History

Andarine was developed by GTx, Inc. with University of Tennessee researchers (the Dalton/Miller group) and first described in the literature around 2002 as part of a class of selective androgen receptor modulators (SARMs). It was investigated for muscle wasting/cachexia, osteoporosis, and benign prostatic hyperplasia, but development was discontinued — reportedly because of visual disturbances observed in clinical studies — and research interest shifted to other SARMs such as enobosarm/ostarine and ligandrol/LGD-4033.

Andarine (S4) is a selective androgen receptor modulator (SARM), a synthetic small molecule — not a peptide and not an anabolic steroid. It is frequently sold in fitness, biohacking, and “research chemical” channels as a muscle-building “safer steroid alternative,” but its real evidence base is limited almost entirely to rodent studies, and its most concretely documented human finding is a side effect (reversible vision changes) rather than a proven benefit.

What it is

Andarine (code names S-4, GTx-007 / GTX-007) is a non-steroidal arylpropionamide-class SARM. It works as an orally active partial agonist of the androgen receptor (AR). Its defining preclinical feature is tissue selectivity: in animal work it behaved as a near-full agonist in anabolic tissue (skeletal muscle) but only a partial agonist in androgenic tissue (prostate). That selectivity is the basis for the “muscle without full prostate stimulation” idea behind SARMs. It is not a peptide.

The claims

In fitness and “research chemical” marketing, andarine is pitched for lean muscle gain, fat loss, body recomposition, strength, and “hardening”/vascularity, often as a “safer steroid alternative” or stacked with other SARMs. These performance and aesthetic claims are not supported by completed human efficacy trials for andarine.

What the evidence actually shows

Preclinical (animal): The best-documented findings are in castrated rats. S-4 maintained or restored levator ani (anabolic) muscle weight toward intact levels while only partially restoring prostate weight, demonstrating tissue-selective anabolic activity (Yin/Gao et al., J Pharmacol Exp Ther 2003; Gao et al., Endocrinology 2004). It also showed bone-preserving effects in rodent osteoporosis models.
Human: Andarine reached only early Phase 1–stage clinical work. There are no completed, published Phase 2/3 efficacy trials establishing benefit for muscle wasting or any other condition.
Discontinued: Development was halted, reportedly due to visual disturbances seen in clinical studies — andarine’s signature reported side effect.

Bottom line on evidence: human benefit is essentially absent from the verifiable record, and the most concrete human finding is a safety signal, not efficacy.

Legal and regulatory status

FDA: Andarine and SARMs generally are not FDA-approved for any use and are not lawful dietary-supplement ingredients. FDA has stated SARMs sold as “supplements” are unapproved drugs, has issued warning letters, and has published consumer warnings (including one aimed at teens and young adults) citing risks of liver injury, heart attack/stroke, and other serious harms. The sport-supplement certifier BSCG also flags andarine as an illegal dietary-supplement ingredient.
DEA: As of June 2026, SARMs (including andarine) are not federally scheduled controlled substances. Bills to add SARMs to Schedule III (the “SARMs Control Act,” e.g. S.2742 in the 115th Congress, 2018, and reintroductions) have not been enacted. Note: this is distinct from anabolic-steroid law — oxandrolone is an actual anabolic-androgenic steroid and a Schedule III controlled substance, and should not be conflated with SARMs.
Anti-doping (WADA): All SARMs, including andarine, are prohibited at all times (in- and out-of-competition) under category S1.2, “Other Anabolic Agents.” For comparison, GW-501516 / cardarine is a PPARδ agonist and SR9009/SR9011 are REV-ERB agonists — not SARMs, though they are often mis-sold as such.

Safety

Vision effects (andarine-specific): The most consistently reported human effect is transient visual disturbance — a yellowish tint to vision, difficulty with night/dark adaptation, and blue-light/flash sensitivity. It is described as dose-related and reversible on discontinuation; the proposed mechanism is AR interaction in retinal tissue (mechanistically inferred, not definitively proven). This is the reported reason clinical development stopped.
Testosterone/HPG suppression: As an AR agonist, andarine — like SARMs as a class — is expected to suppress endogenous testosterone, LH, and FSH via negative feedback. Suppression is a well-established SARM class effect.
Lipids / HDL: SARMs as a class are associated with lowered HDL cholesterol (documented for oral SARMs such as ostarine/enobosarm). Andarine-specific human lipid data are limited.
Liver injury (hepatotoxicity): Drug-induced liver injury, including hospitalizations, has been documented in real-world SARM users and is captured in NIH LiverTox. Most published cases involve other SARMs (ostarine, LGD-4033, RAD140); andarine-specific reports are sparse, but the class signal is real.
For contrast (a different compound): GW-501516 development was halted around 2007 after a long-term rodent study showed tumors across multiple organ systems at chronic high doses. That carcinogenicity finding applies to GW-501516, not andarine — there is no comparable finding for andarine.
What we will not assert: There is no reliable evidence of permanent blindness or QT-interval prolongation specifically attributable to andarine; its reported vision effects are reversible.

This profile includes no dosing amounts, cycles, or protocols by design.

Bottom line

Andarine is a SARM whose tissue-selective anabolic effects are documented only in animals. There are no completed human efficacy trials, it is not approved or lawful as a supplement, and it is banned at all times in sport. The clearest human data point is a side effect — reversible vision disturbance — which is why its clinical development was abandoned. Class-wide signals (testosterone suppression, lowered HDL, and liver injury) add further caution.

Evidence grade: Animal only.