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DPreclinical / mechanistic only
No human data

ACP-105

ACP-105 is an experimental non-steroidal selective androgen receptor modulator (SARM) originally synthesized as a drug candidate (ACADIA Pharmaceuticals) and characterized as a partial agonist at the androgen receptor relative to testosterone. It has never completed human clinical trials, has no regulatory approval anywhere, and its safety in people is essentially unstudied — the only human exposure documented in the literature is a single 100 microgram oral dose given to generate urinary metabolites for anti-doping detection, which measured no safety or efficacy endpoints. It is sold as a research chemical and is used off-label by athletes and bodybuilders to try to gain muscle; it is banned in sport by WADA. Because there is essentially no human safety data, all risks are inferred from preclinical/computational work and from the known behavior of the SARM class. Concerning signals include a computational (in silico) prediction of hERG channel inhibition (potential cardiac/QT risk), predicted genotoxicity and even potential cyanide release from its benzonitrile structure, expected suppression of natural testosterone production (as with all androgen-receptor agonists), and the liver-injury concerns that have been reported clinically for other SARMs. Products sold as "ACP-105" are unregulated and frequently mislabeled or contaminated. This monograph leads with those uncertainties: no one can quote a reliable human risk profile for this compound.

Clinical readoutSARM · sarm
Hepatic strainNone
CardiovascularModerate
HPTA suppressionNone
Half-life
1.2 h
Route
Oral
Evidence
D
Active
Unknown in humans
1.2 h2.4 h3.5 h4.7 h5.9 h
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Not established in humans. An in silico ADME analysis predicted a short plasma half-life of approximately 1.18 hours; this is a computational estimate, not a measured human value.
Pharmacology

Mechanism of action

ACP-105 (2-chloro-4-[(3-endo)-3-hydroxy-3-methyl-8-azabicyclo[3.2.1]oct-8-yl]-3-methylbenzonitrile) is a non-steroidal ligand of the androgen receptor (AR) built on an N-substituted tropanol pharmacophore. It was identified in a high-throughput receptor selection and amplification (R-SAT) screen and characterized as a potent AR partial agonist relative to testosterone. As a SARM it is intended to produce tissue-selective anabolic signaling (muscle/bone) with a theoretically lower androgenic burden than testosterone; in castrated male rats it improved anabolic endpoints over a 2-week course (preclinical). Structurally related analogs from the same chemical series behaved as antiandrogens, including activity at the AR T877A mutant relevant to prostate cancer. Small structural differences within this series flip agonist/antagonist behavior. In gonadectomized transgenic mouse models it has also been used as an AR agonist to probe androgen effects on cognition, anxiety-like behavior and amyloid-beta handling. All mechanistic characterization is preclinical/receptor-level; tissue selectivity and the anabolic-to-androgenic ratio have not been validated in humans.
Kinetics

Pharmacokinetics

Half-life

Not established in humans. An in silico ADME analysis predicted a short plasma half-life of approximately 1.18 hours; this is a computational estimate, not a measured human value.

Active duration

Unknown in humans. Parent drug and metabolites have been detected in equine urine for up to ~72 hours after a single dose, reflecting metabolite elimination windows for doping detection rather than a defined human duration of pharmacologic effect.

Route

Oral (route used in rat, dog and the single documented human administration); the parent compound has also been detected in human hair in forensic/anti-doping screening.

Metabolism & clearance

Predominantly hepatic. In silico and in vitro/in vivo (rat, equine, human microsome) work indicates extensive phase I oxidation to mono-, bis- and tri-hydroxylated metabolites (with a dehydration pathway on the tropanol moiety) followed by phase II glucuronidation. CYP3A4 is the primary predicted enzyme (with contributions from CYP2C9, CYP2C19, CYP2D6). Metabolites are eliminated renally; no OCT2-mediated active renal secretion was predicted. High predicted plasma protein binding (77-99%) with <1% free fraction.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • Androgen receptor partial agonism (mechanistic/receptor-level characterization).
  • Improved anabolic parameters (e.g., muscle/anabolic endpoints) in castrated male rats over 2 weeks - preclinical only, not demonstrated in humans.
  • Reduced anxiety-like behavior and modulation of cognition/amyloid-beta handling in gonadectomized transgenic mouse models - preclinical only.
  • Marketed and used off-label by athletes/bodybuilders for claimed muscle and strength gains; these human benefits are unproven - no human efficacy trial exists.
  • Detectable in urine and hair, making it identifiable on anti-doping tests; it is prohibited in sport by WADA.
Safety

Adverse effects by system

Cardiovascular

No human data. A computational (in silico) toxicity study predicted hERG potassium channel inhibition, a signal associated with QT prolongation and arrhythmia risk; this is a modeling prediction only and has not been confirmed in any living system for ACP-105. Androgenic compounds as a class can adversely affect lipids and blood pressure, but this has not been measured for ACP-105.

