbonyl)-L-phenylalanyl)oxy)-N- (fluoromethyl)-N,N-dimethylethan-1-aminium chloride (230 mg, 0.623 mmol) in trifluoroethanol (2.00 mL) at 0 °C was added chlorotrimethylsilane (0.20 mL) and the resulting mixture stirred at room temperature for 1 h. Thereafter, the reaction mixture was concentrated and lyophilized for 24 h to afford 2-((L-phenylalanyl)oxy)-N-(fluoromethyl)- N,N-dimethylethan-1-aminium chloride hydrochloride (98.0 mg, 50%) as a colourless solid. <sup>1</sup> H NMR (400 MHz, DMSO-d <sub>6</sub> ): δ 1'21 #Z% ,<$% 0'+-&0'-+ #T% .<$% .'.-&.'/- #T% *<$% .'-,& 5.52 (m, 1H), 4.46-4.66 (m, 2H), 4.20-4.32 (m, 1H), 3.7213.91 (m, 2H), 3.24 (dd, J = 6.0 and 14.0 Hz, 1H), 3.08-3.20 (m, 7H). ESI MS: m/z = 269 [M] <sup>+</sup> . HPLC: 95.0% (CAD analysis). HRMS: calculated for C14H <sub>2</sub> 2FN <sub>2</sub> O <sub>2</sub> <sup>+</sup> , 269.1660; found, 269.1656. Compound 8: 2-((L-seryl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1-aminiu m chloride hydrochloride Step 1: A DMF solution (5 mL) of fluoromethylcholine chloride (0.3700 g, 2.3476 mmol) was added to a mixture of TBS-Boc-serine (prepared as in J. Org. Chem.2003, 68, 2979) (1.0572 g, 3.3092 mmol), N,N’-diisopropylcarbodiimide (0.4423 g, 3.5048 mmol), and OxymaPure® (ethyl cyano(hydroxyimino)acetate, 0.4824 g, 3.3946 mmol) in DMF (10 mL). Resulting orange mixture stirred until a homogeneous solution was achieved (~ 5 min). Pyridine (0.40 mL, 5.0 mmol) was added and the resulting solution stirred under a nitrogen environment overnight at room temperature. Reaction mixture turned dark brown. Solvent removed using rotary evaporation and then high vacuum to remove residual DMF to give an orange gummy solid. Crude product used as is. Step 2: The crude product from the previous step was diluted with THF (20 mL) and stirred at room temperature. Tetrabutylammonium fluoride (3.0 mL, 1.0 M in THF) was added and the resulting mixture stirred at room temperature for 1 h. Mass spec no longer showed starting material. Reaction mixture was concentrated using rotary evaporation to give the crude product as an orange gum that was washed with diethyl ether (3 x 5 mL). Washings were discarded. Crude product was subjected to high vacuum for 3 h and then triturated with water (10 mL) to dissolve the product. Mixture was filtered through Celite and rinsed with additional water (5 mL). Aqueous filtrate was collected and concentrated to give an orange gum, 0.6087 g which was used as is. Step 3: The crude product from the previous step (0.6087 g) was dissolved in isopropanol (3 mL) and ethyl acetate (6 mL) and then treated with 4M HCl in dioxane (1 mL). Resulting mixture stirred for 2 h at room temperature whereupon a precipitate formed. Solvent was removed using rotary evaporation and then high vacuum. Product was triturated with EtOH (5 mL) and stirred for 1.5 h. Isopropanol (15 mL) was added which gave a white precipitate. Mixture stirred for 1 h and then sat for 2 h. Mixture was centrifuged (3800 rpm, 10 min) and then the clear solvent removed leaving behind an off-white solid (0.1190 g). <sup>1</sup> H- NMR (400 MHz, DMSO-d6$3 k 1'.1 #IYVHK ZPUNSL[% +'- <$% .'0) #[% = 5.', <a% *<$% .'