Is YK-11 really a SARM?

No, technically not. YK-11 has a steroidal structure (DHT-derivative) unlike true SARMs (LGD-4033, RAD-140, ostarine) which are non-steroidal. Its 'SARM' classification is marketing: Kanno 2011 and 2013 described its mechanisms (partial AR agonism + myostatin inhibition) but it does not have the muscular selectivity of true SARMs. Practical consequence: hepatotoxic profile probably more marked than classic SARMs, and nonexistent human corpus. Its classification remains debated in the literature.

Does myostatin inhibition really work in humans?

Theoretically yes, but the magnitude of YK-11 effect in humans has not been demonstrated in clinical studies. Kanno 2013 shows in vitro and in mice an elevation of follistatin and inhibition of myostatin, with associated muscular hypertrophy. The human translation remains hypothetical. User feedback suggests faster gains than LGD-4033 or ostarine, but without rigorous documentation, these effects could be attributable to partial androgenic activity rather than myostatin inhibition.

Does YK-11 cause transaminase elevation?

Empirically yes, frequently. User reports and case studies (DILI under YK-11) suggest ALT/AST elevations 2-5× normal in majority of users at 10-15 mg/d × 6 weeks. Suspected mechanism: hepatic metabolism of a steroidal compound with aggression pathway similar to 17α-alkylated oral AAS. Mandatory monitoring. Hepatoprotectors recommended. Very short cycles (< 6 weeks) if used.

What realistic gains with YK-11?

Difficult to quantify due to lack of clinical studies. User reports at 10 mg/d × 6 weeks: +3 to +5 kg raw lean mass, of which some potentially linked to simple androgenic activity rather than myostatin inhibition. Strength up +5-10%. Net gains retained at 3 months post-PCT: +2 to +3 kg attributable to YK-11. The gains/risks ratio (hepatotoxicity, product purity, suppression) is unfavorable compared to LGD-4033 or ostarine.

What PCT after YK-11?

Start 3-4 days after last intake (half-life ~6-10 h). Robust scheme: clomid 50/50/25/25 mg × 4-6 weeks + nolvadex 40/20/20/20 mg. T total, LH, FSH panel at W6 post-PCT. Suppression under YK-11 appears more marked than under classic SARMs per user reports, justifying reinforced PCT. If T < 300 ng/dL at W6, extend 2 weeks.

Why is YK-11 less documented?

Compound synthesized in 2011 by Kanno and colleagues without pharmaceutical clinical follow-up (never entered official human phase 1). All human reports come from recreational use without control. No GSK, Glaxo or other big pharma phase 1. Consequence: pharmacokinetic profile, dose-response, long-term safety totally uncharacterized in humans. Any use is experimental, the market offers only underground products of variable purity.

Is YK-11 suitable for women?

Strictly no. Steroidal compound with androgenic structure, unknown pharmacological profile in women, high and unpredictable virilization risk. No reason to take YK-11 in women when ostarine and anavar offer much better documented alternatives. If SARMs for women: ostarine 5-10 mg/d × 6-8 weeks remains the safest experimental standard.

YK-11 or RAD-140 for advanced users?

RAD-140 for the majority of cases. RAD-140, despite its limited human corpus, has at least phase 1 and solid preclinical studies (Miller 2010, Solomon 2019). YK-11 has almost no human data and a concerning hepatic profile. For advanced users seeking a more potent SARM than LGD-4033, RAD-140 remains the more rational option. YK-11 is only justified in very targeted experimentation with reinforced monitoring.

YK-11 vs RAD-140: complete comparison (myostatin vs potent SARM)

Q: What realistic gains with YK-11?

Difficult to quantify due to lack of clinical studies. User reports at 10 mg/d × 6 weeks: +3 to +5 kg raw lean mass, of which some potentially linked to simple androgenic activity rather than myostatin inhibition. Strength up +5-10%. Net gains retained at 3 months post-PCT: +2 to +3 kg attributable to YK-11. The gains/risks ratio (hepatotoxicity, product purity, suppression) is unfavorable compared to LGD-4033 or ostarine.

Q: What PCT after YK-11?

Start 3-4 days after last intake (half-life ~6-10 h). Robust scheme: clomid 50/50/25/25 mg × 4-6 weeks + nolvadex 40/20/20/20 mg. T total, LH, FSH panel at W6 post-PCT. Suppression under YK-11 appears more marked than under classic SARMs per user reports, justifying reinforced PCT. If T < 300 ng/dL at W6, extend 2 weeks.

Q: Why is YK-11 less documented?

