Benefits, Dosage, Risks, and Legal Status Explained – Swolverine

S23 is a nonsteroidal selective androgen receptor modulator (SARM) developed in the same R&D era as other aryl-propionamide SARMs. It’s known for high AR potency with a reputation for marked suppression of natural testosterone—why many consider it an “advanced-only” research compound rather than a starting point.

→ What this guide covers: benefits people seek, real risks (suppression, cardiometabolic markers), community-reported dosing practices (for education, not advice), PCT considerations, legality/testing status, and safer, lower-risk priorities for training and recovery.
→ Bottom line up front: S23 can create a “hard/lean” look and strength bump for some, but carries disproportionately high suppression and no FDA-approved medical use. It’s banned at all times in tested sport.

Preclinical work on S-series SARMs—including S-23—shows potent AR activation with reversible suppression of spermatogenesis and favorable lean-mass effects in rodents. — Jones et al., Endocrinology (OUP Academic)

SARMs (including S23) remain non-approved drugs in the U.S., with FDA warnings about serious safety concerns and enforcement against bodybuilding products. — U.S. FDA, Consumer Update (U.S. Food and Drug Administration)

All SARMs are prohibited in- and out-of-competition under WADA’s “Other Anabolic Agents (S1.2)”—athletes subject to testing should avoid entirely. — WADA Prohibited List 2025 (Wada Ama)

Why it’s controversial:
→ Potency vs. selectivity trade-offs: “tissue selective” in theory, but systemic androgen signaling still impacts HPG axis, lipids, and other biomarkers.
→ Human data are lacking; most mechanistic and efficacy/safety insights come from animal studies and community anecdotes—a poor basis for risk prediction.
→ “Research chemical” supply chains mean variable purity and adulteration risks.

Who this guide is for:
→ Advanced lifters evaluating risk realistically (and who prioritize labs/medical oversight).
→ Coaches/clinicians who need a clear, harm-reduction-first explainer for client questions.
→ Tested athletes who need a reminder: it’s banned, full stop.

What Is S23?

S23 is a research-only SARM—a lab-made compound that sticks to the androgen receptor very tightly. It showed up in early pharma work (think: GTx, Inc.) as a potential male hormonal contraceptive because it could build lean tissue in animals and switch off sperm production while on-cycle, with recovery after stopping. That’s why lifters talk about it as “potent”—but also why suppression is such a big part of the story. (OUP Academic)

→ In plain English: it’s not an approved medicine; it’s a powerful AR “on-switch.” That power cuts both ways—muscle-friendly signaling, but also meaningful signal to your HPG axis (your body’s own testosterone loop). The FDA has repeatedly warned that SARM-labeled products are unapproved drugs and can carry real safety risks, and in tested sports, all SARMs are banned year-round. (U.S. Food and Drug Administration)

→ Chemistry snapshot (for ID only): you’ll see S23 listed in databases by its long IUPAC name and CAS 1010396-29-8. Those listings are useful for confirming you’re reading about the same molecule—not a green light to use it. (PubChem)

Why people even consider it:
→ Reports of a “harder,” leaner look and noticeable strength at relatively small amounts.
→ But that comes with a reputation for pronounced suppression, so it’s not a smart entry point for newcomers. (There’s no human dosing standard—everything online is anecdote.) (OUP Academic)

Mechanism of Action (How S23 Works)

At its core, S23 is a powerful “on-switch” for the androgen receptor (AR). When it binds, the receptor flips from idle to active, moves into the nucleus, and turns on (and off) sets of genes that influence muscle protein synthesis, strength adaptations, and anti-catabolic signaling. That’s the simple version—here’s the nuance that actually matters:

→ Tissue-selective ≠ side-effect-free.
“SARMs are selective,” but not perfectly. Selectivity depends on which co-regulator proteins are present in each tissue (muscle, bone, prostate, brain), how tightly S23 binds, and how long it sits there. The net effect: lots of muscle-friendly signaling, but still systemic androgen signaling your body has to account for.

→ Why people get the “harder/leaner” look.
Strong AR activation nudges gene programs toward building/retaining contractile proteins and resisting breakdown when you’re dieting or training hard. Less muscle loss during a cut can read visually as a “harder” look. It’s not magic fat-loss; it’s mostly better retention of lean tissue under stress.

