Chloromethylandrostenediol

Other Names

4-chloro-17α-methyl-androst-4-ene-3β,17β-diolCMA

Synopsis

Chloromethylandrostenediol (CMA / Promagnon): A Comprehensive Reference

1. Identity and Chemical Characterization

Chloromethylandrostenediol (abbreviated CMA) is the commonly used name for the synthetic steroidal compound formally designated 4-chloro-17α-methyl-androst-4-ene-3β,17β-diol. CMA is a synthetic, orally active anabolic-androgenic steroid (AAS) and a 17α-alkylated derivative of 4-androstenediol that was never marketed. It is sold and discussed under the trade name Promagnon.

According to Wikidata's curated chemical data, CMA carries the molecular formula C₂₀H₃₁ClO₂ and a molecular mass of approximately 338.2 daltons. The compound belongs to the androstane steroid family. Structurally, it features three notable modifications relative to its parent androgen scaffold:

A 4-chloro substituent (chlorine atom at the C4 position of ring A)
A 17α-methyl group (the key alkylation conferring oral bioavailability)
3β,17β-diol functionality (hydroxyl groups at both C3 and C17 in the beta configuration, rather than the more common 3-keto arrangement)

CMA is closely structurally related to, but distinct from, chlorodehydromethylandrostenediol (CDMA, sold as Halodrol-50), which carries an additional double bond (Δ1) in its A-ring. CMA is closely related to chlorodehydromethylandrostenediol (CDMA; Halodrol-50), which was developed by industry veteran Bruce Kneller, and was also briefly sold on the Internet in 2005 and 2006, though by a different company.

Natural source: CMA has no natural botanical or animal source. It is an entirely synthetic, laboratory-created molecule. It does not occur in nature and is not derived from any herbal, plant, or glandular extract. It is therefore not a "natural ingredient" in any pharmacognostic or botanical sense, despite having been commercially positioned as a dietary supplement.

Putative metabolic target / "prohormone" claim: Although CMA was sold as a "prohormone" or "prosteroid" of chloromethyltestosterone (CMT; also known more commonly as methylclostebol), it is likely that the conversion is far from complete and that much of the activity of the drug may be attributable to its unchanged form. Methylclostebol (chloromethyltestosterone) is itself a synthetic, orally active anabolic-androgenic steroid and designer steroid that has been sold on the Internet as a "dietary supplement," but has never been studied for medical use.

2. Common Forms and Preparations

CMA was commercially available in a single primary format: oral tablets or capsules, distributed under the product name Promagnon. It was first encountered in 2005 when it was introduced as a "dietary supplement" and putative prohormone under the name Promagnon by an online vendor called Peak Performance Laboratories. Promagnon was sold exclusively through the internet and was not distributed through conventional retail pharmacy or supplement store channels. A related product, Halodrol-50 (containing the structurally analogous CDMA), was simultaneously sold by Gaspari Nutrition through online and supplement retail outlets.

CMA (Promagnon) was listed in the literature as an oral, "all purpose" product, with reported dosages of 50–100 mg. Forum-era documentation from the period of sale also referenced tablet strengths of 25 mg, with user-reported dosing ranges of 25–75 mg daily. However, these figures derive from uncontrolled user reports, not from clinical studies, and no clinical trial has ever assessed any dosage of CMA in human subjects.

3. Historical and Regulatory Context

3.1 The Prohormone Supplement Era (1994–2006)

The commercial appearance of CMA must be understood against the backdrop of United States dietary supplement regulation and the proliferation of "designer steroid" prohormones in the early 2000s. In the United States, the Dietary Supplement Health and Education Act (DSHEA) classifies dietary supplements as a subcategory of food, allowing manufacturers to distribute their products without submitting proof of safety or efficacy prior to marketing. In the wake of this liberalizing legislation on dietary supplements — which all but usurped the authority of federal regulatory bodies — pro-hormones proliferated in the supplement market, with their efficacy and safety entirely unbeknownst to consumers.

In 1990, Congress passed the Anabolic Steroid Control Act, which placed 27 anabolic steroids into Schedule III of the Controlled Substances Act. The passage of DSHEA in 1994 created a regulatory window in which chemically novel steroidal compounds — not yet named in the Controlled Substances Act — could be sold as dietary supplements. The androstenedione example makes clear that by the time the agencies are able to take action against a specific steroid precursor, unscrupulous manufacturers will already have made minor chemical changes to the product and reintroduced it into the marketplace. Steroid precursor manufacturers fully exploited the protection offered by DSHEA and actively touted precursor products as "natural" and "legal" in order to raise the false implication that they offered a safe alternative to controlled anabolic steroids.