./ #K% JH,F=44.9 Hz, 2H), 4.64 (d, J = 4.6 Hz,2H), 4.14-4.19 (m, 1H), 3.75-3.95 (m, 4H), 3.21 (s, 6H). <sup>13</sup> C-NMR (100 MHz, DMSO-d <sub>6</sub> $3 k */0'2% 2/'2 #K% = <sub>C,F</sub> = 217 Hz), 59.9, 59.7, 59.3, 54.8, 47.9 (2C). HRMS (ESI) m/z: [M - Br] <sup>+</sup> calculated for C <sub>8</sub> H <sub>18</sub> FN <sub>2</sub> O <sub>3</sub> <sup>+</sup> 209.1296; found, 209.1296. Compound 9: 2-((L-seryl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1-aminiu m bromide Step 1: 2-(dimethylamino)ethyl (tert-butoxycarbonyl)-L-serinate. To a solution of (tert-butoxycarbonyl)-L-serine (830 mg, 4.04 mmol, 1.2 equiv) in 5 mL dry-THF was added 1,1’-carbonyldiimidazole (654 mg, 4.04 mmol, 1.2 equiv). The mixture was stirred at 50 ºC for 2 h under nitrogen. A solution of 2-dimethylaminoethanol (300 mg, 3.37 mmol, 1.0 equiv) in dry THF was added. The mixture was stirred at 50 ºC overnight. After cooling to room temperature, the mixture was concentrated and the crude product purified using silica gel column chromatography eluting with 0-10% methanol-dichloromethane to give 2- (dimethylamino)ethyl (tert-butoxycarbonyl)-L-serinate (466 mg, 50.1%) as a colorless oil. LC-MS (API-ES): >95% (214, 254 nm), m/z = 277.2 [M+H] <sup>+</sup> . Step 2: 2-(((tert-butoxycarbonyl)-L-seryl)oxy)-N-(fluoromethyl)-N,N- dimethylethan- 1-aminium bromide. To a solution of 2-(dimethylamino)ethyl (tert-butoxycarbonyl)-L- serinate (100 mg, 0.36 mmol, 1.0 equiv) in acetonitrile (1.5 mL) was added bromofluoromethane (61.4 mg, 0.54 mmol, 1.5 equiv). The mixture was stirred at room temperature for 48 h. The mixture was concentrated and the crude product washed with ethyl acetate (3 x 5 mL) and then dried to give the product 2-(((tert-butoxycarbonyl)-L-seryl)oxy)- N-(fluoromethyl)-N,N-dimethylethan-1-aminium bromide (97 mg, 86.6%) as a colorless oil. LC-MS >95% (214, 254 nm), C13H <sub>2</sub> 7FN2O5 <sup>+</sup> m/z = 310.2 Step 3: 2-((L-seryl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1-aminiu m bromide.2- (((Tert-butoxycarbonyl)-L-phenylalanyl)oxy)-N-(fluoromethyl) -N,N-dimethylethan-1- aminium bromide (97 mg, 0.31 mmol, 1.0 equiv) was dissolved in 48% HBr (1 mL). The mixture was stirred at room temperature for 18 h. The mixture was concentrated to give the product 2-((L-seryl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1-aminiu m bromide (42.2 mg, 64.3%) as a white solid. <sup>1</sup> H-NMR (400 MHz, D2A$3 k .',1 #K% =H,F = 44.8 Hz, 2H), 4.70-4.76 (m, 2H), 4.33 (t, J = 3.6 Hz, 1H), 4.06 (dd, J = 4.0, 12.4 Hz, 1H), 3.96 (dd, J = 3.2, 16.0 Hz, 1H), 3.88 (t, J = 4.0 Hz, 2H), 3.21 (s, 6H). High resolution mass spec: Calculated for C <sub>8</sub> H <sub>18</sub> FN <sub>2</sub> O <sub>3</sub> <sup>+</sup> , 209.1296; found, 209.1292. LC-MS (API-ES): >95% (214, 254 nm), C <sub>8</sub> H <sub>19</sub> FN <sub>2</sub> O <sub>3</sub> <sup>+</sup> m/z = 210.2. Compound 10: (S)-2-((3-amino-3-carboxypropanoyl)oxy)-N-(fluoromethyl)-N,N - dimethylethan-1-aminium chloride hydrochloride Step 1: (S)-2-((4-(tert-butoxy)-3-((tert-butoxycarbonyl)amino)-4-oxo butanoyl)oxy)-N- (fluoromethyl)-N,N-dimethylethan-1-aminium chloride To a stirred solution of (S)-4-(tert- butoxy)-3-((tert-butoxycarbonyl)amino)-4-oxobutanoic acid (1.47 g, 5.09 mmol) in DMF (5.00 mL) was added N,N’-diisopropylcarbodiimide (642 mg, 5.09 mmol), OxymaPure® (ethyl cyano(hydroxyimino)acetate, 723 mg, 5.09 mmol), and fluoromethylcholine chloride (400 mg, 2.54 mmol) under a nitrogen atmosphere and the resulting mixture stirred at room temperature for 16 h. Thereafter, the reaction mixture was quenched with water (10.0 mL) and extracted with ethyl acetate (3 × 50.0 mL). The aqueous layer was concentrated under reduced pressure to obtain the crude product. The crude product was purified by C-18 column chromatography using water as eluent to afford (S)-2-((4-(tert-butoxy)-3-((tert- butoxycarbonyl)amino)-4-oxobutanoyl)oxy)-N-(fluoromethyl)-N, N-dimethylethan-1- aminium chloride (250 mg, 25%) as colourless syrup. <sup>1</sup> H NMR (400 MHz, DMSO-d6$3 k 0',) (d, J = 8.0 Hz, 1H), 5.51 (d, J = 44.8 Hz, 2H), 4.44-4.53 (m, 2H), 4.18-4.27 (m, 1H), 3.73- 3.81 (m, 2H), 3.17 (s, 6H), 2.78-2.87 (m, 1H), 2.61-2.71 (m, 1H), 1.39 (s, 18 H). ESI MS: m/z = 393 [M] <sup>+</sup> Step 2: (S)-2-((3-amino-3-carboxypropanoyl)oxy)-N-(fluoromethyl)-N,N - dimethylethan-1-aminium chloride hydrochloride. To a stirred solution of (S)-2-((4-(tert- butoxy)-3-((tert-butoxycarbonyl)amino)-4-oxobutanoyl)oxy)-N- (fluoromethyl)-N,N- dimethylethan-1-aminium chloride (250 mg, 0.636 mmol) in 1,4-dioxane was added 4M HCl in 1,4-dioxane (4.00 mL) and the resulting mixture stirred at room temperature for 1 h. Thereafter, the 1,4-dioxane was decanted and the reaction mixture was lyophilised for 24 h to afford (S)-2-((3-amino-3-carboxypropanoyl)oxy)-N-(fluoromethyl)-N,N -dimethylethan-1- aminium chloride hydrochloride (63.0 mg, 27%) as syrup. <sup>1</sup> H NMR (400 MHz, DMSO-d <sub>6</sub> $3 k 14.05 (brs, 1H), 8.58 (s, 3H), 5.54 (d, J = 44.9 Hz, 2H), 4.50-4.57 (m, 2H), 4.22-4.31 (m, 1H), 3.79-3.85 (m, 2H), 3.19 (s, 6H), 2.98-3.02 (m, 2H). ESI MS: m/z = 237 [M] <sup>+</sup> ; HPLC: 98.3% (CAD analysis). Compound 11: 2-((L-aspartyl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1-ami nium chloride hydrochloride Step 1: (S)-2-((4-(tert-butoxy)-2-((tert-butoxycarbonyl)amino)-4-oxo butanoyl)oxy)-N- (fluoromethyl)-N,N-dimethylethan-1-aminium chloride. To a stirred solution of (S)-4-(tert- butoxy)-2-((tert-butoxycarbonyl)amino)-4-oxobutanoic acid (1.84 g, 6.36 mmol) in DMF (7.50 mL) was added N,N’-diisopropylcarbodiimide (802 mg, 6.36 mmol), OxymaPure® (ethyl cyano(hydroxyimino)acetate, 904 mg, 6.36 mmol), and fluoromethylcholine chloride (500 mg, 3.18 mmol) under a nitrogen atmosphere and the resulting mixture stirred at room temperature for 16 h. Thereafter, the reaction mixture was quenched with water (10.0 mL), and extracted with ethyl acetate (3 × 50.0 mL). The aqueous layer was concentrated under reduced pressure to obtain the crude compound. The crude product was purified by C-18 column chromatography using water as eluent to afford (S)-2-((4-(tert-butoxy)-2-((tert- butoxycarbonyl)amino)-4-oxobutanoyl)oxy)-N-(fluoromethyl)-N, N-dimethylethan-1- aminium chloride (300 mg, 22% ) as a colourless syrup. <sup>1</sup> H NMR (400 MHz, DMSO-d <sub>6</sub> ): δ 7.41 (d, J = 8.4 Hz, 1H), 5.51 (d, 44.9Hz, 2H), 4.4114.56 (m, 3H), 3.72-3.81 (m, 2H), 3.17 (s, 6H), 2.76 (dd, J = 5.2 and 16.4 Hz, 1H), 2.57 (d, J = 9.2 Hz, 1H),1.39 (s, 9H), 1.38 (s, 9H). ESI MS: m/z = 393 [M] <sup>+</sup> . Step 2: 2-((L-aspartyl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1-ami nium chloride hydrochloride. To a stirred solution of (S)-2-((4-(tert-butoxy)-2-((tert- butoxycarbonyl)amino)-4-oxobutanoyl)oxy)-N-(fluoromethyl)-N, N-dimethylethan-1- aminium chloride (230 mg, 0.585 mmol) in 1,4-dioxane was added 4M HCl in 1,4-dioxane (6.00 mL) and the resulting mixture stirred at room temperature for 1 h. Thereafter, the 1,4- dioxane was decanted and reaction mixture was lyophilized for 24 h to afford 2-((L- aspartyl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1-aminium chloride hydrochloride (100 mg, 60%) as a syrup. 