YK 11 by Dragon Pharma

Dragon Pharma Research Compound

YK-11

Myostatin Inhibitor SARM•10 mg/tab
Class Steroidal Partial AR Agonist / Follistatin Inducer
Half-Life ~6–10 hours
Mechanism AR Partial Agonism + Myostatin Inhibition
Evidence Base In Vitro Only — No Animal / Human Trials
Pack 100 tabs
Form Oral Tablet
Manufactured by Dragon Pharma Third-Party Tested
Availability: In Stock
$145.00
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YK-11 — Steroidal Myostatin Inhibitor / Partial AR Agonist by Dragon Pharma

YK-11 is Dragon Pharma's formulation of the most pharmacologically unique compound in the SARM category at 10mg per tablet — a steroidal partial androgen receptor agonist that simultaneously upregulates Follistatin to inhibit myostatin, combining two distinct anabolic mechanisms in one molecule. The "SARM" label applied to YK-11 is a simplification: unlike all other SARMs in this range (Ostarine, LGD-4033, S23, GW-501516, SLU-PP-332), which are non-steroidal synthetic ligands, YK-11 is a synthetic steroid structurally derived from 5α-dihydrotestosterone (DHT) — with a unique C17 ester that confers oral bioavailability and the partial AR agonist + Follistatin induction profile that distinguishes it from any other compound in performance use. Its evidence base is currently limited to in vitro cell culture studies — no published animal or human pharmacokinetic data exists.

Also searched as: YK-11 10mg, YK11 myostatin inhibitor, YK-11 SARM, YK 11 Dragon Pharma, Follistatin inducer.

Why YK-11 Is Not a Conventional SARM — The Structural Reality

This distinction is the most consistently omitted fact in YK-11 content:

  • Conventional SARMs (Selective Androgen Receptor Modulators) are non-steroidal synthetic compounds — they were designed specifically to bind androgen receptors with a non-steroidal scaffold, aiming to separate anabolic effects (muscle, bone) from androgenic effects (prostate, scalp). Ostarine, LGD-4033, S23 and RAD-140 are all non-steroidal small molecules
  • YK-11 is a synthetic steroid — it shares a steroidal four-ring backbone with DHT, with modifications that make it orally active and create its partial AR agonist profile. Specifically, YK-11 is a C17-methyl-C21-ester derivative of 19-nor-DHT (structurally closer to nandrolone metabolites than to conventional SARMs)
  • This steroidal structure has important implications: unlike non-steroidal SARMs which are metabolised by non-steroidal pathways, YK-11's metabolism may follow steroidal metabolic pathways with potentially different hepatic and endocrine consequences than non-steroidal SARMs
  • The "SARM" designation persists in the performance community because YK-11 demonstrates some tissue selectivity — partial AR agonism rather than full agonism — but it is more accurately described as a synthetic steroidal partial androgen receptor agonist with Follistatin-inducing properties

The Dual Mechanism — AR Partial Agonism and Follistatin Induction

YK-11's anabolic potential derives from two distinct mechanisms operating simultaneously:

  • Partial AR Agonism: YK-11 binds the androgen receptor but activates only a subset of the receptor's downstream signalling compared to full agonists like DHT or testosterone. The partial agonism produces anabolic gene expression in muscle tissue — protein synthesis, satellite cell activation — while potentially producing less complete androgenic effects than a full AR agonist. In practice at higher doses, the distinction from full agonism becomes less clear
  • Follistatin Induction (Myostatin Inhibition): Myostatin (GDF-8) is a TGF-β family protein that functions as a negative regulator of skeletal muscle mass — it limits muscle growth as a biological ceiling. Follistatin is the endogenous antagonist of myostatin — it binds and inactivates myostatin, removing the growth ceiling. YK-11 was shown in cell culture (Kanno et al., 2013, Biology of Chemistry) to significantly upregulate Follistatin expression in C2C12 myoblasts — the muscle precursor cell line. By inducing Follistatin production, YK-11 indirectly inhibits myostatin, theoretically removing or raising the genetic ceiling on muscle mass
  • The combination of direct AR activation (muscle protein synthesis) plus Follistatin-mediated myostatin inhibition (removing the growth ceiling) gives YK-11 its theoretical superposition of anabolic mechanisms that no other SARM or conventional AAS provides simultaneously

