S-4 (Andarine)

1. Overview and Critical Classification Note

S-4, also known as andarine, GTx-007, S-40503, or acetamidoxolutamide, is a non-steroidal small-molecule selective androgen receptor modulator (SARM). It is explicitly NOT a peptide, NOT a peptide derivative, and shares no structural or pharmacological class with the peptide hormones that make up the balance of this reference. S-4 is included on PeptideInsight because it appears repeatedly in the same self-experimentation, bodybuilding, and research-chemical communities that discuss peptides, and users routinely ask whether SARMs and peptides can be stacked, compared, or substituted for one another. Providing accurate, sourced information on S-4 in the same venue where a user might read about BPC-157, IGF-1 LR3, or growth hormone secretagogues is harm-reduction content; it is not an endorsement of use.

Structurally, S-4 is an aryl propionamide with the IUPAC-adjacent name S-3-(4-acetylamino-phenoxy)-2-hydroxy-2-methyl-N-(4-nitro-3-trifluoromethyl-phenyl)-propionamide. Its molecular formula is C17H16F3N3O6, with a molecular weight of approximately 441.35 Da. The scaffold is a chiral propionamide derived from the antiandrogen bicalutamide through a series of structural modifications that converted a pure antagonist into a tissue-selective partial agonist at the androgen receptor [1][3][5]. This places S-4 firmly in the small-molecule medicinal chemistry space, with no amino acids, no peptide bonds, and none of the proteolytic stability issues or parenteral-administration requirements that characterize peptides.

S-4 was developed in the late 1990s and early 2000s by the laboratory of James T. Dalton and Duane D. Miller at the University of Tennessee Health Science Center in Memphis, in partnership with the spin-out company GTx, Inc. GTx was founded specifically to commercialize the SARM platform alongside other small-molecule endocrine agents, and S-4 was among the earliest disclosed clinical candidates in the aryl propionamide SARM series [1][4][5][7]. The company ultimately prioritized a structurally related analog, S-22 (later renamed MK-2866, then ostarine, and finally enobosarm), which showed a superior pharmacokinetic and metabolic profile and advanced through Phase 2 and the Phase 3 POWER trials for non-small cell lung cancer cachexia [7][8]. S-4 was never advanced beyond early preclinical and Phase 1 work, and there are no published Phase 2 or Phase 3 efficacy trials for andarine in any indication.

The hallmark adverse effect of S-4 — and the feature that most clearly differentiates it in the community from other SARMs — is a dose- and duration-dependent visual disturbance. Users report a yellow or green tint to their vision, a marked loss of night vision and low-light sensitivity, and delayed dark adaptation when moving from bright to dim environments. These effects are reversible upon discontinuation but have been consistently reported in case reports and survey literature of recreational SARM users. The proposed mechanism involves binding to or interaction with components of the retinal phototransduction cascade, potentially including cross-reactivity with the intrinsically photosensitive retinal ganglion cell (ipRGC) melanopsin pathway, though a definitive molecular explanation has not been published in peer-reviewed literature.

Classification

Non-steroidal selective androgen receptor modulator (SARM) — small molecule, NOT a peptide

Chemical Name

S-3-(4-acetylamino-phenoxy)-2-hydroxy-2-methyl-N-(4-nitro-3-trifluoromethyl-phenyl)-propionamide

Molecular Weight

~441.35 Da (C17H16F3N3O6)

Developer

GTx, Inc. (Memphis, TN) and Dalton/Miller laboratory, University of Tennessee Health Science Center

Parent Scaffold

Aryl propionamide (derived from bicalutamide/hydroxyflutamide antagonist templates)

Route

Oral (bioavailable in preclinical species)

AR Activity

Partial agonist at androgen receptor; tissue-selective anabolic vs. androgenic

Signature Adverse Effect

Dose-dependent visual disturbance — yellow/green tint, reduced night/low-light vision, delayed dark adaptation

Regulatory Status

Not approved in any jurisdiction; WADA prohibited (S1.2 class); FDA warning on SARM supplement adulteration