Compound synthesized in 2011 by Kanno and colleagues without pharmaceutical clinical follow-up (never entered official human phase 1). All human reports come from recreational use without control. No GSK, Glaxo or other big pharma phase 1. Consequence: pharmacokinetic profile, dose-response, long-term safety totally uncharacterized in humans. Any use is experimental, the market offers only underground products of variable purity.

Q: Is YK-11 suitable for women?

Strictly no. Steroidal compound with androgenic structure, unknown pharmacological profile in women, high and unpredictable virilization risk. No reason to take YK-11 in women when ostarine and anavar offer much better documented alternatives. If SARMs for women: ostarine 5-10 mg/d × 6-8 weeks remains the safest experimental standard.

Q: YK-11 or RAD-140 for advanced users?

RAD-140 for the majority of cases. RAD-140, despite its limited human corpus, has at least phase 1 and solid preclinical studies (Miller 2010, Solomon 2019). YK-11 has almost no human data and a concerning hepatic profile. For advanced users seeking a more potent SARM than LGD-4033, RAD-140 remains the more rational option. YK-11 is only justified in very targeted experimentation with reinforced monitoring.

YK-11 vs RAD-140: complete comparison (myostatin vs potent SARM)

Critère	yk-11	rad-140
Class	Partial AR agonist + myostatin inh.	Non-steroidal SARM
Structure	Steroidal (DHT-derivative)	Non-steroidal
Half-life	~6-10 h	~16-20 h
Hepatotoxicity	Moderate to high	Moderate
HPG axis suppression	Moderate to strong	Moderate to strong
Typical dose	5-15 mg/d	10-20 mg/d
Human studies	Virtually nonexistent	Preclinical + limited phase 1
Risk-benefit	Poorly characterized	Poorly characterized

Quand choisir yk-11

YK-11 is one of the least documented compounds on the SARM market (technically, it is not a true SARM due to unclear tissue selectivity). Kanno 2011 and Kanno 2013 demonstrated in vitro and in mice a dual action: partial agonism of the androgen receptor and inhibition of myostatin via the follistatin/Smad pathway — hence the marketing argument of 'muscle gains without physiological ceiling'. Choose it (with extreme caution) for: (1) an orally accessible myostatin inhibition experience, (2) a short cycle (4-6 weeks) in advanced user accepting a poorly characterized risk, (3) a complement to a classic AAS cycle for already advanced users. Pharmacological profile: steroidal structure derived from DHT (different from classic non-steroidal SARMs), low affinity to androgen receptor but high functional activity, hepatotoxicity empirically documented (marked ALT/AST elevations in majority of users at 10+ mg/d × 6 weeks). Major drawbacks (Pope 2014 on unregulated compounds): virtually nonexistent human corpus (no published phase 1 study, GTx did not develop YK-11 clinically), long-term safety profile totally unknown, very variable underground market purity with analyses showing 40-70% of underdosed or contaminated products, concerning hepatic toxicity signal with reported DILI cases. Typical dose in practice 5-15 mg/d × 4-6 weeks maximum. Mandatory PCT clomid + nolvadex 4 weeks. Not suited for beginners, women, or users wanting a predictable safety profile. To avoid in the absence of solid data — preferable alternative: LGD-4033 or RAD-140.

Quand choisir rad-140

RAD-140 (testolone) is a non-steroidal SARM with high affinity to the muscular androgen receptor, with tissue selectivity proven in preclinical (Miller 2010). Choose it for: (1) an oral cycle without injection with more marked gains than LGD-4033 or ostarine, (2) a milder cutaneous androgenic profile than 17α-alkylated oral AAS (less acne, less hair loss), (3) a SARM experience targeted at fast muscular gains. Pharmacological profile (Solomon 2019, Bhasin 2009): SARM potent in raw anabolic effect, clear muscular selectivity in preclinical, no aromatization, no 5α-reduction. Drawbacks to anticipate (Pope 2014): marked HPG suppression (50-80% at 20 mg/d × 8 weeks), rigorous PCT required, possible transaminase elevation (10-20% of users), degraded lipid profile, limited human safety corpus (essentially preclinical + phase 1). DILI cases reported. Typical dose 10-20 mg/d × 6-8 weeks, single morning intake. PCT clomid + nolvadex 4-6 weeks required. Not suited for women (virilization possible) nor adolescents.

Combinaison ?