Pursuant to the 2004 Anabolic Steroid Control Act, Congress placed an additional 36 steroids and over-the-counter prohormone dietary supplements into Schedule III of the Controlled Substances Act, including androstenedione and its derivatives. The 2004 Act forced the removal of first-generation prohormones (androstenedione, androstenediol, and their immediate derivatives) from the supplement market. This regulatory action created a second wave of "designer" compounds — including CMA — engineered to differ sufficiently in chemical structure from the newly scheduled substances. To circumvent existing laws, the chemical structure of AAS was modified and these designer steroids were sold as nutritional supplements mainly over the Internet.

CMA appeared on the market in 2005, one year after the 2004 Act, precisely in this regulatory gap. Its short commercial lifespan ended in 2006: CMA was voluntarily discontinued by Gaspari Nutrition in late 2006, likely fearing government sanctions if it continued to sell the product. (Note: While Wikipedia's article on CMA names Gaspari Nutrition in connection with discontinuation, the Promagnon product itself was sold by Peak Performance Laboratories; Gaspari Nutrition was the vendor of the related CDMA product Halodrol-50. The close parallel histories of the two products and the same principal industry figure, Bruce Kneller, may account for this overlap in the sourced accounts.)

The regulatory environment continued to tighten in subsequent years. In December 2014, President Barack Obama signed the Designer Anabolic Steroid Control Act of 2014 (DASCA), which replaced two prior versions of the Anabolic Steroid Control Act that had been passed in 1990 and 2004. Congress intended the DASCA to erase the distinction between the substances once called "prohormones" — steroidal substances unlawfully marketed as dietary supplement products — and the substances traditionally regarded as anabolic steroids.

3.2 Traditional Use

CMA has no documented traditional use in any culture, herbal system, or historical period. It is a fully synthetic compound, first described in 2005, and no record exists of its use in Ayurvedic, Traditional Chinese Medicine, Western botanical herbalism, Indigenous medicine, or any other pre-modern therapeutic tradition. No monograph exists for it in the WHO, European Pharmacopoeia, German Commission E, ESCOP, or USP databases. There is accordingly no traditional-use section to report in the ethnopharmacological sense.

4. Active Compounds, Structural Chemistry, and Mechanisms of Action

4.1 The 17α-Methyl Group and Oral Bioavailability

The defining pharmacokinetic feature of CMA is its 17α-methyl substitution. CMA is a 17α-alkylated compound. This alteration protects the drug from deactivation by the liver, allowing a very high percentage of the drug entry into the bloodstream following oral administration. In unmodified androgens, first-pass hepatic metabolism rapidly converts the hormone to inactive glucuronide or sulfate conjugates. The 17α-methyl group sterically hinders this 17-keto oxidation, substantially increasing oral bioavailability. This structural strategy is shared by methyltestosterone, oxandrolone, stanozolol, and other classical oral AAS.

4.2 The 4-Chloro Group: Aromatase Resistance and Modified 5α-Reductase Activity

The chlorine atom at the C4 position confers two important pharmacological properties:

Non-aromatizability: Due to the presence of a chloro group at the C4 position, CMA cannot be aromatized, and for this reason poses no risk of estrogenic side effects like gynecomastia at any dosage. Aromatization is the enzymatic conversion of androgens to estrogens, catalyzed by CYP19A1 (aromatase), which requires a 4,5-double bond and an unsubstituted C4. Halogenation at C4 blocks this conversion entirely.
Reduced 5α-reductase metabolism: CMA is not extensively metabolized by 5α-reductase and exhibits relatively greater anabolic than androgenic activity, but is still capable of producing androgenic side effects like oily skin, acne, and increased growth of facial and body hair, as well as virilization in women. Under normal AAS pharmacology, the androgenic-to-anabolic ratio of a given AR agonist is related to its capacity to be transformed by enzymes such as 5α-reductase in conjunction with the AR activity of any resulting products. For instance, an AAS that is not metabolized by 5α-reductase would not undergo potentiation in 5α-reductase-expressing tissues. Because CMA resists 5α-reduction, it does not produce significantly elevated DHT levels in androgenic tissues such as the prostate and skin/scalp, contributing to a relatively higher anabolic-to-androgenic ratio compared to testosterone.

