AC-262536

Partial Agonism at the Androgen Receptor#

AC-262536 is a non-steroidal small molecule that binds the androgen receptor (AR) with nanomolar affinity but activates it only partially. Unlike testosterone or full-agonist SARMs like RAD-140 and LGD-4033 — which drive AR-mediated transcription to maximal output — AC-262 ceilings at roughly two-thirds of testosterone's signalling capacity. That partial-agonist profile is the defining feature: it sets a lower ceiling on both the upside (muscle signalling) and the downside (HPTA suppression, androgenic load).

"AC-262536 is a potent and selective androgen receptor ligand, which functioned as a partial agonist with maximal efficacy around 66% relative to testosterone in androgen-dependent tissues, but with markedly diminished effects in androgenic tissues such as the prostate." — Piu F. et al., Journal of Steroid Biochemistry and Molecular Biology, 2008

In practical terms: expect modest, steady lean gain and strength creep rather than the explosive recomp of a full-agonist SARM. The trade-off is a gentler suppression curve and lighter androgenic pressure on skin and scalp.

Tissue Selectivity — Muscle vs Prostate#

The whole point of a SARM is anabolic signalling in muscle without the androgenic cost in prostate, skin, and scalp. AC-262 shows this split cleanly in the Acadia preclinical work: in castrated rats, chronic oral dosing built levator ani muscle at levels approaching testosterone, while prostate tissue barely responded.

"In castrated rats, chronic oral dosing of AC-262536 for 14 days stimulated levator ani muscle growth at levels comparable to 66% of the androgenic effect from testosterone propionate, but produced only 27% of the prostate weight increase." — Piu F. et al., Journal of Steroid Biochemistry and Molecular Biology, 2008

That gives a calculated anabolic:androgenic ratio around 2.45:1 — modest compared to RAD-140's ~90:1 on paper, but with a meaningfully prostate-sparing profile. For hair-conscious users, this matters: less AR activation in peripheral androgen-sensitive tissue means less pressure on the scalp than with a full-agonist SARM, though AR activation is still AR activation — topical AR antagonists (RU58841, pyrilutamide) remain the hedge, since oral finasteride won't touch SARM-driven signalling.

Central AR Engagement and HPTA Suppression#

AC-262 crosses into the hypothalamus and pituitary, where AR agonism triggers negative feedback — LH and FSH drop, and endogenous testosterone production follows. This is the mechanism behind post-cycle suppression. Because AC-262 is a partial agonist, the feedback signal it generates centrally is blunted relative to a full agonist at the same receptor occupancy — which is why at 10 mg for 8 weeks most users report mild suppression and natural recovery without a SERM. Push to 20–30 mg or extend the cycle, and the partial-agonist cushion erodes; LH suppression becomes meaningful and a mini-PCT with Nolvadex or enclomiphene becomes the sensible call.

This is also why bloodwork matters more than forum vibes on this compound. "Mild" is a population average — individual recovery varies.

Oral Bioavailability and Clearance#

AC-262 is orally active, which is why community protocols standardize on once-daily morning dosing with or without food. Rat PK from the Piu work showed clean dose-response on oral administration, and anti-doping assays have confirmed systemic exposure in humans.

"AC-262536 was included in our panel of analytes, and the compound was clearly detected in urine at low ng/mL concentrations following oral administration, confirming its systemic bioavailability and excretion profile relevant for anti-doping controls." — Sobolevsky T. & Ahrens B., Drug Testing and Analysis, 2021

Human half-life has not been formally characterized — the ~10–24 hour window cited online is inferred from dosing practice, not measured. Functionally, once-daily dosing produces stable effects, and there's no signal that split dosing adds anything. Anyone running it in a drug-tested context should note that modern LC-MS/MS panels pick it up alongside the mainstream SARMs.

Downstream Anabolic Signalling in Muscle#

Once AC-262 docks the AR in skeletal muscle, the downstream cascade is the standard androgen-response pathway: the AR-ligand complex translocates to the nucleus, binds androgen response elements (AREs) on DNA, and upregulates transcription of genes governing protein synthesis, satellite cell activation, and IGF-1 expression in muscle tissue. The partial-agonist nature means this transcriptional push is submaximal — hence the modest ~0.5–0.6 lb/week lean gain ceiling rather than the 1+ lb/week seen with full-agonist SARMs or low-dose testosterone.

The practical read: AC-262 is a signal modifier, not a signal overdrive. It nudges muscle protein synthesis upward in a prostate-sparing way, which is exactly what you want from a mild recomp tool, a first SARM cycle, or a bridge between heavier runs — and exactly why it disappoints anyone expecting RAD-140-tier gains from it.