'HNMR (400 MHz, DMSO-d <sub>6</sub> ): δ 13.05 (brs, 1H), 8.76 (s, 3H), 5.56 (d, J = 448 Hz, 2H), 4.62 (d, J = 4.8 Hz, 2H), 4.29-4.38 (m, 1H), 3.80-3.88 (m, 2H), 3.20 (s, 6H), 2.99 (d, J = 5.3 Hz, 2H). ESI MS: m/z = 237 [M] <sup>+</sup> . HPLC: 89.6% (CAD analysis). High resolution mass spec: Calculated for C9H18FN2O4 <sup>+</sup> , 237.1245; found, 237.1244. Compound 12: (S)-2-((4-amino-4-carboxybutanoyl)oxy)-N-(fluoromethyl)-N,N- dimethylethan-1-aminium chloride hydrochloride Step 1: (S)-2-((5-(tert-butoxy)-4-((tert-butoxycarbonyl)amino)-5-oxo pentanoyl)oxy)- N-(fluoromethyl)-N,N-dimethylethan-1-aminium chloride. To a stirred solution of (S)-5-(tert- butoxy)-4-((tert-butoxycarbonyl)amino)-5-oxopentanoic acid (1.93 g, 6.36 mmol) in DMF (10.0 mL) was added N,N’-diisopropylcarbodiimide (815 mg, 6.37 mmol), OxymaPure® (ethyl cyano(hydroxyimino)acetate, 904 mg, 6.37 mmol), and fluoromethylcholine chloride (500 mg, 3.18 mmol) under a nitrogen atmosphere and the resulting mixture stirred at room temperature for 16 h. Thereafter, the reaction mixture was quenched with water (10.0 mL) and extracted with ethyl acetate (3 × 50.0 mL). The aqueous layer was concentrated under reduced pressure to obtain the crude product. The crude product was purified by C-18 column chromatography using water as eluent to afford (S)-2-((5-(tert-butoxy)-4-((tert- butoxycarbonyl)amino)-5-oxopentanoyl)oxy)-N-(fluoromethyl)-N ,N-dimethylethan-1- aminium chloride (150 mg, 10%) as colourless liquid. <sup>1</sup> H NMR (400 MHz, DMSO-d <sub>6</sub> ): δ 7.20 (d, J = 8.3 Hz, 1H), 5.48 (d, J = 44.8 Hz, 2H), 4.42-4.49 (m, 2H), 3.79-3.89 (m, 1H), 3.71-3.78 (m, 2H), 3.15 (s, 6H), 2.31-2.35 (m, 2H), 1.86-2.01 (m, 1H), 1.73-1.85 (m, 1H), 1.34-1.42 (m, 18H). ESI MS: m/z = 407 [M] <sup>+</sup> Step 2. (S)-2-((4-amino-4-carboxybutanoyl)oxy)-N-(fluoromethyl)-N,N- dimethylethan-1-aminium chloride hydrochloride. To a stirred solution of (S)-2-((5-(tert- butoxy)-4-((tert-butoxycarbonyl)amino)-5-oxopentanoyl)oxy)-N -(fluoromethyl)-N,N- dimethylethan-1-aminium chloride (150 mg, 0.368 mmol) in 1,4-dioxane was added 4M HCl in 1,4-dioxane (4.00 mL) and the resulting mixture stirred at room temperature for 1 h. Thereafter, the 1,4-dioxane was decanted and reaction mixture was lyophilized for 24 h to afford (S)-2-((4-amino-4-carboxybutanoyl)oxy)-N-(fluoromethyl)-N,N- dimethylethan-1- aminium chloride hydrochloride (61.0 mg, 54%) as syrup. <sup>1</sup> H NMR (400 MHz, DMSO-d <sub>6</sub> ): δ 13.91 (brs, 1H), 8.49 (brs, 2H), 8.32 (brs, 1H), 5.53 (d, J = 45.2 Hz, 2H), 5.48 (d, J = 45.2 Hz, 2H), 4.47 (s, 2H), 3.94 (brs, 1.5H), 3.85 (brs, 1H), 3.78 (brs, 2H), 3.49 (t, J = 3.6 Hz, 1.5H), 3.18 (s, 6H), 3.15 (s, 4H), 2.4912.12 (m, 2.5H), 2.1211.97 (m, 1H). ESI MS: m/z = 251 [M]+. HPLC: 96.1% (CAD analysis). High resolution mass spec: Calculated for C10H <sub>2</sub> 