4.3 3β-Hydroxyl Configuration

CMA's C3 position bears a β-hydroxyl group rather than the 3-keto group found in most classical AAS (including testosterone, methyltestosterone, and its putative metabolite methylclostebol). CMA carries a 3β-hydroxyl group instead of the common 3-keto group that facilitates receptor binding, which makes it somewhat weaker than chloromethyltestosterone in comparison. The 3-keto configuration is generally associated with higher androgen receptor (AR) binding affinity; the 3β-OH must first be oxidized to a 3-keto compound to engage more potently with the AR. This oxidation step — which would yield methylclostebol — is what forms the pharmacological basis for the "prohormone" marketing claim.

4.4 Androgen Receptor Activation

Like all AAS, CMA is understood to act primarily through direct and indirect agonism of the androgen receptor (AR). There are three main action mechanisms: (i) directly on the AR; (ii) via dihydrotestosterone (DHT) produced by the action of 5α-reductase; and (iii) via estrogen receptors by means of estradiol produced by CYP19 aromatase. Free testosterone (or its synthetic analogue) is transported into target tissue cell cytoplasm; binding to the AR takes place either directly or after conversion to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. In the case of CMA, pathway (iii) is blocked by the 4-chloro group (no aromatization), and pathway (ii) is attenuated by the same chloro group (limited 5α-reduction). The compound therefore relies predominantly on direct AR activation and, to an uncertain degree, on metabolic conversion to its putative active metabolite methylclostebol.

Into the cell nucleus, the steroid-AR complex acts on specific nucleotide sequences of chromosomal DNA. The produced mRNA can activate DNA transcription of specific responsive genes. AAS mimics the testosterone physiological effects, and primarily acts via the androgen receptor. These transcriptional effects are proposed to promote nitrogen retention, positive protein balance, and muscle protein synthesis — the mechanism classically attributed to the anabolic effects of AAS as a class.

4.5 Comparative Potency

No direct human or animal pharmacological study has been published specifically for CMA. Comparative data derive from the profile of its proposed metabolite, methylclostebol: In animal assays, chloromethyltestosterone displayed about 30–50% of the anabolic activity of methyltestosterone, with about 10% of the accompanying androgenic activity. Chloromethylandrostenediol is a primarily anabolic but fairly weak steroid milligram for milligram, although it does possess enough potency to be an effective lean mass building drug. These characterizations, however, derive from secondary sources without primary peer-reviewed citation and should be interpreted cautiously.

5. Scientific Evidence by Area of Use

5.1 Skeletal Muscle Hypertrophy and Athletic Performance

Human clinical evidence: None. No peer-reviewed, published clinical trial — randomized or otherwise — has been conducted specifically on CMA in human subjects for any indication, including muscle mass, strength, or athletic performance. This represents an absolute absence of direct human evidence for the compound.

Several side effects are linked with AAS abuse. Only little is known about the pharmacological effects and metabolism of unapproved steroids due to the absence of clinical studies.

The broader class of second-generation prohormone supplements (those entering the market after the 2004 Act) has been studied in a very limited number of small trials. One notable study examined a structurally distinct but related prohormone: Seventeen resistance-trained men (mean age 23 years; 13.1% body fat) were randomly assigned to receive either 330 mg/day of 3β-hydroxy-5α-androst-1-en-17-one (a prohormone) or placebo and complete a 4-week structured resistance-training program. Body composition, muscular strength, circulating lipids, and markers of liver and kidney dysfunction were assessed at study onset and termination. The prohormone increased lean body mass by 6.3 ± 1.2%, decreased fat body mass by 24.6 ± 7.1%, and increased back squat one repetition maximum by 14.3 ± 1.5%. This trial is methodologically relevant as a template for evaluating second-generation AAS prohormones as a class; however, its results cannot be extrapolated to CMA specifically, as the compound studied is chemically distinct.

Contemporaneous to the compounds peaking in popularity was the emergence of a body of scientific research evidencing that pro-hormones had little in the way of ergogenic value, in stark contrast to the promising proprietary claims present in their advertising. This conclusion applies specifically to first-generation prohormones (androstenedione, androstenediol); whether it generalizes to second-generation 17α-alkylated designer steroids like CMA — which have significantly different pharmacokinetics — has not been formally tested.