→ Why suppression is so common (and often pronounced).
Your HPG axis (hypothalamus → pituitary → gonads) runs on feedback. When AR signaling is high from S23, your brain reads “we’re good on androgens” and dials down GnRH → LH/FSH, which suppresses testicular testosterone and can reduce sperm production. That feedback loop is why so many users report needing robust recovery plans after stopping.

→ It’s potent—so small changes matter.
S23 binds AR very tightly, so dose jumps can have outsized effects. More receptor engagement doesn’t linearly equal “more gains”—it often equals more suppression and more strain on lipids, blood pressure, mood/sleep, and other systems.

→ Selectivity can shift with context.
Caloric deficit vs. surplus, sleep debt, training volume, and even other compounds you stack with S23 can change the balance of co-regulators and stress hormones. Translation: the same dose can “feel” different across phases—another reason to avoid chasing effects by bumping dose.

→ What we don’t know (and why it matters).
There’s no validated human half-life or PK profile for S23. Most split-dosing advice online is guesswork. Without reliable PK, you can’t time bloodwork precisely or predict peaks/troughs—so conservative assumptions and frequent labs are the only responsible approach.

Key takeaways (mechanism → practice):
→ S23 turns on AR-driven muscle programs but turns down your own T production via negative feedback.
→ “Hardening” is mainly lean-mass preservation under stress, not a fat-loss superpower.
→ High potency means small increases can escalate side effects quickly.
→ Unknown human PK = treat all dosing folklore as unverified; if someone uses it anyway, labs and guardrails are non-negotiable.

Benefits of S-23 (What the Research Actually Shows)

Reality check up front: there are no controlled human trials on S-23. What follows comes from preclinical (animal) studies and medicinal-chemistry reviews—useful for understanding biology, not guarantees of results in people.

→ Lean-mass support in vivo
Across rat studies, S-23 shows clear myotrophic effects (e.g., larger levator ani muscle) and favorable body-comp signals under androgen receptor (AR) activation. That’s the scientific root of its “hardening” reputation. (PubMed)

→ Body-composition shifts (dose-responsive)
Preclinical work reports lean mass up and fat mass down as exposure increases—consistent with strong AR agonism driving protein synthesis and anti-catabolic pathways in vivo. (PMC)

→ Bone-anabolic signals (preclinical)
Nonsteroidal SARMs—including the S-series—repeatedly show positive effects on bone markers/density in animal models, aligning with AR-mediated skeletal benefits seen with other SARMs. (PMC)

→ Anabolic with relatively lower prostate stimulation vs. testosterone (in animals)
Head-to-head preclinical profiling suggests S-23 can increase muscle while producing less prostate growth than classical androgens at studied doses—the “selective” in SARM. (PubMed)

→ Potency that helps preserve tissue under stress
In models where muscle is at risk (e.g., castration/orchiectomy paradigms), SARMs preserve lean tissue and strength-related endpoints—an effect pattern S-23 shares within this class. (OUP Academic)

What this does not mean

• S-23 is not a validated fat-loss drug; any fat loss remains diet-driven. The consistent preclinical signal is lean-mass preservation, not direct lipolysis. (Class-level evidence, not human S-23 data.) (PMC)

• Benefits come with a trade-off: the same potency that drives myotrophy is why S-23 was explored for male contraception—it suppresses LH/FSH and spermatogenesis during exposure in rats, with reversibility reported after discontinuation in that model. (PubMed)

Bottom line: The strongest evidence for S-23’s “benefits” is preclinical—lean-mass support, body-comp and bone signals, and tissue bias vs. testosterone in animals. Without human trials, magnitude, safety, and durability in people remain unknown.

Dosage & Cycle Length (Educational Overview, Not Advice)

There’s no sugar-coating this: there are no validated human dosing standards for S-23—no peer-reviewed human pharmacokinetics, no clinical half-life, no approved indications. Everything you see online is anecdote. Treat it that way.