Hepatic

No ACP-105-specific human hepatotoxicity data exist. It is an orally administered, CYP3A4-metabolized non-steroidal SARM; drug-induced liver injury has been reported clinically for other SARMs, so hepatic risk cannot be excluded, but there is no direct evidence for ACP-105.

Endocrine / HPTA

No human data. As an androgen receptor agonist it is mechanistically expected to suppress the hypothalamic-pituitary-gonadal axis (lowering LH, FSH and endogenous testosterone) via negative feedback, as seen with the SARM class; the magnitude, time course and reversibility in humans are unknown for ACP-105 specifically.

Reproductive

No human data. HPTA suppression predicts potential impairment of spermatogenesis and fertility and reduced endogenous testosterone as a class effect of AR agonists; not directly studied for ACP-105. Contraindicated in pregnancy on mechanistic grounds (androgenic teratogenic potential) - no data.

Neuropsychiatric

No human data. In rodent models ACP-105 reduced anxiety-like behavior and altered fear conditioning/sensorimotor performance; human neuropsychiatric effects (including the mood changes and aggression associated with androgens generally) have not been studied.

Renal

No human data. Metabolites undergo renal elimination; no OCT2-mediated active secretion was predicted in silico. No specific nephrotoxicity signal has been characterized, and absence of a signal reflects absence of study rather than demonstrated safety.

Hematologic

No human data. Androgens can raise hematocrit/erythropoiesis as a class effect; this has not been measured for ACP-105. An in silico analysis flagged predicted DNA/protein interaction and potential cyanide release from the benzonitrile moiety, raising theoretical genotoxic/toxicologic concern that remains unverified experimentally.

Dermatologic

No human data. In silico screening evaluated skin and eye irritation endpoints; androgenic effects such as acne and hair changes are plausible on a class basis but unstudied for ACP-105.

Recovery

HPTA suppression & recovery

Suppression: Expected but unquantified (no human data)

As an androgen receptor agonist, ACP-105 is mechanistically expected to suppress endogenous testosterone, LH and FSH through negative feedback, consistent with the SARM class; however, the degree and reversibility have never been measured in humans for this compound. Anyone who has used it and has symptoms of low testosterone (low libido, fatigue, mood changes, testicular atrophy) or who is planning use should consult an endocrinologist or physician for individualized evaluation and hormone testing. Recovery should be medically supervised; do not self-manage a 'restart.' This monograph does not endorse or describe any SERM-based or multi-drug recovery protocol - such decisions belong to a qualified endocrinologist.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Total and free testosterone, LH, FSH (baseline and follow-up to detect HPTA suppression)Liver function panel (ALT, AST, ALP, bilirubin)Lipid panel (total, LDL, HDL, triglycerides)Complete blood count including hematocrit/hemoglobinECG/QTc if any cardiac symptoms, palpitations, or concurrent QT-prolonging drugsEstradiol and PSA where clinically indicated by a physician

Cadence: Ideally a baseline before any exposure, then physician-directed follow-up (commonly every 4-8 weeks during any use and again after stopping). Because no validated human protocol exists, testing intervals should be set by a clinician, not self-directed.

Warning signs — seek care
  • Chest pain, palpitations, fainting, or irregular heartbeat - seek emergency care
  • Right-upper-quadrant abdominal pain, nausea, dark urine, jaundice, or itching (possible liver injury) - stop and seek care
  • Marked fatigue, loss of libido, testicular shrinkage, or mood disturbance (HPTA suppression)
  • Unusual bruising, headaches, visual changes, or very elevated blood pressure
  • Any new severe or unexplained symptom - discontinue and consult a physician
Do not use if

Contraindications

  • No established safe use in any population - not an approved medicine; benefit-risk is unknown.
  • Pregnancy and breastfeeding (mechanistic androgenic teratogenic potential; no data).
  • Anyone with, or at risk of, prostate or other androgen-sensitive cancer (AR-active compound; related analogs show AR activity relevant to prostate cancer).
  • Known or suspected QT prolongation, significant arrhythmia, or use of other QT-prolonging drugs (theoretical hERG-inhibition signal).
  • Pre-existing or active liver disease or elevated liver enzymes (oral, CYP3A4-metabolized SARM; class-level hepatic concern).
  • Competitive athletes subject to anti-doping rules (prohibited by WADA; detectable in urine and hair).
  • Adolescents / anyone with an open growth plate or developing endocrine axis.
  • Concurrent strong CYP3A4 inhibitors or inducers (predicted major CYP3A4 metabolism raises interaction/exposure uncertainty).
Combinations