Evidence strength: Absent for CMA specifically. No human trials exist.

5.2 Body Composition

No human data exist for CMA's effects on body composition. The marketed claims of lean mass gain and fat loss are marketing assertions unsupported by any published clinical data. The pharmacological rationale — AR-mediated enhancement of nitrogen retention and protein synthesis — is extrapolated from the general AAS literature, not from CMA-specific studies.

Evidence strength: Absent for CMA specifically.

5.3 Endocrine Effects / Hypothalamic-Pituitary-Testicular Axis Suppression

While no CMA-specific endocrine studies exist, all exogenous AAS suppress the hypothalamic-pituitary-testicular (HPT) axis through negative feedback. Administration of supraphysiological androgens reduces the pulsatile release of gonadotropin-releasing hormone (GnRH), which suppresses LH and FSH secretion from the pituitary, resulting in reduced endogenous testosterone production and, with sustained use, testicular atrophy. The AAS withdrawal syndrome is probably the result of persistent suppression of endogenous testosterone production during the recovery phase, direct effects of AAS withdrawal on brain neurosignaling, and loss of muscle mass that is disproportionately important for some men. Known side effects include reduced fertility that might take 1 to 2 years to normalize after discontinuation of AAS, erythrocytosis, and dyslipidemia. These effects apply to the AAS class and, by pharmacological reasoning, to CMA; no CMA-specific data exist.

Evidence strength: Class-level (AAS) evidence only; no CMA-specific data.

6. Body Systems and Health Areas Associated with CMA

6.1 Musculoskeletal System

CMA was marketed for effects on the musculoskeletal system — specifically, gains in lean muscle mass and muscular strength. The proposed mechanism is AR-mediated upregulation of muscle protein synthesis genes. No direct human evidence supports or refutes these claims for CMA in particular.

6.2 Hepatic (Liver) System

The liver is the organ most directly impacted by CMA's 17α-alkylated structure. As with other 17α-alkylated AAS, CMA may pose a risk of hepatotoxicity. The hepatotoxic potential of the 17α-alkylated AAS class is well-characterized in peer-reviewed literature. Androgenic and anabolic steroids have been implicated in four distinct forms of liver injury: transient serum enzyme elevations, an acute cholestatic syndrome ("bland cholestasis"), chronic vascular injury to the liver (peliosis hepatis), and hepatic tumors including adenomas and hepatocellular carcinoma. The C-17α alkylated androgenic steroids have all been implicated in cases of liver injury, including prolonged cholestasis, peliosis hepatis, nodular regeneration, hepatic adenomas, and hepatocellular carcinoma.

The biochemical mechanism of 17α-AAS hepatotoxicity is not fully resolved. The mechanism of toxicity remains poorly understood, but it has been suggested to result from AR activation in liver cells, leading to an increased production of reactive oxygen species (ROS). Additionally, orally administered 17α-alkylated steroids are considered to be the most hepatotoxic. They increase the number of reactive oxygen species (ROS) which directly injure the liver tissue. This may be manifested as an elevation of liver enzymes, peliosis hepatis, or distinctive acute cholestasis.

The clinical presentation of 17α-AAS-induced liver injury most commonly features a distinctive form of acute cholestasis often referred to as "bland cholestasis." The liver injury generally arises within 1 to 4 months of starting the drug. Use of androgenic steroids is associated with a variable rate of serum enzyme elevations which are usually asymptomatic and self-limited. AAS are recognized to exert a detrimental effect on the liver, and this particularly seems to be the case for 17α-alkylated AAS. Biochemically, this expresses itself in relatively small elevations of blood aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and gamma-glutamyl transpeptidase (GGT) values. Rarely, AAS-induced hepatotoxicity might manifest itself in jaundice and pruritus.

Cases of liver injury specifically attributed to prohormone supplement use have been documented in the medical literature. A reported case from a publication examining drug-induced liver injury in deployed U.S. service members described findings from prohormone supplement use: peak bilirubin of 23.6 mg/dL, alkaline phosphatase of 441 units/L, and AST/ALT of 70/117 units/L. A working diagnosis of acute intrahepatic cholestasis was made. Liver biopsy revealed a centrilobular insult with neutrophilic infiltrates and Ito cell hyperplasia consistent with acute drug-induced cholestasis. This case did not involve CMA specifically but illustrates the hepatic risk profile documented for the designer steroid prohormone supplement class.