The YK-11 + RAD-140 combo is popular in some underground bodybuilding stacks but inadvisable: two compounds with concerning hepatic profile and limited human corpus, stacking risks without clearly additive anabolic benefit. If still combined: YK-11 10 mg/d + RAD-140 15 mg/d × 6 weeks maximum, followed by robust PCT (hCG 1500 IU EOD × 10 days then clomid 50/50/25/25 mg + nolvadex 40/20/20/20 mg × 6 weeks). Strict monitoring: ALT, AST, GGT, total and direct bilirubin at W0 then every 2 weeks during the cycle; complete lipids with apoB and HDL, T total, LH, FSH at W0/W4/W8 of the cycle. Hepatoprotectors (TUDCA 500-1000 mg/d, NAC 1200 mg, milk thistle 600 mg) recommended as support. Any sign of hepatitis (jaundice, dark urine, skin pruritus) or ALT elevation > 3× normal requires immediate stop with hepatology consultation. Regular zone 2 cardio (30-45 min × 3-4 times per week) to support cardiovascular profile during suppression. Minimum 12-16 week break before any new SARM cycle, with complete panel back to normal. Sample 6-week experimental timeline: W0 baseline complete panel + hepatology assessment, W1 start, W2 first ALT/AST + bilirubin check (critical for YK-11), W3 mid-cycle ALT/AST + lipids + T total, W4 ALT/AST + bilirubin recheck, W6 last dose, W6 PCT start immediately, W12 PCT end, W16 post-PCT recovery and hepatic confirmation. Any ALT > 3× normal or bilirubin > 2× baseline forces immediate cycle termination. Independent lab testing imperative: both compounds in the underground market have 40-70% mislabeling rate per various independent analyses — verify product with Janoshik or AnaboLab (~50 €) before starting. Practical dose split: take both compounds in single morning dose with breakfast.

FAQ

Is YK-11 really a SARM?: No, technically not. YK-11 has a steroidal structure (DHT-derivative) unlike true SARMs (LGD-4033, RAD-140, ostarine) which are non-steroidal. Its 'SARM' classification is marketing: Kanno 2011 and 2013 described its mechanisms (partial AR agonism + myostatin inhibition) but it does not have the muscular selectivity of true SARMs. Practical consequence: hepatotoxic profile probably more marked than classic SARMs, and nonexistent human corpus. Its classification remains debated in the literature.
Does myostatin inhibition really work in humans?: Theoretically yes, but the magnitude of YK-11 effect in humans has not been demonstrated in clinical studies. Kanno 2013 shows in vitro and in mice an elevation of follistatin and inhibition of myostatin, with associated muscular hypertrophy. The human translation remains hypothetical. User feedback suggests faster gains than LGD-4033 or ostarine, but without rigorous documentation, these effects could be attributable to partial androgenic activity rather than myostatin inhibition.
Does YK-11 cause transaminase elevation?: Empirically yes, frequently. User reports and case studies (DILI under YK-11) suggest ALT/AST elevations 2-5× normal in majority of users at 10-15 mg/d × 6 weeks. Suspected mechanism: hepatic metabolism of a steroidal compound with aggression pathway similar to 17α-alkylated oral AAS. Mandatory monitoring. Hepatoprotectors recommended. Very short cycles (< 6 weeks) if used.
What realistic gains with YK-11?: Difficult to quantify due to lack of clinical studies. User reports at 10 mg/d × 6 weeks: +3 to +5 kg raw lean mass, of which some potentially linked to simple androgenic activity rather than myostatin inhibition. Strength up +5-10%. Net gains retained at 3 months post-PCT: +2 to +3 kg attributable to YK-11. The gains/risks ratio (hepatotoxicity, product purity, suppression) is unfavorable compared to LGD-4033 or ostarine.
What PCT after YK-11?: Start 3-4 days after last intake (half-life ~6-10 h). Robust scheme: clomid 50/50/25/25 mg × 4-6 weeks + nolvadex 40/20/20/20 mg. T total, LH, FSH panel at W6 post-PCT. Suppression under YK-11 appears more marked than under classic SARMs per user reports, justifying reinforced PCT. If T < 300 ng/dL at W6, extend 2 weeks.
Why is YK-11 less documented?: Compound synthesized in 2011 by Kanno and colleagues without pharmaceutical clinical follow-up (never entered official human phase 1). All human reports come from recreational use without control. No GSK, Glaxo or other big pharma phase 1. Consequence: pharmacokinetic profile, dose-response, long-term safety totally uncharacterized in humans. Any use is experimental, the market offers only underground products of variable purity.
Is YK-11 suitable for women?: Strictly no. Steroidal compound with androgenic structure, unknown pharmacological profile in women, high and unpredictable virilization risk. No reason to take YK-11 in women when ostarine and anavar offer much better documented alternatives. If SARMs for women: ostarine 5-10 mg/d × 6-8 weeks remains the safest experimental standard.
YK-11 or RAD-140 for advanced users?: RAD-140 for the majority of cases. RAD-140, despite its limited human corpus, has at least phase 1 and solid preclinical studies (Miller 2010, Solomon 2019). YK-11 has almost no human data and a concerning hepatic profile. For advanced users seeking a more potent SARM than LGD-4033, RAD-140 remains the more rational option. YK-11 is only justified in very targeted experimentation with reinforced monitoring.