0FN2O4 <sup>+</sup> , 251.1402; found, 251.1403. Compound 13: 2-((acetyl-L-aspartyl)oxy)-N-(fluoromethyl)-N,N-dimethyletha n-1- aminium chloride Step 1: (S)-2-((2-acetamido-4-(tert-butoxy)-4-oxobutanoyl)oxy)-N-(fl uoromethyl)- N,N-dimethylethan-1-aminium chloride. To a solution of (S)-2-acetamido-4-(tert-butoxy)-4- oxobutanoic acid (1.46 g, 6.36 mmol) in DMF (7.50 mL) was added N,N’- dicyclohexylcarbodiimide (1.31 g, 6.36 mmol), 4-dimethylaminopyridine (38.0 mg, 0.3184 mmol), and fluoromethylcholine chloride (500 mg, 3.184 mmol) at room temperature and the resulting mixture stirred at 60 °C for 16 h. Thereafter, the reaction mixture was quenched with water (10.0 mL) and extracted with ethyl acetate (3 × 50.0 mL). The aqueous layer was concentrated under reduced pressure to obtain the crude product. The crude product was purified by C-18 column chromatography using water as eluent to afford (S)-2-((2- acetamido-4-(tert-butoxy)-4-oxobutanoyl)oxy)-N-(fluoromethyl )-N,N-dimethylethan-1- aminium chloride (260 mg, 22%) as a colourless syrup.. <sup>1</sup> H NMR (400 MHz, DMSO-d <sub>6</sub> ): δ 8.50 (d, J = 7.6 Hz, 1H), 5.53 (d, J = 44.8 Hz, 2H), 4.6014.69 (m, 1H), 4.50 (d, J = 4.8 Hz, 2H), 3.78 (t, J = 4.3 Hz, 2H), 3.18 (s, 6H), 2.76 (dd, J = 5.6 and 16.4 Hz, 1H), 2.60 (dd, J = 8.0 and 16.4 Hz, 1H), 1.86 (s, 3H), 1.40 (s, 9H). ESI MS: m/z = 335 [M] <sup>+</sup> . Step 2.2-((acetyl-L-aspartyl)oxy)-N-(fluoromethyl)-N,N-dimethylet han-1-aminium chloride. To a solution of (S)-2-((2-acetamido-4-(tert-butoxy)-4-oxobutanoyl)oxy)-N- (fluoromethyl)-N,N-dimethylethan-1-aminium chloride (40.0 mg, 0.108 mmol) in trifluoroethanol (2.00 mL) at 0 °C was added chlorotrimethylsilane (0.20 mL) and the resulting mixture stirred at room temperature for 1 h. Thereafter, the reaction mixture was concentrated and lyophilized for 24 h to afford 2-((acetyl-L-aspartyl)oxy)-N-(fluoromethyl)- N,N-dimethylethan-1-aminium chloride (10.0 mg, 30%) as a colourless solid. <sup>1</sup> H NMR (400 MHz, CD3A9$3 k .',0 #K% J = 44.9 Hz, 2H), 4.65 (t, J = 6.4 Hz, 1H), 4.48-4.56 (m, 2H), 3.74 (t, J = 4.8 Hz, 2H), 3.16 (d, J = 2.0 Hz, 6H), 2.77 (dd, J = 2.0 & 6.4 Hz, 2H), 1.89 (s, 3H). ESI MS: m/z = 279 [M] <sup>+</sup> . High resolution mass spec: Calculated for C11H <sub>2</sub> 0FN2O5 <sup>+</sup> , 279.1351; found, 279.1349. Compound 14: 2-((L-glutamyl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1-ami nium chloride hydrochloride (S)-2-((5-(tert-butoxy)-2-((tert-butoxycarbonyl)amino)-5-oxo pentanoyl)oxy)-N- (fluoromethyl)-N,N-dimethylethan-1-aminium chloride. To a solution of (S)-5-(tert-butoxy)- 2-((tert-butoxycarbonyl)amino)-5-oxopentanoic acid (964 mg, 3.18 mmol) in DMF (3.50 mL) was added N,N’-dicyclohexylcarbodiimide (655 mg, 3.18 mmol), 4-dimethylaminopyridine (38.0 mg, 0.159 mmol), and fluoromethylcholine chloride (250 mg, 1.59 mmol) and the resulting mixture stirred at room temperature for 16 h. Thereafter, the reaction mixture was quenched with water (10.0 mL), and extracted with ethyl acetate (3 × 50.0 mL). The aqueous layer was concentrated under reduced pressure to obtain the crude compound. The crude product was purified by C-18 column chromatography using water as eluent to afford (S)-2- ((5-(tert-butoxy)-2-((tert-butoxycarbonyl)amino)-5-oxopentan oyl)oxy)-N-(fluoromethyl)- N,N-dimethylethan-1-aminium