The Evidence Gap — Critical Context

This is the most important section for any user considering YK-11:

  • YK-11's entire published scientific evidence base consists of in vitro studies only — specifically Kanno et al. (2013) demonstrating AR binding, partial agonism and Follistatin induction in cultured cell lines. No published peer-reviewed animal pharmacokinetic data exists. No human trials have been conducted or published
  • In vitro results in cell culture do not reliably predict in vivo pharmacokinetics, bioavailability, metabolism, tissue distribution or safety. The Follistatin induction observed in C2C12 cells may or may not translate to meaningful Follistatin elevation in living skeletal muscle — which operates in a very different biochemical environment than cell culture
  • This places YK-11 in a categorically different evidence tier from even preclinical-only SARMs like S23 (which has rodent in vivo data) — YK-11's in vivo behaviour is essentially uncharacterised in published literature
  • Community use and anecdotal reports provide the only practical performance data — which consistently suggest significant anabolic effects and significant HPG suppression, but are not peer-reviewed and cannot characterise safety with the reliability of controlled studies

YK-11 in the Full SARM/Research Compound Hierarchy

Compound Structure Mechanism Evidence Level HPG Suppression
Ostarine Non-steroidal Partial AR agonist Phase III human trials Mild
LGD-4033 Non-steroidal Full AR agonist Phase I human trial Significant
S23 Non-steroidal Full AR agonist Rodent in vivo High to complete
YK-11 Steroidal (DHT-derived) Partial AR agonist + Follistatin induction In vitro only Significant (anecdotal)

Effects and Benefits

  • Dual anabolic mechanism — AR activation plus Follistatin-mediated myostatin inhibition; theoretically the most comprehensive anabolic signalling available from a single oral compound
  • Lean mass gains — consistent with significant AR agonism; community reports suggest LGD-4033-comparable or superior lean mass accumulation
  • Strength gains — significant; reported as one of YK-11's most prominent effects
  • Muscle fullness and density — consistent with both AR and anti-myostatin mechanism activity
  • No aromatisation — steroidal but no estrogenic conversion at typical doses

Dosage and Administration

Experience Level Daily Dose Cycle Length PCT
First YK-11 cycle 5–10 mg/day 6 weeks Full PCT — mandatory
Experienced 10–15 mg/day 6–8 weeks Full PCT; HCG advisable

The ~6-10 hour half-life requires twice-daily dosing for stable blood levels — split morning and evening. Given the steroidal structure and significant suppression reports, hepatic monitoring (ALT/AST) is advisable at higher doses — unlike non-steroidal SARMs, YK-11's steroidal scaffold may have hepatic metabolism consequences that are not fully characterised. PCT with Clomid or Nolvadex is mandatory; begin 24-48 hours after the last tablet.

Side Effects

  • HPG suppression — significant; comparable to LGD-4033 or greater at higher doses; testosterone recovery requires full PCT
  • Potential hepatotoxicity concern — steroidal structure with unclear hepatic metabolism; liver enzyme monitoring advisable at 10-15mg/day doses
  • Androgenic effects — acne, possible hair acceleration; steroidal androgen with partial AR agonism still carries androgenic side effect potential
  • No estrogenic effects documented — no aromatisation pathway identified in vitro

Stacking Context

  • MK-677 — non-suppressive GH/IGF-1 elevation alongside YK-11's dual anabolic mechanism; injectable-free mass stack with three complementary mechanisms (AR, Follistatin/myostatin, GH/IGF-1)
  • GW-501516 (Cardarine) — non-suppressive endurance and fat oxidation support during a YK-11 cycle; addresses cardiovascular demands of high-volume training without additional HPG burden

"YK-11 is not a conventional SARM — it is a synthetic steroid that partially agonises the androgen receptor while upregulating Follistatin to inhibit myostatin. The combination of two anabolic mechanisms from one oral compound is theoretically compelling; the absence of any published in vivo data demands that users apply greater caution than with compounds that have human or animal pharmacokinetic data."