→ What the research actually gives us

• Preclinical only. S-23 was profiled in animals for male contraception: potent AR activation, lean-mass signals, strong HPG-axis suppression—and reversibility after cessation in those models. That’s biology, not a dosing playbook. (PubMed)

• No human PK/half-life. Major reference listings identify S-23 but do not provide validated human dosing or half-life data. If you can’t time exposure, you can’t time labs or predict peaks/troughs with confidence. (DrugBank)

→ Why “split dosing” advice online is shaky
Without human PK, assumptions about absorption, time-to-peak, or distribution are guesswork. Split dosing is often copied from other SARMs or from stimulant playbooks—not from S-23 human data. (There aren’t any.)

→ Cycle length: shortest practical exposure
Because S-23 is high-potency and suppressive, risk generally scales with dose × time. A harm-reduction stance prioritizes minimal exposure and objective monitoring over chasing marginal cosmetic changes. (Preclinical potency is exactly why caution matters.) (PubMed)

→ Monitoring framework (what responsible looks like)

• Before: CBC, CMP (ALT/AST, creatinine/eGFR), fasting lipids, hormones (total T, free T or calc, LH, FSH), BP/resting HR baseline.

• During: Repeat CMP/lipids at ~3–4 weeks; track BP, resting HR, sleep, mood, performance. If things trend the wrong way, adjust training first—don’t escalate exposure.

• After (recovery): Re-check hormones/lipids/CMP 3–6 weeks post and continue until baseline returns. No re-runs until both labs and symptoms normalize.
  These guardrails reflect the suppression and systemic signals seen in animal work and the FDA’s broader safety warnings around SARM-labeled products. (PubMed)

→ Tested athletes: zero room for error
All SARMs (including S-series) are banned at all times under WADA S1.2. Detection windows can be unpredictable with research-chemical supply chains. If you’re tested, avoidance is the only rational choice. (Wada Ama)

Risks & Side Effects (Research-Driven, No Spin)

Context: There are no controlled human trials on S-23. Risk signals come from (1) animal work on S-23 itself (potent AR activation with marked HPG-axis suppression), and (2) human reports and class-level data on other SARMs (liver injury, lipid changes, regulatory warnings). Read this like a pre-flight checklist.

Endocrine & Fertility

→ Strong suppression is the headline. In rat contraception models, S-23 consistently suppressed LH/FSH, reduced spermatogenesis, and did so in a dose-responsive manner (reversible after discontinuation in those studies). That’s the biological basis for expecting significant testosterone suppression in people, even though human S-23 data are lacking. (PubMed)

Hepatic Signals

→ Drug-induced liver injury (DILI) has been documented with SARMs (e.g., ligandrol/LGD-4033, ostarine/RX-24, RAD-140) in case series and reports, including biopsy-proven cholestatic patterns. While these are not S-23 specifically, they indicate a class risk that warrants labs and caution. (PMC)

Lipids & Cardiometabolic

→ HDL tends to fall with SARM exposure. Human and translational studies on SARMs show significant HDL-C reductions (with variable effects on LDL/TG) and mechanistic shifts in HDL subspecies—signals that push you to monitor lipids, blood pressure, and training stress. (PMC)

Regulatory & Safety Warnings

→ The FDA has repeatedly warned that SARM-labeled bodybuilding products are unapproved drugs linked to serious safety concerns (liver, cardiac, stroke risk) and has taken enforcement action against marketers. Translation: no approval, no validated dosing, and real safety flags. (U.S. Food and Drug Administration)
→ For athletes, all SARMs are prohibited year-round under WADA S1.2; detection windows are unpredictable across gray-market products. (Wada Ama)

CNS, Dermatologic, and Other Androgenic Signals

→ Community and clinician reports around the SARM class include sleep fragmentation, irritability, low mood (especially post-cycle), acne/oily skin, hair shedding in predisposed users, and shifts in resting HR/BP—consistent with potent AR modulation plus endocrine disruption. (Mechanistic alignment from S-series preclinical work + class surveillance.) (PMC)

What to Monitor (practical guardrails)