Development Status

Abandoned; GTx prioritized enobosarm; no active clinical program

2. Mechanism of Action

Androgen Receptor Binding and Partial Agonism

S-4 binds to the ligand-binding domain of the human androgen receptor (AR) with a dissociation constant (Ki) of approximately 4 nM, comparable to dihydrotestosterone (DHT) but with functional activity characterized as partial agonism rather than full agonism [3]. In cell-based reporter assays, S-4 produces approximately 50 to 80 percent of the maximal transcriptional activation observed with DHT, depending on the promoter context and coactivator expression. This partial agonism is central to the tissue-selective profile of S-4: in tissues with abundant coactivator expression (such as skeletal muscle and bone), S-4 recruits sufficient transcriptional machinery to drive anabolic gene expression, whereas in tissues more dependent on specific coactivator repertoires (prostate, seminal vesicles), S-4 activity is attenuated.

Tissue Selectivity (Anabolic vs. Androgenic Dissociation)

The defining pharmacological feature of SARMs, including S-4, is dissociation of anabolic effects on skeletal muscle and bone from androgenic effects on the prostate, seminal vesicles, and skin [1][4][5]. In the standard Hershberger assay in castrated male rats, S-4 at oral doses of 0.3 to 3 mg/kg/day restored levator ani muscle weight to or above intact-control values while producing only partial restoration of ventral prostate and seminal vesicle weights, substantially below the effect produced by testosterone propionate at equipotent muscle-restoring doses [2][3]. The pharmacological selectivity index, calculated as the ratio of muscle effect to prostate effect, was several-fold higher than for testosterone.

The molecular basis of this tissue selectivity remains an area of active research. Proposed contributors include: (a) S-4 induces a distinct AR ligand-binding domain conformation compared with steroidal agonists, which alters the surface available for coregulator binding [6][7]; (b) S-4 is not a substrate for 5-alpha-reductase, so unlike testosterone it cannot be locally amplified to DHT in androgen-sensitive tissues such as prostate and skin [4]; and (c) differential expression of AR coactivators and corepressors across tissues creates context-dependent transcriptional output for a partial agonist.

Downstream Gene Expression

Activated AR–S-4 complexes translocate to the nucleus, bind androgen response elements (AREs) in target gene promoters, and recruit coactivators (SRC-1, SRC-2, SRC-3, p300/CBP) to drive transcription of anabolic target genes including IGF-1, myostatin regulators, and myogenic transcription factors in muscle. In bone, AR activation enhances osteoblast function and suppresses osteoclast activity, producing the pro-osteogenic phenotype observed preclinically with several SARMs. Kazmin and colleagues demonstrated by gene expression profiling that different AR ligands, including aryl propionamide SARMs, produce distinct transcriptional signatures, providing a mechanistic framework for the tissue selectivity of SARMs like S-4 [6].

HPG Axis Suppression

Like other AR agonists, S-4 at biologically active doses suppresses the hypothalamic-pituitary-gonadal (HPG) axis through negative feedback, lowering serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), and consequently endogenous testosterone. This suppression is a predictable pharmacological consequence of AR activation in the hypothalamus and pituitary and is not unique to S-4; it is observed across essentially all SARMs with meaningful AR agonism at clinically relevant doses. The extent and reversibility of suppression in humans are incompletely characterized because no controlled clinical trial of S-4 has been published.

Visual Disturbance — Proposed Mechanisms

The signature S-4 adverse event is dose-dependent visual disturbance, classically described by users as a yellow-green tint to vision and a loss of night vision, with delayed adaptation to darkness after exposure to bright light. The proposed mechanisms (none definitively proven in peer-reviewed literature) include:

1. Direct interaction with melanopsin (OPN4): Melanopsin is the photopigment in intrinsically photosensitive retinal ganglion cells (ipRGCs) that mediates non-image-forming visual functions including pupillary light reflex and circadian entrainment. The chromophore and opsin structure of melanopsin involves a retinal Schiff base linkage that may be susceptible to allosteric modulation by non-steroidal ligands with the right physicochemical profile. Hypotheses in the harm-reduction community invoke S-4 binding to or allosterically modulating melanopsin, producing altered photopigment kinetics and the reported symptoms.