6.3 Cardiovascular System

Chronic supraphysiological AAS exposure is associated with serious cardiovascular consequences, ranging from hypertension and lipid disorders to cardiomyopathy, atherosclerosis, and sudden cardiac death. The most robustly documented cardiovascular effect of oral alkylated AAS is dyslipidemia: AAS have consistently been associated with low serum high-density lipoprotein (HDL) cholesterol concentrations in men and women; orally ingested alkylated AAS may cause profound suppression of serum HDL cholesterol.

Even short-term steroid cycles (lasting several weeks) can reduce HDL cholesterol by 20–70% and concomitantly raise LDL cholesterol by approximately 20%, often with a moderate rise in total cholesterol. The mechanism involves disruption of hepatic cholesterol metabolism: AAS affect the lipid profile by modifying key hepatic cholesterol metabolism pathways. They suppress apolipoprotein A-I expression and enzymes involved in HDL production, while upregulating hepatic very-low-density lipoprotein (VLDL)/LDL synthesis. AAS also accelerate HDL catabolism, further exacerbating dyslipidemia. Abnormalities of HDL and LDL may arise within 9 weeks of AAS self-administration.

Key cardiovascular pathways include endothelial dysfunction, adverse lipid profile changes, prothrombotic and vasospastic effects, myocardial hypertrophy with fibrosis, and electrical remodeling contributing to arrhythmias. Again, these effects pertain to the AAS class broadly and to 17α-alkylated oral AAS specifically; no cardiovascular studies have been conducted for CMA.

6.4 Reproductive and Endocrine System

The androgenic activity of CMA — though attenuated relative to testosterone by virtue of limited 5α-reduction and the 3β-OH configuration — means it retains the potential for androgenic adverse effects. CMA exhibits relatively greater anabolic than androgenic activity, but is still capable of producing androgenic side effects like oily skin, acne, and increased growth of facial and body hair, as well as virilization in women. The absence of aromatization means no estrogen-mediated effects (such as water retention or gynecomastia) are expected from CMA itself.

6.5 Dermatological Effects

As an androgen, CMA shares the dermatological side-effect profile of the AAS class: many adverse effects have been associated with AAS misuse, including disturbance of endocrine and immune function, alterations of sebaceous system and skin. The 4-chloro, non-5α-reduced pharmacology of CMA theoretically attenuates the androgenic stimulation of sebaceous glands and hair follicles relative to testosterone, but does not eliminate it.

7. Dosage Forms and Reported Dosages

CMA was manufactured and sold exclusively in oral tablet/capsule form. No injectable, transdermal, sublingual, or other dosage form has been documented.

Dosages reported in the scientific and grey literature for CMA include:

50–100 mg as noted in a published review of AAS used in the United Kingdom, where CMA (Promagnon, oral) was listed as an "all purpose" compound at those doses.
An earlier forum-sourced profile described by the original vendor indicated tablet strengths of 25 mg, with a usage range of 25–75 mg daily.

No clinical trial has ever evaluated any dose of CMA in humans. The dosages cited above come from user-reported data and review-level collation of gym/bodybuilding community practices, not from controlled pharmacological investigations. There is no established safe or effective dose, no pharmacokinetic data (e.g., half-life, Cmax, AUC) published in peer-reviewed literature, and no toxicity threshold determined by systematic study.

8. Safety Considerations and Interactions

8.1 Hepatotoxicity

This is the most well-characterized risk for 17α-alkylated AAS as a class and the risk most directly applicable to CMA. As with other 17α-alkylated AAS, CMA may pose a risk of hepatotoxicity. Use of 17α-alkylated anabolic-androgenic steroids (17α-AAS) has been connected to hepatotoxicity. Side effects such as cholestatic jaundice only occurred in a small number of patients taking the recommended doses of 17α-AAS. Peliosis hepatis, hepatic tumors, and hepatocellular adenomas are other reported side effects. The NIH LiverTox database confirms that the C-17α alkylated androgenic steroids have all been implicated in cases of liver injury, including prolonged cholestasis, peliosis hepatis, nodular regeneration, hepatic adenomas, and hepatocellular carcinoma.