→ Before: CBC; CMP (ALT/AST, creatinine/eGFR); lipid panel; hormones (total T, free T or calculated, LH, FSH); BP & resting HR baseline. (Suppression + hepatic + lipid rationale.) (PubMed)
→ During (≈ week 3–4): CMP, lipids; track BP, resting HR, sleep, mood, performance. If markers trend the wrong way, fix training, sleep, and diet first—don’t escalate dose. (PMC)
→ After (recovery): Repeat hormones/lipids/CMP 3–6 weeks post to confirm axis rebound and hepatic/lipid normalization before resuming high-stress training phases. (PubMed)

Red Flags → Stop & Seek Care

Chest pain/shortness of breath; persistent BP ≥140/90; jaundice, dark urine, RUQ pain; severe fatigue; major mood changes or anhedonia; ALT/AST spikes or sharp HDL collapse on labs. (These mirror the FDA’s safety concerns and published DILI cases.) (U.S. Food and Drug Administration)

Bottom line: S-23’s potency is exactly why suppression is expected; class data add liver and lipid risk on top. With no human S-23 dosing/PK, the only responsible stance is conservative exposure, objective labs, and a clear exit plan—and for tested athletes, zero use. (Wada Ama)

Post-Cycle Therapy (PCT) Considerations

S23’s calling card is strong suppression. If someone runs it anyway, assume you’ll need a real recovery plan—measured by labs, not vibes.

→ Why PCT is usually necessary
S23 drives AR signaling high enough that your hypothalamus/pituitary read “androgens are abundant,” dialing down GnRH → LH/FSH. The result: endogenous testosterone drops and sperm parameters can tank. Coming off, you’re relying on your axis to restart—PCT is about nudging that process while you protect health and training.

→ What “good PCT” means (principles, not prescriptions)

• Objective baselines: Before the last on-cycle week, get total T, free T (or calc), LH, FSH, plus lipids and CMP (ALT/AST, creatinine/eGFR).

• Timing the start: Begin recovery support after the compound’s effects have meaningfully waned (with S23, human PK is unknown—err on a short washout rather than stacking uncertainty).

• Duration: Plan for 4–6 weeks of recovery support as a starting frame, then extend or taper based on labs/symptoms—not the calendar.

• Training during PCT: Reduce systemic fatigue—dial in volume, intensity, and frequency to prioritize quality reps and technique. Insert a deload in week 1–2 of PCT.

• Nutrition during PCT: Slight calorie bump to maintenance or +5–10%, 0.8–1.0 g protein/lb, consistent carbs around training, micronutrient sufficiency (iodine, selenium, zinc from food first).

• Lifestyle: 7–9 hours sleep, alcohol at or near zero, manage stress (HRV/resting HR are useful reality checks).

→ What to monitor (and when to change course)

• Weeks 2–3 of PCT: Repeat LH, FSH, total/free T, lipids, CMP. Look for up-trending LH/FSH and rising T with symptoms improving (energy, sleep, drive).

• If labs stall or worsen: Extend recovery, tighten training stress, reassess sleep/steps, and consider clinician-guided options.

• Red flags: Persistently low mood, marked fatigue, BP elevation, pronounced ALT/AST rise, or any concerning symptoms → escalate to a clinician promptly.

→ Guardrails that actually help

• Don’t stack more compounds “to feel normal.” Recovery is a hormonal and behavioral process.

• Keep conditioning in, but make it repeatable (zone 2 or tempo work) to support lipids, BP, and mood without pounding recovery.

• Supplements to prioritize: basic, low-risk pillars—creatine monohydrate, omega-3s, electrolytes, vitamin D if deficient. Skip the “PCT miracle” blends.

→ When to consider medical help

• No upward movement in LH/FSH or testosterone by week 4–6 post-cycle

• Severe mood/sleep disruption or sexual function not improving

• Lipids or liver enzymes that remain materially off-baseline

Dosage & Cycle Length (Educational Overview, Not Advice)

There’s no clinical playbook for S-23—no validated human half-life, dosing, or PK. Anything you see online is anecdote, not evidence. Read this as a framework for safety thinking, not a how-to.

→ What we actually know

• Preclinical only. S-23 is potent and suppressive in animal models. Useful for understanding risk, not for calculating doses.

• Human PK unknown. Without a verified half-life, “split dosing” schedules you see on forums are guesswork. Peaks, troughs, and washout timing are unpredictable.