2. AR in retinal tissue: The androgen receptor is expressed in several retinal cell types including retinal pigment epithelium and retinal ganglion cells. Acute AR activation in these tissues could plausibly alter gene expression or downstream signaling in ways that affect dark adaptation and color perception. This mechanism, if operative, would predict similar effects from other SARMs; the fact that visual disturbances are characteristic of S-4 but are not classically associated with enobosarm or LGD-4033 argues against a purely AR-mediated mechanism.

3. Off-target binding to rhodopsin or related opsins: S-4 or a metabolite may interact with the rod photoreceptor opsin (rhodopsin) or cone opsins, directly altering the phototransduction cascade and producing the reported reductions in low-light sensitivity and altered color perception.

The weight of community and clinical-review evidence supports a real, reproducible visual effect of S-4 at dose ranges reported by recreational users, but the molecular target has not been definitively identified in published research. The effect is reversible upon discontinuation, typically resolving over days to weeks.

3. Researched Applications

Muscle Wasting and Sarcopenia (Preclinical Only)

Evidence level: Preclinical only — no published Phase 2 or 3 trials

S-4 restored castration-induced losses of skeletal muscle mass and contractile function in castrated rat models at oral doses of 0.3 to 3 mg/kg/day, with efficacy approaching that of testosterone while producing substantially less prostate stimulation [2][3]. These data served as the proof-of-concept for the SARM platform. However, GTx did not advance S-4 to later-stage clinical development for sarcopenia, instead prioritizing enobosarm (S-22), which showed a better metabolic stability and safety profile in comparative preclinical studies [8][15].

Cancer Cachexia (Not Advanced)

Evidence level: Preclinical only

While the SARM class, via enobosarm, was tested in Phase 2 and Phase 3 cachexia trials (POWER and ASTRID programs) in non-small cell lung cancer, S-4 itself was never advanced to cachexia studies in humans [8]. The POWER Phase 3 trials failed to meet co-primary endpoints despite showing benefit on lean body mass, and the FDA declined to approve enobosarm for this indication, effectively halting late-stage development of the SARM class for cachexia. There is no realistic prospect of S-4 being developed for this or any other indication by GTx or its successors.

Benign Prostatic Hyperplasia (Paradoxical Early Hypothesis — Not Pursued)

Evidence level: Early preclinical hypothesis; not pursued clinically

Some early GTx disclosures suggested that the partial-agonist profile of S-4 could, in principle, reduce net androgenic signaling in the prostate in men receiving supraphysiological endogenous stimulation, providing a potential benefit in benign prostatic hyperplasia (BPH). This rationale was superseded by the recognition that 5-alpha-reductase inhibitors (finasteride, dutasteride) and alpha-1 adrenergic antagonists were already established, approved options, and GTx did not pursue S-4 for BPH.

Osteoporosis (Preclinical Only)

Evidence level: Preclinical only

Preclinical osteoporosis models showed that S-4 and related aryl propionamide SARMs preserve or increase bone mineral density, bone strength, and trabecular architecture in orchiectomized and ovariectomized rodent models. These data supported the SARM concept for osteoporosis but, like the muscle-wasting indication, did not translate into S-4-specific clinical development.

Recreational / Off-Label Bodybuilding Use (Not Recommended; No Safety Data)

S-4 is widely sold as a research chemical and as an adulterant in dietary supplements marketed to bodybuilders. Self-reported use patterns involve oral doses of 25 to 75 mg/day, often split into two or three doses because of the relatively short estimated half-life, cycled for 6 to 12 weeks [10][12][13]. There are no controlled safety or efficacy data to support any dose or duration in humans. Reported effects include modest gains in lean mass and strength, increased vascularity, and the characteristic visual disturbances that typically emerge within one to two weeks of use at doses of 50 mg/day or higher.

4. Clinical Evidence Summary

5. Dosing Reported in Literature and in Recreational Use

The following table summarizes doses reported in the preclinical literature, community survey literature, and adulteration analyses. No dose of S-4 has been established as safe or effective in humans by controlled clinical trials. Inclusion in this table is descriptive and for harm-reduction purposes; it is not a recommendation.