chloride (125 mg, 18%) as colourless solid. <sup>1</sup> H NMR (400 MHz, DMSO-d <sub>6</sub> ): δ 0',. #K% J = 8.0 Hz, 1H), 5.52 (d, J = 45.0 Hz, 2H), 4.51 (d, J = 4.3 Hz, 2H), 4.05-4.13 (m, 1H), 3.77 (t, J = 4.2 Hz, 2H), 3.18 (s, 6H), 2.29 (t, J = 7.3 Hz, 2H), 1.90- 2.02 (m, 1H), 1.70-1.83 (m, 1H), 1.37-1.42 (m, 18H). ESI MS: m/z = 407 [M] <sup>+</sup> . Step 2: 2-((L-glutamyl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1-ami nium chloride hydrochloride. To a solution of (S)-2-((5-(tert-butoxy)-2-((tert- butoxycarbonyl)amino)-5-oxopentanoyl)oxy)-N-(fluoromethyl)-N ,N-dimethylethan-1- aminium chloride (200 mg, 0.4914) in trifluoroethanol (2.00 mL) at 0 °C was added chlorotrimethylsilane (0.20 mL) and the resulting mixture stirred at room temperature for 1 h. Thereafter, the reaction mixture was concentrated and lyophilized for 24 h to afford 2-((L- glutamyl)oxy)-N-(fluoromethyl)-N,N-dimethylethan-1-aminium chloride hydrochloride (80.0 mg, 53%) as colourless solid. <sup>1</sup> H NMR (400 MHz, DMSO-d <sub>6</sub> ): δ *+',2 #IYZ% *<$% 1'10 #Z% 3H), 5.61 (d, J = 44.9 Hz, 2H), 4.62 (d, J = 6.4 Hz, 2H), 4.01-4.14 (m, 1H), 3.82-3.95 (m, 2H), 3.23 (s, 6H), 2.39-2.46 (m, 2H), 2.00-2.13 (m, 2H). ESI MS: m/z = 251 [M] <sup>+</sup> . HPLC: 92.2% (CAD analysis).. High resolution mass spec: Calculated for C10H <sub>2</sub> 0FN2O4 <sup>+</sup> , 251.1402; found, 251.1397. Example 2: In vitro TMA inhibition Full-length, recombinant CutC/D was expressed through the use of competent E. coli cells transformed with the expression plasmids encoding for the cutC and cutD genes from P. mirabilis as described (Wang Z et al., Cell 2015 Dec 17;163(7):1585-95). CutC/D over- expressing cells were grown in nutrient-rich LB medium with the addition of ampicillin (100 µg/mL). The cell pellets were kept on ice and re-suspended in the lysis buffer: 200 mM HEPES, 50 mM NaCl, 10 mM MgCl <sub>2</sub> , pH 8.0. Clarified lysate was aliquoted and flash frozen for storage at -80 ºC until use. Choline TMA lyase enzymatic activity assays were conducted to measure the conversion of isotope-labeled d9-choline to d9-TMA. Upon thawing an aliquot of frozen clarified lysate on ice and gentle mixing, clarified lysate was diluted to 5 mg/mL in lysis buffer and the necessary co-factors were added (final concentration: 1 mM SAM, 10 mM NaDT, and 2 mM NADH). Potential inhibitor compounds (typically dissolved in H <sub>2</sub> O) were serially diluted (10-fold) and added to individual reaction mixtures (done in triplicate). The mixture was then allowed to incubate for at least 15 minutes at 22 ºC before the addition of substrate (300 µM final d9-choline) to initiate the reaction, which was carried out for 2 hours at room temperature (22 ºC) in the dark in gas tight sealed reaction vials. The reactions were quenched with the addition of 200 µL of 1 M NaOH and 0.5 µM of the internal standard ([ <sup>13</sup> C <sub>3</sub> <sup>15</sup> N <sub>1</sub> ]TMA), vortexing and placement in ice. d <sub>9</sub> -TMA production was quantified using mass spectrometry by measuring the peak area ratio of the precursor to product ion transition of d <sub>9</sub> -TMA (m/z 69 # 49) to the internal standard [ <sup>13</sup> C <sub>3</sub> <sup>15</sup> N <sub>1</sub> ]TMA (m/z 64 # 47). Calculated