Interaction profile

  • ModerateWith a thermogenic stimulant: Additive cardiovascular strain
  • ModerateWith an anabolic steroid: Hormonal
  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • The most important point: ACP-105 has no human safety data and no approval. Choosing not to use it is the only fully evidence-based way to avoid its unknown risks.
  • It is not a substitute for medically supervised testosterone therapy; anyone considering it for a hormonal or health reason should see a physician/endocrinologist instead.
  • Products sold as 'ACP-105' are unregulated research chemicals that are commonly mislabeled, underdosed, overdosed, or contaminated with other active SARMs or drugs - you cannot assume the contents match the label.
  • If used despite these warnings, get baseline bloodwork (testosterone, LH/FSH, liver panel, lipids, CBC) and repeat with a clinician; do not rely on 'feel.'
  • Stop immediately and seek medical care for chest pain, palpitations or fainting (possible cardiac effect), or for jaundice, dark urine, or right-upper-quadrant pain (possible liver injury).
  • Expect suppression of your own testosterone; if you develop low-testosterone symptoms, see an endocrinologist rather than self-treating, and do not undertake any self-directed SERM or drug 'recovery' protocol.
  • Avoid entirely if pregnant, trying to conceive, breastfeeding, an adolescent, or if you have liver disease, cardiac/QT risk, or androgen-sensitive cancer risk.
  • Competitive athletes: this is a WADA-prohibited substance detectable in urine and hair.
  • Disclose any use to your doctor, including before surgery or when starting new medications, because of possible CYP3A4 drug interactions.
Evidence

Citations (8)

Every clinical claim above is tied to a primary source. Overall evidence grade D — this compound lacks adequate human data; claims rest on preclinical or mechanistic evidence.

  1. 01

    ACP-105 is a novel non-steroidal SARM and androgen receptor partial agonist (relative to testosterone) discovered via R-SAT screening; it improved anabolic parameters in castrated male rats over 2 weeks, and structurally related analogs in the same series were antiandrogens including activity at the AR T877A prostate-cancer mutant.

    PreclinicalSynthesis, structure-activity relationships, and characterization of novel nonsteroidal and selective androgen receptor modulators.PMID 19856921 ↗

  2. 02

    In silico ADME: high GI absorption, moderate lipophilicity, strong plasma protein binding (77-99%, <1% free), predominant CYP3A4 metabolism (with CYP2C9/2C19/2D6), predicted short half-life ~1.18 h, predicted blood-brain-barrier penetration, no OCT2-mediated renal excretion, and predicted DNA/protein interaction with potential cyanide release.

    PreclinicalFirst multifaceted ADME profile of ACP-105 (CAS: 1048998-11-3): a novel non-steroidal selective androgen receptor modulator used as doping in sports-integrative in silico toxicological studies for clinical and forensic toxicology purposes.PMID 40928534 ↗

  3. 03

    In silico toxicity screening predicted cardiotoxicity via hERG inhibition, and evaluated genotoxicity (Ames), organ toxicity, and skin/eye irritation endpoints; the compound's human safety profile is described as insufficiently explored.

    PreclinicalToxicity of ACP-105: a substance used as doping in sports: application of in silico methods for prediction of selected toxicological endpoints.PMID 40064700 ↗

  4. 04

    Only documented human exposure: a single 100 microgram oral dose given to identify urinary metabolites (two monohydroxylated forms as main targets) for doping control - a metabolite-detection study with no safety or efficacy endpoints.

    Case reportA multivariate data analysis approach for the investigation of in vitro derived metabolites of ACP-105 in comparison with human in vivo metabolites.PMID 37972465 ↗

  5. 05

    SARMs including ACP-105 have been prohibited by WADA since 2008 and detected in doping-control samples despite none having full clinical approval; ACP-105 bears an N-substituted tropanol pharmacophore.

    ReviewDetection of SARMs in doping control analysis.PMID 28137616 ↗

  6. 06

    In gonadectomized transgenic mouse Alzheimer models, ACP-105 (an AR agonist) decreased anxiety-like behavior and, in combination with an ERbeta agonist, affected amyloid-beta degrading enzymes and cognition - preclinical neurobehavioral effects only.

    PreclinicalNonsteroidal selective androgen receptor modulators and selective estrogen receptor beta agonists moderate cognitive deficits and amyloid-beta levels in a mouse model of Alzheimer's disease.PMID 24020966 ↗

  7. 07

    In female mice, the SARM ACP-105 altered sensorimotor (rotorod) performance and cued fear conditioning and changed cortical MAP-2 immunoreactivity - preclinical neurobehavioral data.

    PreclinicalEffects of the SARM ACP-105 on rotorod performance and cued fear conditioning in sham-irradiated and irradiated female mice.PMID 21219889 ↗

  8. 08

    ACP-105 undergoes extensive oxidative metabolism (mono-, bis-, tri-hydroxylation plus dehydration) with phase II glucuronidation; metabolites detectable in equine urine up to ~72 h, supporting hepatic metabolism and renal metabolite elimination.

    PreclinicalDetection and identification of ACP-105 and its metabolites in equine urine using LC/MS/MS after oral administration.PMID 32852865 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice