ACP-105 vs. Testosterone: What the Research Actually Shows

Key takeaways

What is ACP-105, and how is it different from testosterone?

ACP-105 is a synthetic, non-steroidal compound belonging to the class of selective androgen receptor modulators (SARMs). It was developed by ACADIA Pharmaceuticals, which presented preclinical data on the compound at the Experimental Biology 2008 meeting and published the underlying medicinal chemistry in 2009. According to Wikipedia's referenced summary, ACP-105 is an aniline-based SARM and is structurally related to two other experimental compounds, AC-262536 and vosilasarm (RAD140), though it is chemically unrelated to testosterone, a steroid hormone built on the cholesterol backbone.

Testosterone is the principal endogenous androgen in humans and drives both anabolic effects (on muscle and bone) and androgenic effects (on the prostate, voice, hair growth, and spermatogenesis) throughout the body. ACP-105 was designed with the opposite goal in mind: tissue-selective activation of the androgen receptor so that anabolic effects could, in theory, be separated from androgenic ones. In its own preclinical announcement, ACADIA reported that ACP-105 is <cite index="1-1,1-2">shown to be as potent and efficacious as testosterone in in vitro assays without interaction at other hormone receptors, and demonstrates potent anabolic effects on muscle and bone with minimal effect on prostate in preclinical models</cite>. This is a company-generated claim from a conference press release, not an independently replicated finding, and it predates any peer-reviewed publication of the full dataset.

Independent product-chemistry listings citing the peer-reviewed discovery paper describe ACP-105 as an <cite index="29-1">orally available and potent selective androgen receptor modulator (SARM) with pEC50 of 9.0 and 9.4 for AR wild type and AR mutation T877A, respectively</cite>, indicating high in vitro binding potency. However, potency at the receptor is not the same as producing testosterone's full physiological effect. The peer-reviewed discovery paper itself, published by Schlienger and colleagues in the Journal of Medicinal Chemistry, describes the compound this way in its own words, as reproduced in citation databases: <cite index="11-1">ACP-105 (1), a novel and potent nonsteroidal selective androgen receptor modulator (SARM) with partial agonist activity relative to the natural androgen testosterone</cite>, and notes that <cite index="11-4">in vivo, 1 improved anabolic parameters in a 2-week chronic study in castrated male rats</cite>. Partial agonist activity means the compound occupies the androgen receptor without producing the maximal response a full agonist like testosterone or DHT can produce.

A note on a common source of confusion: ACP-105 vs. AC-262536

Much of the online material about ACP-105 blends its data with that of AC-262536, a separate, structurally related non-steroidal SARM that ACADIA Pharmaceuticals developed around the same time. The two compounds are often described together in doping-detection and structural-chemistry literature because both belong to the same tropane-related chemical series, but the animal pharmacology data reported for each compound is not interchangeable. The frequently repeated claims that this class of compound 'potently suppressed the luteinizing hormone surge' and had only minimal prostate trophic effects in castrated rats actually come from the separate pharmacological characterization of AC-262536, not ACP-105: the primary paper states that <cite index="31-4,31-5,31-6">using a functional cell-based assay AC-262536 was identified as a potent and selective AR ligand, with partial agonist activity relative to the natural androgen testosterone, and a 2-week chronic study in castrated male rats indicated that AC-262536 significantly improves anabolic parameters in these animals, especially in stimulating the growth of the levator ani and in suppressing elevated LH levels, with weak androgenic effects as measured by prostate and seminal vesicle weights in sharp contrast to testosterone</cite>. Numeric selectivity figures circulating on commercial and forum sites (for example, specific percentages of DHT-equivalent anabolic or androgenic activity, or ratios such as 3:1) likewise trace back to AC-262536's characterization or to unsourced vendor marketing material rather than to a peer-reviewed, dose-response study of ACP-105 itself. Readers should treat any quantitative anabolic-to-androgenic ratio attributed specifically to ACP-105 with caution, since no verifiable primary source for such a figure was identified for this page.

Mechanism of action and receptor pharmacology

Testosterone activates the androgen receptor directly and is also converted by 5-alpha-reductase to dihydrotestosterone (DHT), a more potent androgen responsible for much of the effect on skin, hair, and prostate tissue, and by aromatase to estradiol, which contributes to effects on bone density, libido, and lipid metabolism. This dual metabolism is part of why testosterone produces broad, non-selective effects across many tissues.

Non-steroidal SARMs such as ACP-105 lack the steroid backbone required for conversion by aromatase or 5-alpha-reductase in the same way testosterone is converted, which is the pharmacological rationale offered for reduced estrogen-related side effects in this compound class generally. This reasoning is structural and theoretical for ACP-105 specifically, since no controlled human data exist to confirm reduced water retention or gynecomastia risk relative to testosterone.

Because ACP-105 is a partial agonist rather than a full agonist at the androgen receptor, pharmacology principles predict that it could, in some circumstances, blunt the effect of a full agonist such as testosterone when both are present at the receptor simultaneously, similar to how partial agonists behave with other receptor systems. This has not been directly demonstrated for ACP-105 in a controlled experiment identified for this page, and should be regarded as a theoretical extension of general receptor pharmacology rather than an established finding specific to this compound.

Anabolic and androgenic effects: what the animal data actually show

The specific quantitative Hershberger-assay data for ACP-105 (levator ani muscle growth vs. prostate and seminal vesicle regrowth in castrated rats, benchmarked against DHT or testosterone) have not been located in a peer-reviewed, publicly accessible dataset for this page. The 2009 discovery paper reports that ACP-105 improved anabolic parameters in castrated male rats over a two-week study, but the detailed percentage breakdowns often cited online for ACP-105 (such as specific percentages of the DHT maximum for muscle versus prostate) could not be traced to a verifiable primary source for this compound and may originate from confusion with the related compound AC-262536, described above, or from unsourced commercial material.

Because of this gap, this page does not report specific anabolic-to-androgenic dissociation ratios for ACP-105 as established fact. What can be said with confidence is that ACP-105 was characterized by its developers as a partial agonist with in vitro potency comparable to testosterone and with anabolic activity in castrated rats, but the degree of tissue selectivity has not been independently confirmed through published dose-response data specific to this molecule.

Beyond muscle, ACP-105 has also been studied in a small number of exploratory rodent neuroscience papers that are not typical targets of testosterone research. One study examined the effects of ACP-105 on motor coordination and fear conditioning in irradiated and non-irradiated female mice, published as <cite index="21-12,21-13,21-14,21-15">Dayger C, et al. Effects of the SARM ACP-105 on rotorod performance and cued fear conditioning in sham-irradiated and irradiated female mice, Brain Res. 2011 Mar 24;1381:134-40</cite>. A separate paper examined ACP-105, alone and combined with a selective estrogen receptor beta agonist, in a triple-transgenic Alzheimer's disease mouse model, published as <cite index="27-19,27-20,27-21,27-22,27-23">George S, Petit GH, Gouras GK, Brundin P, Olsson R. Nonsteroidal selective androgen receptor modulators and selective estrogen receptor β agonists moderate cognitive deficits and amyloid-β levels in a mouse model of Alzheimer's disease. ACS Chem Neurosci. 2013 Dec 18;4(12):1537-48</cite>. These are exploratory rodent findings only. There is no evidence any of these effects translate to humans, and no human trials of ACP-105 for any neurological, cognitive, muscle, or bone indication have been conducted or registered.

Human evidence: SARM research vs. decades of testosterone data

This is the area of greatest asymmetry between the two compounds. Testosterone is an FDA-approved prescription hormone with an extensive human evidence base, including the large, FDA-mandated TRAVERSE cardiovascular safety trial. According to the FDA, testosterone <cite index="55-3">is approved solely for use in men who lack or have low testosterone levels in conjunction with an associated medical condition</cite>, and the agency has retained 'Limitation of Use' language specifically excluding age-related low testosterone from the approved indication while updating labeling based on newer trial data.