IC <sub>50</sub> values are provided in Table 1. Table 1. IC50 Values Example 3: In vivo d9-Choline Challenge Model--q3 hr In this model, the indicated drug and isotope tracer labeled choline (d9-choline) were provided via oral gavage concomitantly (like giving inhibitor at same time of a glucose tolerance test), while animals were maintained ad lib on a 1% Choline diet (average plasma TMAO levels on 1% Choline added diet are 201.7 +/- 104.5 µM, n = 121), and plasma was recovered at the indicated times post gavage to monitor the impact of inhibitor on d <sub>9</sub> -TMA and d9-TMAO generation. This model helps to define whether an agent can inhibit TMA and TMAO production when given orally, provided it has PK properties that permit it to reach the gut microbiota compartment within the time frame monitored. 7YPLMS`% 8.0IS(/ ;LTHSL TPJL #=HJRZVU " )//-$ c1 ^RZ VM HNL ^LYL MHZ[LK MVY * OY PU a clean empty cage with water ad libitum. Mice were given a single bolus of 2 mg d ₉ -choline and the indicated dose (in mg/kg) of Compound in 0.2 mL of sterile water. Blood was collected at the indicated time point(s). Plasma was analyzed for d ₉ -TMA and d ₉ -TMAO production by stable isotope dilution tandem mass spectrometry. After observing near comparable results (in terms of calculated ED50) when looking at multiple different time points post gavage (1.5, 3 and 4.5 hr), results are reported at peak levels (3h post gavage). Results were plotted using GraphPad Prism (v9.1) in comparison to either a same-day control (n=4 -5) or a compiled control (n=15-24 mice, across 5 independent experiments) and a Mann Whitney test was conducted. The plotted data is shown in FIG.1. Example 4: In vivo Q24 hr Model In this model, drug was provided via oral gavage once daily in an animals placed on a high choline diet ad libitum, and plasma was recovered on a daily (Q24h) basis to monitor therapeutic response (TMAO level) at time of trough blood level (just before gavage). This model can help to define minimal daily oral regimen to achieve desired TMAO reduction throughout the entire duration of study. 7YPLMS`% 8.0IS(/ ;LTHSL TPJL #=HJRZVU ")//-% c1 ^RZ VM HNL$ ^LYL THPU[HPULK WYPVY to initiation of the study on a 1% Choline diet for at least 48 hrs. At the start of this study, mice were given the indicated dose (in mg/kg) of compound via oral gavage (typically in 0.2 mL of sterile water or vehicle). Blood was collected prior to gavage (baseline) and q24hr after gavage for analysis of TMA, TMAO and creatinine. Data was plotted in Graphpad prism (v9) and a paired t-test (Wilcoxon) was completed, p < 0.05 was considered significant. The plotted data is shown in FIG.2. Example 5: Pharmacokinetic Data Female mice (Jackson #00664 or Taconic Swiss Webster) at least 8 weeks of age were placed on 1% choline added diet (Teklad, TD.09041) ad libitum. After at least 48 hours on diet, animals were given a bolus gavage of 0.2 mL aqueous solution (2 mg d <sub>9</sub> -choline + 100 mg/kg (TEST COMPOUND)) After gavage animals were singly-housed in a cage fitted with collection wires on the cage floor. Blood and urine samples were collected prior to gavage, 1 hour, 2 hours, 3 hours, 4 hours, and 24 hours after gavage. Blood was collected via saphenous vein. Urine was collected by manual expression of the bladder. Feces were pooled from the cage floor at the end of the 24 hours. 