8.2 Dyslipidemia and Cardiovascular Risk

Severe side effects including hepatotoxicity, cholestasis, renal failure, hypogonadism, gynecomastia, and infertility have been reported secondary to the use of designer steroid products. The lipid-altering effects of oral alkylated AAS are particularly pronounced: Of these potential adverse effects, the strongest data relate to dyslipidemia. AAS have consistently been associated with low serum HDL cholesterol concentrations in men and women; orally ingested alkylated AAS may cause profound suppression of serum HDL cholesterol. These adverse lipid changes, combined with AAS-induced endothelial dysfunction, lead to accelerated atherosclerosis in AAS users.

8.3 HPT-Axis Suppression and Hypogonadism

Exogenous administration of any androgenic compound suppresses the body's endogenous testosterone production via negative feedback on the hypothalamic-pituitary-testicular axis. Upon discontinuation of the exogenous AAS, the HPT axis recovery may be prolonged. Known side effects include reduced fertility that might take 1 to 2 years to normalize after discontinuation of AAS, erythrocytosis, and dyslipidemia.

8.4 Androgenic Side Effects

Although CMA's profile suggests it is less androgenic than testosterone or methyltestosterone due to limited 5α-reductase metabolism, it is not free from androgenic adverse effects. CMA is not extensively metabolized by 5α-reductase and exhibits relatively greater anabolic than androgenic activity, but is still capable of producing androgenic side effects like oily skin, acne, and increased growth of facial and body hair, as well as virilization in women.

8.5 Absence of Estrogenic Side Effects

Unlike testosterone and most classical oral AAS, CMA's 4-chloro substitution prevents aromatization, eliminating estrogen-mediated adverse effects. Due to the presence of a chloro group at the C4 position, CMA cannot be aromatized, and for this reason poses no risk of estrogenic side effects like gynecomastia at any dosage.

8.6 Lack of Safety Data and Regulatory Status

Several side effects are linked with AAS abuse. Only little is known about the pharmacological effects and metabolism of unapproved steroids due to the absence of clinical studies. CMA was never approved or authorized as a pharmaceutical drug in any jurisdiction. It was never subjected to the preclinical or clinical testing required for pharmaceutical approval. Consequently, no formally determined safety profile, maximum tolerated dose, pharmacokinetic characterization, or drug interaction data exist in the peer-reviewed literature.

Under U.S. law, CMA falls within the scope of the Designer Anabolic Steroid Control Act of 2014 by virtue of being chemically and pharmacologically related to testosterone. The statutory definition of AAS includes "any drug or hormonal substance, chemically and pharmacologically related to testosterone (other than estrogens, progestins, corticosteroids and dehydroepiandrosterone)." The WADA Prohibited List prohibits all anabolic androgenic steroids when administered exogenously, as anabolic agents are prohibited, covering anabolic androgenic steroids when administered exogenously. Any athlete subject to anti-doping rules would face a potential violation from CMA use, regardless of whether it is specifically named.

8.7 Adulteration and Mislabeling Risk

As with other designer steroid products sold in the supplement marketplace, methylclostebol (a closely related compound to CMA's putative active metabolite) was found as a listed ingredient in currently sold "dietary supplements." Common to many designer steroid products, the labeled ingredient was written in a convoluted and outdated nomenclature. This pattern of obfuscatory labeling makes it difficult for consumers, clinicians, and regulators to identify the actual pharmacological agents present in such products.

9. Absence of Peer-Reviewed Clinical Evidence: Summary Assessment

A systematic review of the available peer-reviewed literature reveals that no clinical trial, pharmacokinetic study, randomized controlled trial, or systematic review has been published specifically investigating chloromethylandrostenediol (CMA) in human subjects for any purpose — including muscle hypertrophy, body composition, performance enhancement, endocrine effects, or safety. The compound was never subjected to formal pharmaceutical development and was never studied in preclinical animal models in published research.

The entirety of what is scientifically stated about CMA derives from:

Its chemical structure and the mechanistic inferences drawn therefrom (i.e., what it should do based on its pharmacological class).
Extrapolation from the literature on related compounds — methyltestosterone, methylclostebol (its proposed active metabolite), and CDMA (Halodrol, its structural analogue).
The general AAS literature regarding class-level mechanisms and toxicities.
Uncontrolled, anecdotal user reports from the period of its commercial availability (2005–2006).

This constitutes one of the weakest possible evidence bases for any compound discussed in a health or clinical context. No efficacy or safety claim for CMA can be made with scientific validity.

References

Health Conditions

Health conditions that Chloromethylandrostenediol may help support.

No conditions available.

Body Systems

Body systems that Chloromethylandrostenediol may help support.

No body systems available.