6. Pharmacokinetics

Oral Absorption and Bioavailability

Preclinical rat studies established oral bioavailability in the range of approximately 30 percent, with a time-to-peak plasma concentration (Tmax) of approximately 1 to 2 hours after oral gavage [2][15]. Human pharmacokinetic data are limited to unpublished Phase 1 work and community-derived estimates; published peer-reviewed human PK studies of S-4 are scarce because the compound was not advanced in clinical development.

Half-Life and Dose Frequency

The estimated terminal half-life in rats is approximately 3 to 4 hours, which informs the community practice of dividing the total daily dose into two or three administrations across the day. If human pharmacokinetics follow the preclinical pattern, a multi-dose daily regimen would be required to maintain sustained AR occupancy, which is likely relevant to both the desired anabolic effect and the dose-related visual adverse effects.

Metabolism and Excretion

S-4 undergoes Phase I metabolism including hydrolysis of the acetamide group to generate a free amine metabolite, reduction of the nitro group, and hydroxylation of the aromatic rings. Phase II conjugation (glucuronidation, sulfation) follows, and metabolites are excreted primarily in urine. The Phase I metabolites form the analytical signature used by WADA-accredited laboratories and equine doping-control laboratories to detect S-4 abuse; the parent compound and multiple metabolites remain detectable in urine for multiple days after a single oral dose [14].

Drug Interactions and CYP Involvement

Detailed CYP phenotyping of S-4 metabolism is incomplete in published literature. Based on the structural similarity to bicalutamide and related aryl propionamides, CYP3A4 is likely a contributor to hepatic oxidative metabolism, with the implication that strong CYP3A4 inhibitors (e.g., ketoconazole, ritonavir, grapefruit juice constituents) could increase S-4 exposure and vice versa. This has not been systematically studied and should not be used as a basis for clinical decision-making.

7. Safety and Side Effects

Visual Disturbances (Signature Adverse Effect)

Frequency: Common (dose-dependent)

The most distinctive adverse effect of S-4 is a dose-related visual disturbance consisting of:

1. A yellow or greenish tint to vision, particularly noticeable when viewing white surfaces or looking at lights
2. Marked reduction in night vision and low-light sensitivity, with users reporting difficulty driving at night or navigating dimly lit environments
3. Delayed dark adaptation, such that moving from a brightly lit environment to a dim one produces prolonged periods of near-blindness before the eyes adjust

These effects are typically reversible, resolving over days to a few weeks after cessation, but have been consistently reported across community surveys and clinical review literature [9][16]. The exact molecular mechanism is not definitively established but is hypothesized to involve interaction with melanopsin, rhodopsin, or AR in retinal tissues (see Section 2). Individuals with pre-existing retinal disease, poor baseline night vision, or professions requiring reliable night vision (aviation, trucking, military) should regard this as a serious contraindication.

HPG Axis Suppression and Hypogonadism

Frequency: Common at active doses

Like all active SARMs at pharmacologically relevant doses, S-4 suppresses LH, FSH, and endogenous testosterone through negative feedback at the hypothalamus and pituitary. Recovery timelines after discontinuation have not been systematically studied for S-4 specifically. Based on analogous data from enobosarm and LGD-4033, recovery is generally expected but can be protracted, and post-cycle hypogonadism with symptoms including fatigue, low libido, low mood, and erectile dysfunction is a recognized concern. Recreational users commonly attempt post-cycle therapy (PCT) with selective estrogen receptor modulators (clomiphene, tamoxifen) to accelerate HPG axis recovery, but this practice is itself unregulated and unsupervised.

Hepatotoxicity

Frequency: Uncommon but documented

Although S-4 is not classically associated with the severe hepatotoxicity seen with some 17-alpha-alkylated oral anabolic steroids, case reports and case series of SARM-associated drug-induced liver injury (DILI) have been published, with a typical pattern of cholestatic or mixed hepatocellular-cholestatic injury in previously healthy young men [11][17]. A complicating factor is that many commercial SARM products are adulterated, contaminated, or mislabeled, such that a user believing they are taking S-4 may be exposed to other SARMs or to approved pharmaceutical agents without their knowledge [10]. Attribution of DILI to S-4 specifically versus co-exposure to other hepatotoxic compounds is therefore difficult.