Common (most users)#

• Mild HPTA suppression — LH dips are reported at 15 mg+ and become more reliable at 20–30 mg. Partial agonism blunts the crash you'd see on RAD-140 or LGD-4033, but it's not zero. Mitigation: cap solo runs at 8 weeks, titrate up from 10 mg, and confirm recovery with post-cycle bloods (LH, FSH, total T) 2–3 weeks after dropping.
• Mild lipid shift (HDL drop) — expected on any oral SARM. Mitigation: cardio 3×/week, keep saturated fat reasonable, add 2–4 g EPA/DHA daily, and pull a lipid panel at week 4 to see where you are.
• Slight liver enzyme elevation — ALT/AST creep is common at 20 mg+. Mitigation: TUDCA 500 mg/day on cycle, avoid alcohol, and recheck LFTs mid-cycle. Back off if ALT trends past ~2× upper limit.
• Mild androgenic skin effects (acne, oilier skin) — milder than RAD-140 at equivalent doses given the 2.45:1 ratio, but not absent. Mitigation: standard topical routine (adapalene, benzoyl peroxide), manage it like any AR-driven breakout.
• Low-grade scalp shedding in hair-prone users — SARM AR activation isn't addressed by oral 5-AR inhibitors. Mitigation: topical RU58841 or pyrilutamide, or topical finasteride as an AR-pathway-adjacent hedge.

"AC-262536 … stimulated levator ani muscle growth at levels comparable to 66% of the androgenic effect from testosterone propionate, but produced only 27% of the prostate weight increase." — Piu et al. 2008

Uncommon (dose-dependent or individual)#

• More pronounced suppression at 25–30 mg — users pushing the top of the range for the full 8 weeks more often need a mini-PCT. Check LH/FSH and total T at week 6; if LH is floored, plan on Nolvadex 20/20/10/10 or enclomiphene 12.5 mg/day × 3–4 weeks.
• RUQ discomfort / upper-abdominal ache — reported at 20 mg+, usually resolves on dose reduction. If it persists, stop the compound and pull a liver panel including GGT.
• Libido swings — most users report neutral libido; a minority report either bump or dip. Usually resolves post-cycle. If libido tanks and doesn't recover by week 3 post, run bloods rather than guessing.
• Mood flatness / mild aggression — rare and dose-linked. Back off 5–10 mg and reassess.
• Moderate LDL rise — less consistent than the HDL drop but worth watching if you have baseline dyslipidemia. Recheck at week 4.

Rare but serious#

• Meaningful transaminitis (ALT/AST >3× ULN) — uncommon but reported. Warning signs: persistent RUQ pain, dark urine, scleral yellowing, unexplained fatigue. Stop immediately and pull a full hepatic panel.
• Significant lipid derangement — HDL floored, LDL spiking, trigs climbing. Warning sign: panel at week 4 shows an aggressive shift. Stop if the movement is severe; this is the delta that matters long-term, not the absolute numbers on a single draw.
• Prolonged HPTA recovery — the rare user who stacks AC-262 on top of other SARMs and runs long ends up with slow recovery. Warning sign: LH still suppressed 4+ weeks post-cycle. Plan a proper SERM PCT and retest at 8 weeks post.
• Counterfeit-compound reactions — AC-262 is low-volume in the grey market; mislabeled product (often LGD-4033 or RAD-140 in the vial) produces disproportionate sides. If sides feel like a full-agonist SARM, they probably are. Insist on a batch-matched HPLC COA before running.

Hard contraindications#

• Pregnancy or lactation — AR agonism is a hard no.
• Women pursuing near-term conception — AR activity in utero is a category risk; do not run this on the "just in case" window.
• Pre-existing untreated dyslipidemia or hypertension — address baseline lipids and BP before cycling any oral SARM. AC-262 will make both worse.
• Active liver disease, viral hepatitis, or current hepatotoxic medication stack — including concurrent orals, high-dose NSAID use, or heavy alcohol intake. Do not add another hepatic load.
• Drug-tested competition — AC-262536 is detectable on modern WADA-tier LC-MS/MS panels. Do not assume "niche SARM = invisible."

"AC-262536 … was clearly detected in urine at low ng/mL concentrations following oral administration, confirming its systemic bioavailability and excretion profile relevant for anti-doping controls." — Sobolevsky & Ahrens 2021

"AC-262536 is now covered by advanced screening protocols used in anti-doping laboratories, indicating its relevance and detectability alongside classic SARMs like ostarine and LGD-4033." — Mazzarino et al. 2022

Gender-specific and PCT notes#

Women: not recommended for women of reproductive age. Virilization risk (voice deepening, clitoral enlargement, menstrual disruption) applies to any AR agonist, and some virilization effects are permanent. Women who run it anyway stay at ≤5 mg/day and stop at the first sign of vocal or clitoral changes — these are non-negotiable stop-signals, not "push through it" sides.

Men — PCT: at 10 mg × 8 weeks, most users recover natural production without a SERM; confirm with LH/FSH/total T at 2–3 weeks post. At 15–20 mg, have a mini-PCT ready and use it if LH is still suppressed at week 8. At 25–30 mg or stacked runs, plan on SERM PCT from the start — Nolvadex 20/20/10/10 or enclomiphene 12.5 mg/day for 3–4 weeks, starting 24 hours after your last dose. Retest bloods 4 weeks after PCT ends. If LH hasn't recovered by then, that's a conversation with bloodwork in hand — not a reason to run another cycle on top.