YK-11 vs RAD-140: complete comparison (myostatin vs potent SARM)

Critère	yk-11	rad-140
Class	Partial AR agonist + myostatin inh.	Non-steroidal SARM
Structure	Steroidal (DHT-derivative)	Non-steroidal
Half-life	~6-10 h	~16-20 h
Hepatotoxicity	Moderate to high	Moderate
HPG axis suppression	Moderate to strong	Moderate to strong
Typical dose	5-15 mg/d	10-20 mg/d
Human studies	Virtually nonexistent	Preclinical + limited phase 1
Risk-benefit	Poorly characterized	Poorly characterized

Quand choisir yk-11

Quand choisir rad-140

Combinaison ?

FAQ

Is YK-11 really a SARM?: No, technically not. YK-11 has a steroidal structure (DHT-derivative) unlike true SARMs (LGD-4033, RAD-140, ostarine) which are non-steroidal. Its 'SARM' classification is marketing: Kanno 2011 and 2013 described its mechanisms (partial AR agonism + myostatin inhibition) but it does not have the muscular selectivity of true SARMs. Practical consequence: hepatotoxic profile probably more marked than classic SARMs, and nonexistent human corpus. Its classification remains debated in the literature.
Does myostatin inhibition really work in humans?: Theoretically yes, but the magnitude of YK-11 effect in humans has not been demonstrated in clinical studies. Kanno 2013 shows in vitro and in mice an elevation of follistatin and inhibition of myostatin, with associated muscular hypertrophy. The human translation remains hypothetical. User feedback suggests faster gains than LGD-4033 or ostarine, but without rigorous documentation, these effects could be attributable to partial androgenic activity rather than myostatin inhibition.
Does YK-11 cause transaminase elevation?: Empirically yes, frequently. User reports and case studies (DILI under YK-11) suggest ALT/AST elevations 2-5× normal in majority of users at 10-15 mg/d × 6 weeks. Suspected mechanism: hepatic metabolism of a steroidal compound with aggression pathway similar to 17α-alkylated oral AAS. Mandatory monitoring. Hepatoprotectors recommended. Very short cycles (< 6 weeks) if used.
What realistic gains with YK-11?: Difficult to quantify due to lack of clinical studies. User reports at 10 mg/d × 6 weeks: +3 to +5 kg raw lean mass, of which some potentially linked to simple androgenic activity rather than myostatin inhibition. Strength up +5-10%. Net gains retained at 3 months post-PCT: +2 to +3 kg attributable to YK-11. The gains/risks ratio (hepatotoxicity, product purity, suppression) is unfavorable compared to LGD-4033 or ostarine.
What PCT after YK-11?: Start 3-4 days after last intake (half-life ~6-10 h). Robust scheme: clomid 50/50/25/25 mg × 4-6 weeks + nolvadex 40/20/20/20 mg. T total, LH, FSH panel at W6 post-PCT. Suppression under YK-11 appears more marked than under classic SARMs per user reports, justifying reinforced PCT. If T < 300 ng/dL at W6, extend 2 weeks.
Why is YK-11 less documented?: Compound synthesized in 2011 by Kanno and colleagues without pharmaceutical clinical follow-up (never entered official human phase 1). All human reports come from recreational use without control. No GSK, Glaxo or other big pharma phase 1. Consequence: pharmacokinetic profile, dose-response, long-term safety totally uncharacterized in humans. Any use is experimental, the market offers only underground products of variable purity.
Is YK-11 suitable for women?: Strictly no. Steroidal compound with androgenic structure, unknown pharmacological profile in women, high and unpredictable virilization risk. No reason to take YK-11 in women when ostarine and anavar offer much better documented alternatives. If SARMs for women: ostarine 5-10 mg/d × 6-8 weeks remains the safest experimental standard.
YK-11 or RAD-140 for advanced users?: RAD-140 for the majority of cases. RAD-140, despite its limited human corpus, has at least phase 1 and solid preclinical studies (Miller 2010, Solomon 2019). YK-11 has almost no human data and a concerning hepatic profile. For advanced users seeking a more potent SARM than LGD-4033, RAD-140 remains the more rational option. YK-11 is only justified in very targeted experimentation with reinforced monitoring.