• Risk scales with exposure. More milligrams × more weeks = more suppression and more chances to ding lipids, liver markers, mood, and sleep.

→ Practical guardrails (if someone uses it anyway)

• Lowest effective exposure, shortest practical duration. Think minimalist trial, not “blast.”

• No stacking “just because.” Overlapping toxicity (lipids, liver, BP, CNS) compounds quickly.

• Training first. Fix volume, intensity, sleep, and nutrition before touching dose—S-23 magnifies whatever system you already run.

• Deloads are non-negotiable. Schedule one during the back half of the run or at the front of recovery to keep fatigue in check.

→ Monitoring cadence (objective > vibes)

• Before: CBC; CMP (ALT/AST, creatinine/eGFR); lipid panel; hormones (total T, free T or calculated, LH/FSH); baseline BP and resting HR.

• During (week 3–4, then as needed): CMP, lipids; track BP, resting HR, sleep, mood, performance notes. If trends slide, adjust training/sleep first—not dose.

• After (recovery): Repeat hormones/lipids/CMP 3–6 weeks post; don’t consider another run until labs and symptoms normalize.

→ Cycle-length mindset

• Conservative windows only. Shorter runs limit cumulative suppression and make recovery more predictable.

• Plan the exit on day one. Book your post-cycle labs and set your training/nutrition for recovery before you start.

→ Red-flag checkpoints (stop and reassess)

• Persistent BP ≥140/90, notable resting-HR rise

• Marked ALT/AST elevation, dark urine, jaundice, RUQ pain

• Major mood changes, sleep breakdown, or anhedonia

• Sharp HDL drop or LDL spike on interim labs

→ Tested athletes

• SARMs are banned year-round. With gray-market variability and unknown metabolites, detection windows are unpredictable. If you’re tested, the only safe move is don’t use.

Stacking & Combinations (Proceed with Caution)

Short version: S-23 is already high-potency and suppressive. Stacking it with other SARMs or orals usually means more suppression, more liver/lipid strain, and more variables you can’t control. The FDA explicitly warns that SARM-labeled products are unapproved drugs linked to serious risks; in tested sport, they’re banned year-round. (U.S. Food and Drug Administration)

Common stacks people talk about — and why risk compounds

→ S-23 + RAD-140 or LGD-4033. Users chase “hardness + size,” but both RAD-140 and LGD-4033 have documented cholestatic drug-induced liver injury (DILI) cases. Additive liver risk + deeper endocrine suppression = bad trade. (PMC)
→ S-23 + another SARM (“kitchen-sink” SARM stacks). Class data show HDL drops with SARMs; stacking makes lipid headwinds worse while offering diminishing returns. (PMC)
→ S-23 + oral AAS (e.g., winstrol, anavar). Even if S-23 isn’t 17-aa, the overlapping hepatic and lipid toxicity profile compounds—and sourcing/label accuracy in the gray market is its own risk multiplier. (U.S. Food and Drug Administration)
→ S-23 + “PCT in a bottle” during the run. Case series note DILI from SARMs and/or PCT adjuncts; more pills ≠ more safety. (PMC)

What not to combine (overlapping-toxicity watchlist)

→ Any hepatotoxic oral (AAS, prohormones, “designer” steroids): stacks raise DILI odds; case literature keeps growing. (PMC)
→ Multiple SARMs at once: expect larger HDL suppression and harder recoveries; there is no clinical upside demonstrated to justify the risk. (PMC)
→ Stimulant-heavy fat burners: add BP/HR strain to a compound class already linked with lipid deterioration; not a smart pairing. (PMC)
→ Anything if you’re a tested athlete: SARMs are prohibited under WADA S1.2 all year; detection windows are unpredictable. (Wada Ama)

Smarter supports to prioritize instead of stacking (lower-risk pillars)

→ Sleep & recovery: 7–9 hours/night, scheduled deloads, steps/zone-2—these improve lipids, BP, and mood without adding hepatic load. (Pairs directly against the lipid/BP headwinds observed with SARMs.) (PMC)
→ Electrolytes & hydration: performance and BP stability with zero endocrine downside.
→ Protein & creatine monohydrate: supports strength/lean mass without liver/lipid penalties seen in SARM stacks; creatine is among the most studied, safe ergogenics.
→ Omega-3s (EPA/DHA): cardio-metabolic support while you monitor lipids—useful in a class that tends to knock HDL down. (PMC)
→ Vitamin D if deficient: fix the deficiency; don’t “stack” more SARMs.