6UHS`ZPZ VM WSHZTH3 *. m> TV\ZL WSHZTH ^HZ HSPX\V[LK PU[V H *'. T> :WWLUKVYM [\IL HUK /) m> JVSK TL[OHUVS JVU[HPUPUN *) m? K ₉ -choline and d ₉ -betaine as internal standards was added and vortexed for one minute. The samples were spun down at 20000 g, at 4 ºC for *) TPU\[LZ HUK [OLU /) m> Z\WLYUH[HU[ ^HZ [YHUZMLYYLK [V H + T> THZZ ZWLJ ]PHS ^P[O H plastic insert for LC/MS/MS analysis. 6UHS`ZPZ VM \YPUL3 EYPUL ^HZ KPS\[LK +)&MVSK PU ^H[LY HUK [OLU *. m> VM [OPZ KPS\[PVU ^HZ HSPX\V[LK [V H *'. T> :WWLUKVYM [\IL' /) m> JVSK TL[OHUVS JVU[HPUPUN *) m? K9-choline and d9-betaine as internal standards was added to the tube and the resulting mixture vortexed MVY VUL TPU\[L' DOL ZHTWSLZ ^LYL ZW\U KV^U H[ +)))) N% - d8 MVY *) TPU\[LZ HUK [OLU /) m> of the supernatant was transferred to a 2 mL mass spec vial with plastic insert for LC/MS/MS HUHS`ZPZ' CLYPHS JVUJLU[YH[PVUZ VM Z[HUKHYKZ ^LYL TP_LK ^P[O - ]VS\TLZ VM *) m? K9-choline and d9-betaine to prepare a standard curve. Analysis of feces: Feces were homogenized in 10 volumes water (assuming 1 mg MLJLZ PZ * m> PU ]VS\TL$ JVU[HPUPUN *) m? K ₉ -choline and d ₉ -betaine as internal standards MVSSV^LK I` JLU[YPM\NH[PVU H[ /))) N% - d8 MVY *+ TPU\[LZ' +)) m> Z\WLYUH[HU[ ^HZ MPS[LYLK through a 3K cut-off filter (Amicon® Ultra-0.5 mL centrifugal filters). The filtrate was collected in a 2 mL mass spec vial with a plastic insert. Serial concentrations of standards ^LYL TP_LK ^P[O *) ]VS\TLZ VM *) m? K <sub>9</sub> -choline and d <sub>9</sub> -betaine to prepare a standard curve. DOL WYLWHYLK ZHTWSL #* m>$ ^HZ HUHS`aLK I` PUQLJ[PVU VU[V H ZPSPJH JVS\TU #+')i *.) TT% . mT >\UH ZPSPJH48H[' @V' ));&-+0-&7)% BOLUVTLUL_% DVYYHUJL% 86$ H[ H MSV^ YH[L VM )'+. T> TPUh* \ZPUN H + FHUX\PZO W\TW Z`Z[LT #DOLYTV CJPLU[PMPJ% GHS[OHT% ?6$% interfaced with a TSQ mass spectrometer (Thermo Scientific, Waltham, MA). A discontinuous gradient was generated to resolve the analytes by mixing solvent A (0.2% formic acid in water) with solvent B (0.2% formic acid in methanol) at different ratios starting from 0% B linearly to 15% B over 5 min, then linearly to 100% B over 2.5 min, then hold for 3 min, and then back to 0% B. Fluoromethylcholine, fluoromethylbetaine and their corresponding internal standards, d ₉ -choline and d ₉ -betaine, were monitored using electrospray ionization in positive-ion mode with multiple reaction monitoring (MRM) of precursor and characteristic product-ion transitions of m/z 122 l .14 *,/ l 0/4 HUK **, l 69; 127 l // HT\% YLZWLJ[P]LS`' DOL WHYHTL[LYZ MVY [OL PVU TVUP[VYPUN ^LYL HZ MVSSV^Z3 spray voltage, 3.5 kV; sheath gas, 50; Aux gas, 10; sweep gas, 1; CE, 16.9 V for fluoromethylcholine, 26.7 V for fluoromethylbetaine, 30.3 V for d9-choline, and 27.0 V for d9-betaine; RF lens 47 for fluoromethylcholine, 58 for fluoromethylbetaine, 53 for d9-choline, and 60 for d ₉ -betaine. Nitrogen (99.95% purity) was used as the source and argon (99.95 purity) was used as collision gas. Various concentrations of fluoromethylcholine and fluoromethylbetaine standards undergoing the same procedure were used to prepare the calibration curves for quantification of fluoromethylcholine and fluoromethylbetaine, respectively. Data are shown in Table 2. Table 2. PK Data