Ostarine
Extensively StudiedNon-steroidal SARM with bone/muscle tropism — milder than LGD-4033 in both efficacy and HPG suppression, but not innocent. | SARM · Oral
Aliases (6)
▸ Cycle structure & PCT AAS oral
Ramp dose over week 1, hold steady through cycle weeks. Track baseline labs (TT/FT/E2/SHBG/HCT/lipids/LFTs) at week 0; recheck at week 4 and end-of-cycle.
On the last dose, the ester clears over its half-life window . PCT begins after the active compound has cleared.
Standard PCT is enclomiphene 12.5-25 mg/day or clomid 50/50/25/25 over 4 weeks (or nolvadex 20/20/10/10). HCG bridge optional during cycle to preserve testicular volume + faster restart. Bloodwork at PCT week 4 + 8 to confirm HPG axis recovery (LH, FSH, TT back to baseline).
▸ Overview TL;DR
Non-steroidal SARM with bone/muscle tropism — milder than LGD-4033 in both efficacy and HPG suppression, but not innocent. SKIP-AT-20 HIGH: real but smaller HPG-axis suppression, scattered case reports of cholestatic hepatotoxicity, no long-term safety data, and the only legal source is FDA-prohibited research-chem with rampant adulteration. There is zero indication in a healthy 20yo with peak natural T, and no upside that creatine + sleep + protein doesn't deliver more safely.
▸ Mechanism of action
Ostarine (MK-2866 / enobosarm) is a non-steroidal aryl-propionamide developed at the University of Tennessee by Dalton/Steiner/Miller and licensed to GTx Inc. It binds the androgen receptor (AR) as a partial agonist with conformational selectivity — its ligand-receptor complex recruits a different set of nuclear coactivators than testosterone or DHT, producing tissue-selective transcription: strong anabolic effects in muscle and bone, weaker effects in prostate, sebaceous glands, hair follicles, and (to a lesser extent) the HPG axis. This selectivity is the entire pharmacological pitch of SARMs vs. AAS.
Ostarine specifically:
- Structurally a non-steroidal aryl-propionamide (chemically related to bicalutamide, an AR antagonist used in prostate cancer — same scaffold, opposite functional outcome).
- Oral bioavailability (rats) ~80%; t-max ~3-6h in humans; half-life ~24h (supports once-daily dosing).
- Metabolism via CYP3A4 with phase II glucuronidation; renal/biliary excretion of metabolites.
- AR binding affinity high but partial-agonist Emax — ostarine cannot drive AR-mediated transcription as fully as DHT in any tissue, which is why effects (and side effects) are dose-and-duration-dependent but plateau lower than AAS.
HPG suppression (the relevant downside for a 20yo):
- Ostarine does suppress LH, FSH, and total testosterone in healthy male subjects in dose-dependent fashion. Published Phase 1/2 data show ~25-40% drops in total T at 3mg/day across 12-16 weeks — milder than LGD-4033 (~50-65% at 1mg/day) but not zero. Recovery typically within 4-6 weeks of cessation in young men with intact axes; longer in older or already-marginal users.
- The AR is also expressed at the hypothalamus and pituitary; partial agonism still produces partial negative feedback. The "non-suppressive SARM" framing common in bodybuilding forums is wrong.
What ostarine is NOT:
- Not aromatized (no estradiol elevation from ostarine itself — though endogenous T suppression can shift the T:E2 ratio).
- Not 5α-reduced to a more potent androgen (unlike testosterone → DHT). This is part of the prostate/scalp sparing.
- Not hepatically alkylated (unlike oral AAS like methyltestosterone, oxandrolone, stanozolol). The hepatotoxicity reports are not 17α-alkylation-mediated; mechanism appears cholestatic/idiosyncratic.
- Not a true tissue-exclusive agonist — "selective" is relative, not absolute.
▸ Pharmacokinetics Approximate
Approximate decay curve drawn from the half-life mention(s) in the source notes. Real PK data not yet ingested per compound.
▸Quality indicators4 checks
▸ What to expect From notes
- 1Week 1-2Nothing perceptible most days; occasional users report mild appetite increase, slightly improved gym recov…
- 2Week 3-6Recovery between training sessions feels noticeably better; lean mass starts visibly accumulating; pump/fu…
- 3Week 6-12~3-6 lbs LBM, ~5-10% strength gains on compound lifts at moderate doses (15-25mg/day). Joint comfort often…
▸ Side effects + safety
Common (>10% users at typical 15-25 mg/day):
- HPG suppression — dose-dependent T drop (~25-40% at 3mg/day; higher at 25mg/day). LH/FSH suppression follows.
- Mild HDL reduction — ostarine reduces HDL cholesterol in essentially all users at 8+ weeks. Magnitude varies (~10-30% drop).
- Mild ALT/AST elevation — often subclinical, often resolves on cessation; concerning when persistent or symptomatic.
Less common (1-10%):
- Cholestatic hepatotoxicity — clinically apparent jaundice, dark urine, pruritus, marked LFT elevation. Multiple published case reports, mostly young men, mostly resolves on cessation but recovery can take 1-3 months and a minority require hospitalization.
- Suppression-related symptoms in PCT — fatigue, low libido, mood drop in the 4-8 week recovery window.
- Mild gyno — rare, related to T:E2 shift during recovery rather than direct estrogenic activity (ostarine doesn't aromatize).
- Visual disturbances — uncommon but reported; mechanism unclear (some SARMs interact with retinoid receptors at high doses).
- Headache, GI upset, mild nausea — minor, typical research-chem side-effect grab-bag.
Rare-serious (<1% but worth knowing):
- Severe cholestatic hepatitis with prolonged recovery — published cases; mechanism appears idiosyncratic (not predictable by dose alone). Some users with 5-10 mg/day developed clinical hepatitis; others on 50 mg/day did not.
- Drug-induced liver injury requiring transplant evaluation — at least one published case.
- Rhabdomyolysis (rare, training-context confounded).
- Cardiac concerns from chronic HDL suppression — theoretical, no MACE data exist for SARMs in any population.
- Counterfeit / contamination-related toxicity — ostarine sold as "ostarine" has been independently lab-tested (Cohen et al. 2017, JAMA, n=44 SARM products: 52% accurate label, 39% contained no SARM, 9% contained SARM not on the label, 25% contained substances banned by FDA) — so a "side effect" can be from an entirely different undisclosed compound.
- WADA AAF / banned-list positives — long detection window (multiple weeks); ostarine metabolites are detectable in urine for 6-9 weeks at very low concentrations.
Specific watch periods:
- Weeks 4-8: First likely window for LFT derangement to appear — many published case reports cluster here.
- End of cycle and into PCT (week 8-16): HPG axis recovery monitoring. T, LH, FSH, E2, hematocrit at 2 and 6 weeks post-cycle.
- Lipid panel at 6 weeks on, end of cycle, and 6 weeks post: HDL trajectory.
▸Interactions9 compounds
- CreatineSynergisticindependent additive lean-mass effect, no pharmacological collision. A-tier rationale.
- Adequate protein (≥1.6 g/kg)Synergisticsubstrate for any anabolic stimulus. A-tier.
- Vitamin D + zinc + magnesium (Dylan's V4 already)Synergisticsupports endogenous T axis during PCT recovery.
- LGD-4033, RAD-140, other SARMs:AvoidCompounds suppression, no proven additive efficacy. Common community mistake.
- AAS (testosterone, trenbolone, anavar, etc.):AvoidDefeats the "milder than AAS" pitch; combines suppression and toxicity profiles.
- 17α-alkylated oral AAS (oxandrolone, methyltestosterone, stanozolol, oxymetholone):AvoidLiver-load stacking — ostarine's idiosyncratic hepatotoxicity plus 17α-alkyl liver strain is a known bad combination.
- Hepatotoxic medications or supplementsAvoid(acetaminophen ≥3g/day chronic, isoniazid, methotrexate, high-dose niacin, etc.).
- Heavy alcohol:AvoidLiver-load compounding.
- Other research-chem compounds with unknown contamination profilesAvoidmultiplies counterfeit risk.
▸References16 sources
POWER 1 + POWER 2 Phase 3 cancer cachexia trials — GTx press release / Lancet Oncology summary
70168-3/abstract) — pivotal Phase 3, mixed outcomes
Dalton et al. 2011, Journal of Cachexia, Sarcopenia and Muscle — Phase 2 ostarine in elderly
2011body composition Phase 2
Cohen et al. 2017, JAMA — Variability in label accuracy of SARM products
2017contamination / mislabeling data
FDA Consumer Update — Body Building Products with SARMs Prohibited
2017FDA position, 2017 + reaffirmed
FDA Warning Letters to SARM-containing supplement vendors, 2017 batch
2017regulatory action
Flores et al. 2020 — Ostarine-induced cholestatic liver injury case report
2020hepatotoxicity case literature
Bedi et al. 2021 — SARM hepatotoxicity case series, ACG Case Reports
2021hepatotoxicity case literature
Barbara et al. 2020 — SARM-associated hepatotoxicity in young man
2020hepatotoxicity case literature
Veru Inc. — enobosarm pipeline (ENABLAR-2 breast cancer, QUALITY weight loss)
current clinical program
Veru Q4 2024 / 2025 readouts — investor materials
2024partial readouts, mixed
USADA — SARMs banned substance profile
anti-doping context (S1.2)
WADA Prohibited List 2026 — S1.2 Other Anabolic Agents
2026current banned-list status
GTx Inc. enobosarm SEC filings 2013-2014
2013original sponsor regulatory documentation
Dalton, Steiner, Miller — original SARM medicinal chemistry, University of Tennessee
discovery / medicinal chemistry
Ostarine pharmacokinetics and metabolism — published Phase 1 data
PK/metabolism reference
Mohideen 2024 — SARM hepatotoxicity systematic review
2024most recent hepatotoxicity literature review