Bottom line: S-23 already carries suppression, lipid, and potential hepatic signals. Stacking with SARMs or orals mostly multiplies risk without evidence-based upside. If someone insists on running it, keep it solo, shortest practical duration, with labs, and build your results on sleep, nutrition, and programming—not on a bigger supplement pile. (U.S. Food and Drug Administration)

S-23 vs. Other Compounds (What the Evidence Suggests)

Quick frame: S-23 sits in the “very potent, very suppressive” bucket with no human PK or dosing data. Compare it to what we do know from other SARMs and from oral AAS.

S-23 vs RAD-140 (Testolone)

Potency/suppression: S-23 binds AR extremely tightly (Kᵢ ≈ 1.7 nM in assay work), which helps explain its reputation for hardness and pronounced HPG-axis suppression in animals. RAD-140 is also high-affinity, but the data that matter for risk are the human case reports: biopsy-proven cholestatic DILI has been documented after RAD-140 use. Bottom line: if your goal is to minimize downside, S-23’s suppression + RAD’s documented DILI are both heavy costs. (caymanchem.com)

Side-effect profile: RAD-140 has multiple published liver-injury reports (including steroid-responsive cholestatic injury); S-23 lacks human case series but carries class-level hepatic and lipid risk warnings from FDA for SARMs generally. Both are prohibited at all times in tested sport. (PMC)

S-23 vs LGD-4033 (Ligandrol/VK5211)

Size vs hardness: LGD-4033 has the most human data in this group. In healthy men (Phase 1), 1 mg/day for 21 days increased lean mass with a 24–36 h half-life (once-daily PK). That profile skews toward “size” at low clinical doses, while S-23’s lore is “hardness” via hard AR signaling—but that’s preclinical + anecdote, not head-to-head data. (PubMed)

Recovery: LGD has human PK to time washouts and labs; S-23 does not. However, LGD also carries documented DILI cases in real-world use, and SARMs as a class tend to lower HDL—so recovery isn’t trivial. S-23’s strong suppression in animals suggests a tougher hormonal rebound even if hepatic events are less documented. (Lippincott Journals)

Takeaway: LGD-4033 = some human clinical data + known DILI case reports; S-23 = no human PK + high suppression. Both are banned in sport. (PubMed)

S-23 vs YK-11 / “myostatin” agents

Claims vs plausibility: The “myostatin inhibitor” pitch for YK-11 traces to cell data showing follistatin upregulation in C2C12 myoblasts (in vitro). That’s not human proof—and newer preclinical work flags potential neurotoxicity/oxidative stress concerns. Doping-control studies exist for metabolism detection, but there are no controlled human efficacy/safety trials. Against that backdrop, S-23 at least has in vivo rat data and consistent suppression signals; YK-11’s “myostatin block” remains unproven in humans. (PubMed)

Takeaway: Treat YK-11’s myostatin claims as hypothesis-level (cell models), not clinical reality. If the goal is “hardening,” training/diet manipulation beats betting on a compound with no human data and emerging safety questions. (PubMed)

S-23 vs Oxandrolone (Anavar) — oral AAS reference point

Efficacy signal: Unlike S-23, oxandrolone has real human clinical data (e.g., burn recovery) showing increases in lean body mass, strength, and functional recovery under medical supervision. (PMC)

Risk & regulation: Oxandrolone is a 17-α-alkylated AAS with well-documented HDL↓/LDL↑ effects and hepatotoxicity risk on its FDA label—hence intense monitoring and controlled-substance status. Meanwhile, S-23 isn’t approved at all; SARMs in “bodybuilding products” carry FDA warnings for serious safety issues, and all are prohibited in sport. (FDA Access Data)

Use-case reality: If someone is comparing “research SARM” to a prescription AAS, recognize the trade: S-23 has no human dosing/PK and uncertain purity in the gray market; oxandrolone has formal labeling and trials but brings known lipid/liver liabilities and legal controls. Neither is a free lunch. (FDA Access Data)

Bottom line (zoomed out)

• S-23 vs RAD-140: S-23 → more suppression; RAD-140 → more human DILI reports. Both banned. (PMC)

• S-23 vs LGD-4033: LGD has human PK + lean-mass data and DILI cases; S-23 lacks human PK but shows strong suppression preclinically. (PubMed)

• S-23 vs YK-11: YK-11’s “myostatin” angle is cell-culture level with no human trials and emerging safety concerns; treat as unproven. (PubMed)

• S-23 vs Oxandrolone: Oxandrolone has clinical efficacy in niche settings but clear HDL/liver risks and legal controls; S-23 has no human dosing data and sits under FDA warnings for SARM-labeled products. (PMC)

Legal Status of S23

Here’s a breakdown of where S23 stands legally — important to understand since the compound resides in a legally murky zone.

United States

• S23 and other selective androgen receptor modulators (SARMs) are not approved by the U.S. Food & Drug Administration (“FDA”) for any medical use. They are considered unapproved drugs. (U.S. Food and Drug Administration)

• Companies cannot legally market S23 (or any SARM) as a dietary supplement or as an over-the-counter drug in the U.S. (Council for Responsible Nutrition)

• The U.S. Senate introduced bills aiming to classify SARMs under the Controlled Substances Act (for example, the “SARMs Control Act of 2018”). The status of S23 specifically under these laws may vary by jurisdiction. (Congress.gov)

• From a sports doping perspective, the World Anti‑Doping Agency (“WADA”) prohibits all SARMs, including S23, for athletes in and out of competition. They fall under “Other Anabolic Agents (S1.2)”. (NPC Hello)

International / Other Considerations

• Because S23 is considered a research chemical or investigational compound, its legal regulation varies significantly by country. In many jurisdictions, marketing it as a supplement or human-use product is illegal. (Wikipedia)

• Even when sold online, products labelled “research use only” or “not for human consumption” may still violate local drug, supplement, or health-regulation laws. These labels do not guarantee legality. (PMC)

Key Practical Takeaways

• If you find S23 marketed as a “supplement” or “performance enhancer” in the U.S., that marketing is likely illegal under FDA policy.

• Athletes governed by anti-doping rules must treat S23 as prohibited at all times; even a trace could lead to sanctions.

• Legal risk includes not only regulatory/listing issues, but also product purity and liability risk — unapproved compounds often lack standard manufacturing controls.

• For non-athletes, while personal possession/use may not always trigger criminal prosecution (depending on jurisdiction), purchases and labeling can still run afoul of import/export, prescription-drug, or supplement-fraud laws.

Conclusion

S-23 sits at the far end of the SARM spectrum: potent AR signaling, high suppression, zero human dosing/PK, and no medical approval. Preclinical data explain the “hardening” reputation (lean-mass preservation in animals), but they also explain the cost—robust HPG-axis shutdown, class-level lipid and hepatic concerns, and a permanent spot on the WADA banned list. In plain terms: the “upside” is theoretical; the downsides are real.

What smart lifters do instead

• Build your look on training clarity (progressive overload, honest RPE, planned deloads).

• Lock in nutrition (adequate protein, consistent carbs around training, fiber and micros).

• Prioritize sleep and stress (7–9 hours, steps/zone-2, caffeine discipline).

• Use well-supported basics (creatine monohydrate, omega-3s, electrolytes, vitamin D if deficient) and keep labs for real health monitoring—not to justify risky cycles.

Bottom line: If you’re a tested athlete, the answer is simple—don’t touch SARMs. If you’re not, the evidence still points to a better play: skip unapproved, highly suppressive research chemicals and invest in the fundamentals that actually scale—training quality, recovery, nutrition, and consistency.

Educational disclaimer: This guide is for information only and is not medical advice. S-23 and other SARMs are not FDA-approved for any use, may carry serious health risks, and are prohibited in sport at all times. Always consult a qualified healthcare professional before making decisions that affect your health.