Cardiovascular Effects

Frequency: Uncommon but serious

Case reports have documented severe cardiomyopathy and other cardiovascular events in young men using SARMs including S-4 [16]. Reported findings include unexplained dilated cardiomyopathy with severely reduced left ventricular ejection fraction, with at least some cases showing recovery after SARM cessation and initiation of guideline-directed heart failure therapy. Adverse lipid profile changes (reduced HDL cholesterol) have also been reported with SARM use in general, though S-4-specific controlled data are limited.

Adulteration and Contamination Risk (Supplement Market)

Frequency: Very common in commercial products

A 2017 analysis published in JAMA by Van Wagoner and colleagues examined 44 products sold online as SARMs: 52 percent contained a SARM matching the label, 39 percent contained a substance different from what was labeled, 25 percent contained no SARM at all, 9 percent contained an approved drug not declared on the label, and the quantities of SARM present varied widely from the labeled amounts [10]. Andarine (S-4), along with ostarine and LGD-4033, was among the three most commonly detected actual SARMs. This means that a consumer purchasing a product labeled as S-4 has at best about a one-in-two chance of receiving what is advertised; the remainder of purchases may contain different SARMs, adulterants, undeclared pharmaceutical agents, or no active compound at all. This variability makes both therapeutic effect and safety impossible to predict at the individual level and is a primary reason why regulators including the FDA and WADA have repeatedly warned consumers against SARM-containing supplements.

Regulatory and Anti-Doping Status

S-4 is not approved for human use in any jurisdiction. The U.S. Food and Drug Administration has issued warning letters to companies marketing S-4 and other SARMs in dietary supplements, citing violations of the Federal Food, Drug, and Cosmetic Act. The World Anti-Doping Agency (WADA) added SARMs including andarine to the Prohibited List under class S1.2 (Other Anabolic Agents) effective January 1, 2008, and they remain prohibited both in-competition and out-of-competition. The U.S. Anti-Doping Agency (USADA) has sanctioned numerous athletes across multiple sports for positive andarine findings, including many cases linked to supplement contamination rather than intentional doping. Many national authorities, including those in the United Kingdom, Canada, and Australia, have taken additional regulatory action against importation and sale of SARMs.

8. Development History and Abandonment

Early Development at University of Tennessee and GTx

The aryl propionamide SARM program at the University of Tennessee, led by James Dalton and Duane Miller, began in the late 1990s with the observation that certain modifications to the bicalutamide antiandrogen scaffold could convert the compound from a pure AR antagonist into a partial agonist with tissue-selective effects [1][3][5]. S-1 and S-4 were among the earliest disclosed compounds in this series. GTx, Inc. was founded in 1997 and acquired rights to the UT SARM platform, pursuing S-4 as an initial clinical candidate.

Prioritization of Enobosarm (S-22) Over S-4

Comparative preclinical pharmacokinetic and pharmacodynamic work demonstrated that S-22 (later enobosarm, MK-2866, ostarine) had a longer half-life, more favorable oral bioavailability, greater metabolic stability, and an apparently cleaner adverse event profile than S-4, particularly with respect to visual effects [7][15]. GTx accordingly prioritized enobosarm for advancement into Phase 2 and Phase 3 clinical development, licensing it for a time to Merck (hence the MK-2866 designation) before repatriating rights. S-4 was effectively shelved as a clinical candidate.

Clinical Outcome of the SARM Class and Regulatory Landscape

Enobosarm was tested in Phase 3 POWER trials for non-small cell lung cancer cachexia (POWER 1 and POWER 2). While lean body mass endpoints were met, the FDA declined to approve enobosarm for cachexia, citing questions about functional outcome measures. Subsequent trials have explored enobosarm in breast cancer and stress urinary incontinence with mixed results. No SARM has received regulatory approval in the United States or European Union as of this reference's update date.

Current Status: Research Chemical Only

S-4 today exists almost exclusively as a research chemical sold online for ostensibly non-human research use, and as an adulterant in bodybuilding and dietary supplement products [10]. There is no active clinical development program for S-4 anywhere in the world, and the compound's principal relevance in 2026 is as a case study in the pharmacology of tissue-selective AR modulators and as a recognized subject of anti-doping control and consumer protection concerns.