Storage and Handling

Store YK-11 at room temperature, away from direct sunlight and moisture. Keep in original packaging until use.

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Not in the strict pharmacological sense. Conventional SARMs are non-steroidal synthetic compounds designed to bind androgen receptors with a non-steroidal scaffold. YK-11 is a synthetic steroid structurally derived from 5α-dihydrotestosterone (DHT) — it has the four-ring steroidal backbone, not a non-steroidal small molecule structure. It demonstrates some AR selectivity (partial agonism rather than full), which is why the "SARM" label has stuck in the performance community, but it is more accurately described as a steroidal partial androgen receptor agonist with Follistatin-inducing properties.

Myostatin (GDF-8) is a TGF-β signalling protein that functions as the body's primary brake on skeletal muscle growth — it limits how much muscle can be built, acting as a biological ceiling on hypertrophy. Follistatin is an endogenous protein that binds and neutralises myostatin, removing this growth ceiling. YK-11 does not directly bind myostatin — instead, it upregulates Follistatin production in muscle cells (demonstrated in C2C12 myoblast cell culture by Kanno et al., 2013), indirectly removing the myostatin brake. This mechanism is theoretically additive with YK-11's direct AR agonism — two anabolic signals from one compound.

Currently, the published evidence consists only of in vitro cell culture studies — primarily Kanno et al. (2013) demonstrating AR partial agonism and Follistatin upregulation in C2C12 myoblast cell lines. No peer-reviewed animal pharmacokinetic studies have been published. No human trials exist. This places YK-11 in the lowest evidence tier of all compounds in the Dragon Pharma range — below S23 (which has rodent in vivo data), and far below LGD-4033 (Phase I in humans) or Ostarine (Phase III). In vitro results in cell culture cannot reliably predict bioavailability, metabolism, tissue distribution or safety in living organisms.

Yes — community use consistently reports significant HPG axis suppression comparable to LGD-4033. Despite being labelled a SARM, YK-11's steroidal structure and significant AR activity produce meaningful testosterone suppression requiring full SERM PCT. PCT begins 24-48 hours after the last tablet. At 10-15mg/day for 6-8 weeks, a 4-6 week PCT with Clomid and/or Nolvadex is appropriate. Given YK-11's steroidal structure and potentially greater suppression depth at higher doses, HCG use during or before PCT is more advisable than with mild non-steroidal SARMs.

Potentially — and this is an important unresolved question. YK-11's steroidal structure undergoes hepatic metabolism through steroidal metabolic pathways rather than the non-steroidal pathways of conventional SARMs. Whether this produces hepatotoxic metabolites or elevated liver enzyme levels is not established in published literature. Community reports include some cases of liver enzyme elevation at higher doses. Liver enzyme monitoring (ALT/AST at baseline and mid-cycle) is advisable for anyone using YK-11 at 10mg/day or above — prudent given the absence of published safety data and the steroidal metabolic pathway.

Both are reported as among the most anabolically potent oral compounds in the SARM/research category. LGD-4033 has Phase I human pharmacokinetic data confirming meaningful lean mass gains at just 1mg/day, with a well-characterised safety and suppression profile. YK-11 has only in vitro evidence but community reports suggest comparable or superior lean mass gains — potentially attributable to the additional Follistatin/myostatin mechanism. LGD-4033 offers significantly better-characterised safety data; YK-11 offers the theoretical advantage of dual anabolic mechanisms. For users prioritising evidence-based safety alongside potency, LGD-4033 is the more defensible choice.

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