The TRAVERSE trial, a randomized, placebo-controlled study in men with hypogonadism and pre-existing or high cardiovascular risk, found that <cite index="50-4">testosterone replacement therapy was noninferior to placebo regarding the incidence of major adverse cardiac events (7.0% versus 7.3%; hazard ratio 0.96; 95% CI, 0.78-1.17; P < .001)</cite>. Based on this trial together with required postmarket ambulatory blood pressure monitoring studies, the FDA has since <cite index="55-1,55-2">required the addition of TRAVERSE results to all testosterone product labeling, retained limitation-of-use language for age-related hypogonadism, removed boxed-warning language about cardiovascular risk, and added new or product-specific warnings about increased blood pressure</cite>.

ACP-105, by contrast, has never been tested in a published human clinical trial. Every study identified in the literature for this compound used animal models (rats, mice), in vitro assays, or in silico/computational modeling. A 2025 in silico toxicology paper on the compound states that <cite index="28-8,28-9,28-10">ACP-105 is a novel non-steroidal Selective Androgen Receptor Modulator (SARM) used by athletes, whose action aims to increase muscle mass, and whose safety profile remains insufficiently explored, particularly regarding its toxicity in humans</cite>. A related 2026 pharmacokinetic modeling paper likewise notes that ACP-105 is <cite index="22-1">a compound first characterized in 2008 conference proceedings and a 2009 medicinal chemistry paper</cite>, and that researchers have had to rely on computational prediction tools rather than measured human pharmacokinetic data, because none exists. This means the evidence grade for ACP-105 in humans is effectively zero: no controlled dosing studies, no measured human pharmacokinetics, no systematic human adverse-event data, and no basis for extrapolating a safe or effective human dose from the animal literature.

Regulatory and legal status: FDA and WADA positions

No SARM, including ACP-105, is approved by the FDA for any human use, and the FDA has repeatedly warned that SARMs marketed as research chemicals or dietary supplements are unapproved drugs associated with serious health risks, including liver injury, and cardiovascular and endocrine effects. The agency has pursued warning letters and enforcement actions against companies distributing SARM products for human consumption.

Testosterone, in contrast, has multiple FDA-approved formulations for a defined medical indication (diagnosed hypogonadism with an associated medical condition), with prescribing governed by product labeling and monitoring guidance from professional societies. It is a Schedule III controlled substance in the United States, requiring a prescription, but it is legally manufactured, prescribed, and dispensed for its approved indication.

Both compounds are prohibited in competitive sport, but under different categories of the WADA Prohibited List that reflect their different biochemical classifications. SARMs, including ACP-105, are listed under <cite index="53-2">the category of 'Other Anabolic Agents' under section S1.2 of the WADA Prohibited List</cite>, and <cite index="53-1">all SARMs are prohibited at all times (both in and out-of-competition) for all athletes, from those competing at the highest level of sport to those competing at the recreational level</cite>. Testosterone, when used exogenously by an athlete, falls under the separate S1.1 category for anabolic androgenic steroids, and its exogenous use is detected using methods such as the urinary testosterone-to-epitestosterone ratio and carbon isotope ratio mass spectrometry to distinguish it from the athlete's endogenous testosterone.

Bottom line

ACP-105 and testosterone both act on the androgen receptor, but they occupy opposite ends of the evidence spectrum. Testosterone is a naturally occurring hormone with an FDA-approved indication, decades of prescribing history, and a large randomized cardiovascular safety trial behind its current labeling. ACP-105 is a partial androgen receptor agonist that was characterized in rodent and in vitro studies by its originating pharmaceutical company roughly two decades ago, was never advanced into human trials, and remains an unapproved substance whose human safety profile is, in the words of the toxicology literature, insufficiently explored. Claims that ACP-105 replicates testosterone's anabolic benefits while avoiding its androgenic risks in humans are not supported by any published human data, and some of the specific selectivity figures attributed to ACP-105 online appear to be misattributed from a different, related compound.

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