9. Comparison with Other SARMs

S-4 (Andarine) vs. Ostarine (Enobosarm, MK-2866, S-22)

• Development status: S-4 abandoned at early preclinical/Phase 1; enobosarm reached Phase 3 POWER trials but not FDA-approved
• Half-life: S-4 ~3-4 hours (rats); enobosarm approximately 24 hours in humans, enabling once-daily dosing
• Visual effects: Prominent with S-4; not a classical enobosarm adverse event at studied doses
• AR potency: Both sub-nanomolar to low-nanomolar Ki at human AR
• Tissue selectivity index: Both favor muscle/bone over prostate; enobosarm generally regarded as modestly cleaner
• Hepatotoxicity: Both reported in SARM DILI case series; enobosarm more extensively characterized in humans

S-4 vs. LGD-4033 (Ligandrol)

• Chemistry: S-4 is aryl propionamide; LGD-4033 is a distinct pyrrolidine-benzonitrile scaffold from Ligand Pharmaceuticals
• Potency: LGD-4033 is considerably more potent at AR (sub-nanomolar) and effective at lower daily doses (recreational use typically 5-10 mg vs. 50-75 mg for S-4)
• HPG suppression: Both suppress; LGD-4033 suppression has been studied in Phase 1 (Basaria 2013) and is dose-dependent
• Visual effects: Characteristic of S-4, not reported with LGD-4033

S-4 vs. RAD-140 (Testolone)

• Chemistry: RAD-140 is a non-steroidal distinct from aryl propionamides
• Development: RAD-140 has been studied by Radius Health in androgen receptor-positive breast cancer; S-4 has no active program
• Potency: RAD-140 more potent at AR than S-4 on a weight basis
• Adverse events: RAD-140 has been associated with hepatotoxicity case reports; visual effects characteristic of S-4 are not reported with RAD-140

S-4 vs. GW-501516 (Cardarine) and SR9009 (Stenabolic)

Cardarine is a PPAR-delta agonist, and SR9009 is a REV-ERB agonist; neither is a SARM and neither acts through AR. They are mentioned here only because they are commonly stacked with S-4 in the bodybuilding community and because cardarine has its own distinct regulatory history (development halted due to rodent carcinogenicity signals). These compounds share none of the AR-mediated effects or adverse events of S-4.

10. Practical Harm-Reduction Information (Not a Recommendation)

Given that individuals do self-administer S-4 despite the absence of controlled safety data and against regulatory advice, the following harm-reduction points are offered as factual information rather than as endorsement or guidance to use:

• Product identity is unreliable: As documented by Van Wagoner et al., the majority of labeled SARM products contain something other than what is on the label [10]. Third-party laboratory testing of the specific batch being consumed is the only way to have any confidence in product identity and dose.
• Visual adverse effects are dose- and duration-dependent: The yellow tint and night-vision loss typically emerge at daily doses of 50 mg or higher and worsen with continued exposure. They are generally reversible on cessation.
• Driving and operating machinery: Users who notice any visual change should not drive at night, operate aircraft, or perform other safety-critical activities requiring reliable night vision.
• HPG suppression is expected: Users should anticipate LH, FSH, and total testosterone suppression and should have baseline and post-cycle blood work rather than relying on subjective symptoms.
• Hepatic monitoring: Baseline and on-cycle liver function tests (ALT, AST, bilirubin, GGT, alkaline phosphatase) are advisable given documented SARM-class hepatotoxicity.
• Cardiovascular monitoring: Baseline lipid profile and awareness of cardiovascular symptoms are appropriate given documented SARM-class cardiovascular case reports.
• Athletes: S-4 is on the WADA Prohibited List (S1.2). Any athlete subject to drug testing should not use S-4 under any circumstances, including as a component of a supplement product where its presence may be undeclared due to adulteration.
• Interaction with other hepatotoxic or cardiotoxic agents: Co-use with alcohol, acetaminophen at high doses, 17-alpha-alkylated oral anabolic steroids, or other SARMs increases hepatic and cardiovascular risk.

11. Related Peptides and SARMs

See also: Ostarine (MK-2866, Enobosarm, S-22), LGD-4033 (Ligandrol), RAD-140 (Testolone), GW-501516 (Cardarine), SR9009 (Stenabolic)

12. References

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