Cyanostane

Cyanostane (Cynostane)

Identity and Chemical Characterization

Names and Nomenclature

Cyanostane is a synthetic anabolic–androgenic steroid (AAS) marketed in the early 2010s as a dietary supplement and prohormone. It is also known as Cynostane, and its chemical name is 2-cyano-17α-methyl-17β-hydroxy-androst-3-one. The active ingredient is listed under two nomenclatures: 2-cyano-17α-methyl-17β-hydroxy-5α-androst-3-one and 2-cyano-17α-methyl-17β-acetoxy-5α-androst-2-ene, both of which refer to the same compound. Many individuals use the name "Cyanostane" because some manufacturers chose it as a commercial brand name for their Cynostane-based products.

Chemical Structure and Molecular Properties

Cyanostane has the molecular formula C₂₁H₃₁NO₂ and a molecular weight of approximately 329.48 g/mol. It is sometimes described as 2-cyano-dromostanolone — a compound bearing a cyano group (CN) attached to the 2 position of the steroidal A-ring, with a chemical structure otherwise identical to methyldrostanolone (Superdrol), except that it has a CN group at the 2 position instead of a methyl group.

Cyanostane is classified as a prohormone — a type of chemical that is a precursor to active hormones. It is converted in the body to testosterone and other sex hormones. The 17α-methylation on cyanostane enables oral administration by decreasing inactivation during first-pass hepatic metabolism, though liver toxicity increases correspondingly.

Natural Source

Cyanostane is an entirely synthetic compound; it has no botanical or natural origin and does not occur endogenously in humans or in plants. It belongs to the broader family of designer synthetic androgens that do not appear naturally in biology. Most designer AAS are analogues of compounds initially developed in the 1960s — early-generation synthetic androgens abandoned in the pharmaceutical pipeline in favor of better alternatives.

Common Forms and Preparations

Cynostane/cyanostane prohormones were first introduced to the market by Anabolic Innovations under the "Cynostane" label, after which many supplement manufacturers launched their own formulations. Notable commercial preparations included Cyanostane RX by Iron Mag Labs, Cynostane by Anabolic Innovations, Supernova C2 by Galaxy Supplements, eStrength 3 by Galaxy Supplements, and Cyanobol by Hardcore Formulations. The product Cyanostane RX, for example, contained two compound ingredients: 17β-hydroxy-2α,17β-dimethyl-5α-androstan-3-one-azine (dymethazine) and 2-cyano-17α-methyl-17β-hydroxy-5α-androst-3-one (cynostane). Products were primarily supplied as oral capsules or tablets. Cynostane prohormone products are no longer available on the market.

Traditional and Historical Use

Cyanostane has no traditional or historical use in any cultural, ethnomedical, or herbal tradition. It is a fully synthetic molecule without a history of use in Ayurvedic, Traditional Chinese, Western herbal, or any other traditional medicine system. Most designer AAS of this type are analogues of compounds initially developed in the pharmaceutical research of the 1960s that were never approved or brought to clinical use.

The emergence of cyanostane as a supplement ingredient is entirely a product of the early 21st-century "designer steroid" era, in which chemical structures of AAS were systematically modified to circumvent existing laws, and these designer steroids were sold as nutritional supplements mainly over the Internet. Cynostane was used for bodybuilding purposes including bulking, body recomposition, and cutting, but was most widely used for bulking.

Key Constituents and Active Compounds

The Active Molecule

Cynostane/cyanostane prohormone products contain one principal active ingredient: 2-cyano-17α-methyl-17β-hydroxy-5α-androst-3-one. The defining structural feature is the cyano group (–C≡N) at the 2α-position on the androstane skeleton. The chemical structure is otherwise the same as methyldrostanolone (Superdrol), except that it has a CN group on the 2 position instead of a methyl group. Cyanostane/cynostane is a methylated prohormone, meaning it carries a 17α-methyl group — a modification that is standard to this class of orally active synthetic androgens.

Structural Relationship to Methyldrostanolone (Superdrol)

Methyldrostanolone (methasterone, trade name Superdrol) is itself a structural analogue of drostanolone with an added 17α-methyl group. The oral designer steroid methasterone, also known as methyldrostanolone, is an example of the hepatotoxicity associated with the consumption of 17α-alkylated steroids; it was sold in the USA as a dietary supplement until 2012 and is a methylated (17α-alkylated) version of the injectable steroid drostanolone. Cyanostane is a second-generation structural modification of that same compound, substituting the 2α-methyl group of Superdrol with a 2α-cyano group.

Relationship to 2-Cyanosteroid Chemistry

The 2-cyano substitution on steroidal scaffolds has been investigated in pharmaceutical research separate from cyanostane itself. Cyanoketone — a structurally related compound known as 2α-cyano-4,4′,17α-trimethylandrost-5-en-17β-ol-3-one (CTM) — is a synthetic androstane steroid and steroidogenesis inhibitor used in scientific research. On account of its structural similarity to pregnenolone, cyanoketone binds to and acts as a potent, selective, and irreversible inhibitor of 3β-hydroxysteroid dehydrogenase (3β-HSD), an enzyme responsible for converting pregnenolone into progesterone, 17α-hydroxypregnenolone into 17α-hydroxyprogesterone, DHEA into androstenedione, and androstenediol into testosterone. As such, cyanoketone inhibits the production of both gonadal and adrenal steroids, including progesterone, androgens, estrogens, and corticosteroids — and the drug is too toxic for therapeutic use in humans.

There are studies about other 2-cyano steroids such as 2-cyano-DHT and 2-cyano-progesterone; in separate studies, one conducted on dogs, both of these 2-cyano steroids caused inhibition of the 3β-HSD enzyme, and this inhibition was found to cause severe adrenal suppression. Whether this mechanism applies to cyanostane specifically is unknown, but users have been cautioned about this possibility.

Proposed Mechanisms of Action

Androgen Receptor Agonism

Like all synthetic AAS of the androstane series, cyanostane is expected to exert its primary biological effects via direct binding to and activation of the androgen receptor (AR). As a prohormone, cyanostane is converted in the body to testosterone and other sex hormones. Community-level characterizations have described cyanostane as an extremely anabolic compound with remarkably low androgenic action, making it qualitatively similar to oxandrolone or methenolone (Primobolan). These claims are based on structural inference rather than formal receptor-binding studies.

Non-Aromatizing Character

Cyanostane is non-aromatizing, meaning it is claimed not to produce estrogen-related side effects; its high degree of anabolic action is cited as making it attractive for athletes concerned with losing body fat while maintaining or increasing muscle mass. Reduction of estrogen-related side effects can be achieved structurally by elimination of the C19-methyl group, introduction of a 1,2-double bond, or methylation at C2, which does not allow the aromatase enzyme complex to aromatize the A-ring — though aromatization cannot be avoided completely even with such modifications. The 2-cyano group in cyanostane serves a structurally analogous purpose to 2-methyl substitution in blocking aromatase access to the A-ring.

Oral Bioavailability via 17α-Methylation

In particular, 17α-alkylated AAS appear to be hepatotoxic, whereas non-alkylated AAS appear not to be; the 17α-alkyl substitution retards hepatic metabolism of the AAS, rendering it orally bioavailable. Cyanostane carries this same 17α-methyl modification, which confers oral activity but simultaneously introduces a hepatotoxic liability inseparable from that structural feature.

Possible 3β-HSD Inhibition

3β-HSD is potently inhibited by compounds including cyanoketone, azastene, epostane, and trilostane. 3β-Hydroxysteroid dehydrogenase/Δ5-4 isomerase (3β-HSD) is an enzyme that catalyzes the biosynthesis of progesterone from pregnenolone, 17α-hydroxyprogesterone from 17α-hydroxypregnenolone, and androstenedione from DHEA in the adrenal gland. Given the structural similarity of the 2-cyano moiety in cyanostane to that in cyanoketone, inhibitory effects on 3β-HSD have been raised as a theoretical concern with cyanostane. However, this has not been formally demonstrated for cyanostane in human studies; it remains a mechanistic hypothesis based on analogy with structurally related compounds.

Scientific Evidence by Area of Use

Overview of Evidence Quality

Cyanostane is used for weight loss, to improve athletic performance, to reduce sexual problems, and for other purposes, but there is no good scientific evidence to support its use. Only little is known about the pharmacological effects and metabolism of unapproved steroids due to the absence of clinical studies. The following subsections therefore describe claims that have been made, but must be read with the understanding that all claims lack support from controlled human clinical trials specifically involving cyanostane.

Muscle Mass and Body Composition

Cyanostane has been marketed primarily for its purported anabolic effects on skeletal muscle. Cyanostane is characterized as a prohormone featuring an alteration of the superdrol compound, with a cyano bond instead of the 2α-methyl superdrol bond. Expected results were described as lean gain, since the compound cannot convert to estrogen; based on the chemical structure, the anabolic potency would appear to be very potent, and since it is anti-estrogenic, users could expect very dry gains.

No peer-reviewed, controlled clinical trials specifically assessing the effect of cyanostane on muscle mass, lean body mass, or body composition in humans have been identified in the scientific literature. The available evidence is limited to mechanistic inference from chemical structure and anecdotal reports from supplement forums and bodybuilding communities. These sources are not valid scientific evidence for efficacy claims. Only little is known about the pharmacological effects and metabolism of unapproved steroids due to the absence of clinical studies.

Broader research on prohormones has provided some relevant context. A study in recreational sports was conducted in 17 men given either the prohormone 3β-hydroxy-5α-androst-1-en-17-one or placebo, where the treated group showed negative effects on cardiovascular and liver parameters. This study involved a different compound, but illustrates the general approach and findings in comparable prohormone trials, which tend to reveal safety problems alongside any performance-related outcomes.

Athletic Performance

Performance enhancement claims for cyanostane rest entirely on structural analogy to known anabolic steroids and on informal self-reports. Anabolic androgenic steroids are some of the most common performance-enhancing drugs among society; despite the broad spectrum of adverse effects and legal consequences, AAS are illicitly marketed and distributed in many countries. No randomized controlled trial, systematic review, or other rigorous human study on cyanostane's effects on strength, power, endurance, or athletic performance has been published in the peer-reviewed literature.

Weight Loss and Body Fat Reduction

Claims of fat-loss effects of cyanostane are based on its non-aromatizing character and its structural similarity to oxandrolone — an approved AAS associated with body composition improvements in specific medical populations. However, there is no good scientific evidence to support the use of cyanostane for weight loss. No clinical trial specifically evaluating cyanostane's effects on adipose tissue or body weight has been identified.

Sexual Function

Cyanostane has been used with the aim of reducing sexual problems, again without any clinical evidence specific to this compound. Indeed, data on AAS as a class indicate the opposite direction of effect: exogenous androgen administration suppresses the hypothalamic-pituitary-gonadal (HPG) axis, frequently resulting in secondary hypogonadism upon discontinuation, with clinical manifestations including decreased libido, erectile dysfunction, infertility, testicular atrophy, and mood disturbances.

Body Systems and Health Areas Associated with Cyanostane

Endocrine and Reproductive System

Anabolic androgenic steroids adversely impact male fertility by suppressing the hypothalamic-pituitary-gonadal axis, leading to reduced intratesticular testosterone levels, impaired spermatogenesis, testicular atrophy, and azoospermia. The HPG axis is fine-tuned by negative feedback according to circulating testosterone levels; the higher the circulating androgen levels in the body, the lower the activity of the HPG axis, ultimately leading to the cessation of endogenous production of FSH, LH, and testosterone. A well-known complication of AAS use is infertility, due to the suppression of the HPG axis and subsequent suppression of spermatogenesis in the testes; cessation of AAS use can restore spermatogenesis, but recovery can take several months to years.

In female individuals, AAS misuse can cause virilization, menstrual irregularities, clitoromegaly, and voice deepening, some of which may be irreversible.

Hepatic System

The liver is the primary organ of concern with cyanostane given its 17α-methylation. 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; these adverse events have been most closely linked with the C-17α alkylated testosterones.

Pure cholestasis without hepatitis is observed most frequently with contraceptive and 17α-alkylated androgenic steroids, and the mechanism most likely involves interference with hepatocyte canalicular efflux systems for bile salts, organic anions, and phospholipids. The mechanism responsible for hepatotoxicity induced by 17α-alkylated AAS remains poorly understood; however, oxidative stress has been repeatedly shown to be associated with it. Several pathophysiological mechanisms have been proposed, including androgen receptor-mediated inflammatory response, disturbance of hepatic antioxidant factors, promotion of hepatocyte hyperplasia, and upregulation of bile acid synthesis.

As a C-17αα steroid, cyanostane will be liver toxic; although, due to the lack of the 4-ene on ring A and lack of 2-methylation, liver toxicity may be reduced relative to a di-methylated steroid such as Superdrol. This claim of relatively lower hepatotoxicity compared to Superdrol is speculative and based on structural inference; no formal comparative hepatotoxicity data specific to cyanostane are available.

Cardiovascular System

AAS misuse can increase the risk of sudden cardiac death, stroke, suicide, and other complications. AAS use is closely linked to hepatotoxicity and serious hepatic conditions, as well as steatohepatitis and dyslipidemia, with multiple studies supporting a causal association. Adverse lipid effects — in particular suppression of HDL cholesterol and elevation of LDL cholesterol — are a widely documented class-wide effect of oral 17α-alkylated androgens and are relevant to cyanostane by structural analogy.

Neuropsychiatric System

The central nervous system is another important target for AAS side effects. Reported side effects of cyanostane include behavioral changes, consistent with the known neuropsychiatric effects of this class of compounds. It has been suggested that AAS misuse and abuse lead to adverse effects in all body tissues and organs, especially long-term toxicity involving the cardiovascular system and the reproductive system.

Adrenal System

Based on the pharmacology of structurally similar 2-cyanosteroids, there is a theoretical concern that cyanostane may affect adrenal steroidogenesis. There are studies on other 2-cyano steroids such as 2-cyano-DHT and 2-cyano-progesterone; in separate studies, one conducted on dogs, both 2-cyano steroids caused inhibition of the 3β-HSD enzyme — an inhibition that would cause severe adrenal suppression, considered a very unsafe inhibition — and whether this occurs with cyanostane is unknown, but users need to be aware of this possibility.

Dosage Forms and Reported Dosages

Cyanostane was formulated exclusively for oral administration in capsule form. There is not enough reliable information to know what an appropriate dose of cyanostane might be. No formally established therapeutic or safe dose exists, as cyanostane was never studied in controlled clinical trials, and no regulatory body has evaluated or approved a dosage recommendation.

The dosages that have appeared in informal community documentation are: an average dose of 40–50 mg per day as a standalone preparation, or 20–30 mg per day when combined ("stacked") with other compounds, with no specific average cycle length formally established. These figures are derived from bodybuilding forum discussions and supplement product labeling, not from clinical research, and should not be interpreted as recommendations or evidence of safety.

Regulatory Status

On December 18, 2014, President Obama signed the Designer Anabolic Steroid Control Act of 2014 (DASCA), which cracked down on the over-the-counter "prohormone" segment of the sports nutrition supplement market. 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 such as testosterone, nandrolone, trenbolone, and boldenone. DASCA gave the DEA additional authority to identify and quickly respond when new designer anabolic steroids are falsely marketed as dietary supplements.

In the US, prohormones are considered the same as anabolic steroids and are not legally permitted in supplement products. Cyanostane is banned by the World Anti-Doping Agency (WADA) and the National Collegiate Athletic Association (NCAA).

To circumvent existing laws, the chemical structures of AAS are modified and these designer steroids are sold as nutritional supplements mainly over the Internet. The large number of designer steroid findings in dietary supplements and the detection of new compounds combined with legal loopholes for their distribution in many countries show that stricter regulations and better information policy are needed.

Safety Considerations and Drug Interactions

Hepatotoxicity

Cyanostane is possibly unsafe for most people when taken by mouth; side effects include liver damage, infertility, behavioral changes, and hair loss, among others. Therapy with anabolic steroids is linked to 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 compound. Predictors of severe clinical course include the cholestatic pattern of injury at presentation and significantly elevated peak serum total bilirubin (greater than 40 mg/dL); renal dysfunction has occurred in approximately 20% of reported AAS DILI cases, with all experiencing renal recovery.

The 17α-alkyl structural modification appears to be inextricably linked to hepatotoxicity. AAS drug-induced liver injury demonstrates a clinical phenotype of impaired bile salt excretion similar to that seen in patients with mutations in genes associated with progressive familial intrahepatic cholestasis syndromes; genotyping in a US case series demonstrated that 7 of 44 patients had damaging missense mutations in those genes (ABCB11, ATP8B1, and ABCB4).

Absence of Benefit from "Liver Protector" Supplements

Some patients have reported using dietary supplement products branded as "liver protectors," believing that these products mitigate the hepatotoxicity of 17α-alkylated compounds; however, these "liver protectors" typically contain N-acetylcysteine, milk thistle extract, and other herbs, none of which have been demonstrated to have any protective effect against oral androgen-induced hepatotoxicity.

HPG Axis Suppression and Reproductive Effects

Most individuals with longstanding AAS exposure exhibit low gonadotropin and testosterone levels even after discontinuation; administration of exogenous AAS suppresses the hypothalamic-pituitary-gonadal axis, reducing endogenous testosterone production and impairing testicular function in men, including decreased testicular volume and sperm output. In men with a history of androgen use, sperm counts typically recover within approximately 4 months to 1 year after discontinuation, with older men requiring longer recovery periods; androgen intake may result in low sperm count, small testes, elevated hemoglobin and hematocrit, suppressed or nondetectable serum luteinizing hormone, and reduced sex hormone–binding globulin.

Pregnancy and Breastfeeding

Cyanostane is possibly unsafe when pregnant or breastfeeding; its use during these periods should be avoided.

Mislabeling and Adulteration Risk

Supplement adulteration with anabolic-androgenic steroids has been reported, and AAS-associated drug-induced liver injury is clinically variable. Variable hepatotoxicity patterns of AAS have been documented, and inaccurate supplement labeling raises concern for consumers who may be unaware of the actual ingredients present. Detection of AAS use is challenging, as AAS may be unknowingly present in supplements (either unlabeled or mislabeled) or may be acquired illicitly and thus unreported by patients.

Cardiovascular Risks

The androgen fluoxymesterone has been shown to inhibit 11β-hydroxysteroid dehydrogenase, which may lead to decreased glucocorticoid inactivation and therefore to cortisol-induced mineralocorticoid receptor activation, ending up in electrolyte disturbances — a possible cause of hypertension. Analogous mechanisms may apply to structurally related 17α-alkylated androgens including cyanostane, though specific data for cyanostane do not exist.

Drug Interactions

No formal drug interaction studies specific to cyanostane have been published. By class-level pharmacology, oral 17α-alkylated androgens are known to interact with anticoagulants (particularly warfarin, with potentiation of anticoagulant effects), may alter insulin sensitivity, and can affect the metabolism of co-administered hepatically processed drugs due to CYP enzyme modulation. Despite the broad spectrum of adverse effects and legal consequences, AAS are illicitly marketed and distributed in many countries, often without any pharmacovigilance, making identification and reporting of interactions difficult.

Summary of Evidence Assessment

Cyanostane is a synthetic 17α-methylated, 2-cyano-substituted androgenic steroid without any approved medical use, any traditional history of use, or any published controlled clinical trials supporting its efficacy for any claimed purpose. It is used for weight loss, improving athletic performance, and reducing sexual problems, but there is no good scientific evidence to support its use. Safety evidence from the broader class of 17α-alkylated oral androgens consistently shows hepatotoxic, reproductive, cardiovascular, and neuropsychiatric risks. Cyanostane is currently illegal to sell as a dietary supplement in the United States under DASCA, and is prohibited in sport by WADA and the NCAA.

References

• WebMD Natural Medicines — Cyanostane [Fast Facts]
• LearnSkin / Natural Medicine Database — Cyanostane [Fast Facts]
• ChemicalBook — Cyanostane: 2-cyano-17α-Methyl-17β-hydroxy-androst-3-one
• Joseph JF, Parr MK. Synthetic Androgens as Designer Supplements. Current Neuropharmacology. 2015;13(1):89–100. PMC4462045
• Rahnema CD et al. Designer steroids — over-the-counter supplements and their androgenic component: review of an increasing problem. Andrology. 2015;3(2):150–155.
• NIH LiverTox: Androgenic Steroids. NCBI Bookshelf.
• Anabolic steroid-associated liver injury. PMC11168845. NIH/PMC.
• Anabolic androgenic steroid-induced liver injury: An update. PMC9331524. NIH/PMC.
• Solimini R et al. Anabolic androgenic steroid-induced hepatotoxicity. Mini Rev Med Chem. 2017;17(9):821–828. PubMed 27372877.
• NIH NCBI Bookshelf — Drug-Induced Cholestatic Liver Disease.
• Stickel F et al. Mission Compromised? Drug-Induced Liver Injury From Prohormone Supplements Containing Anabolic-Androgenic Steroids. PubMed 27612377.
• StatPearls — Anabolic Steroid Use Disorder. NCBI Bookshelf NBK538174.
• Rahnema CD et al. Diagnosis and Management of Anabolic Androgenic Steroid Use. J Clin Endocrinol Metab. 2019;104(7):2490–2500.
• Frontiers in Toxicology — Abusive use of anabolic androgenic steroids, male sexual dysfunction and infertility: an updated review. 2024.
• Understanding and managing suppression of spermatogenesis caused by TRT and AAS. PMC9243576. NIH/PMC.
• Wikipedia — Cyanoketone
• Wikipedia — 3β-Hydroxysteroid dehydrogenase
• Wikipedia — Designer Anabolic Steroid Control Act of 2014
• Federal Register — Implementation of the Designer Anabolic Steroid Control Act of 2014 (2023)
• Council for Responsible Nutrition — The Designer Anabolic Steroid Control Act of 2014
• NIH Dietary Supplement Label Database (DSLD) — Cyanostane
• MSD Manual Professional — Anabolic Androgenic Steroids
• Pandemic of testosterone abuse: Considerations for male fertility. Androgens: Clinical Research and Therapeutics. 2025.
• Frontiers in Endocrinology — Non-medical use of exogenous testosterone and AAS in young men: health, psychological, and fertility consequences. 2026.