WADA prohibited-status registry: peptides and competitive sport

For competitive athletes — anyone subject to testing by a national anti-doping organization, the International Testing Agency, a sport federation, the military, or a professional league that adopts WADA standards — the question of whether a peptide is on the World Anti-Doping Agency's Prohibited List is the first filter, not the last. The regulatory exposure is independent of whether a substance is safe, effective, or legal to acquire under a country's drug laws. A peptide can be prescribed legally by a physician in one jurisdiction, accessed routinely through compounding pharmacies, and still trigger a doping violation that results in a two-to-four-year competition ban.

This dossier documents the 2026 WADA Prohibited List status for every peptide in the corpus. The framing is informational. The page does not tell drug-tested athletes how to evade testing — it documents the regulatory landscape so that decisions about peptide use can be made with the regulatory exposure in view. For athletes outside drug-tested competition, the WADA list is still a useful taxonomy: WADA's pharmacology committee tracks the literature on novel performance-enhancing compounds with more resources than most national regulators, and the list functions as a rough proxy for which compounds the field of sports-medicine experts considers likely to produce ergogenic effects.

The authoritative reference is the WADA 2026 Prohibited List, approved by WADA's Executive Committee on 11 September 2025 and in force from 1 January 2026. The List is updated annually each January following an extensive consultation process; athletes subject to testing should reverify status before each season.

The WADA framework

The Prohibited List groups substances into classes prefixed S0–S9 and methods prefixed M1–M3. Two distinctions are load-bearing for peptide users.

Prohibited at all times versus prohibited in-competition only. Classes S0 through S5 and methods M1–M3 are prohibited both in- and out-of-competition: an out-of-competition test (which can happen at any time on any day) detecting the substance is sufficient for a doping violation. Classes S6–S9 (stimulants, narcotics, cannabinoids, glucocorticoids) and P1 (beta-blockers in particular sports) are prohibited only in-competition, with an in-competition period defined by default as beginning at 11:59 p.m. the day before competition through the end of sample collection. Every peptide of concern to this corpus falls under at-all-times classes. There is no "wash-out before competition" pathway that produces a clean test if a peptide was used during preparation; out-of-competition testing closes that loop.

Specified versus non-Specified. A non-Specified violation carries a default four-year sanction; Specified-Substance violations can be reduced to two years or less if the athlete proves no significant fault. S0 substances are Specified; S2 substances are non-Specified. This means a positive for a research peptide caught under the S0 catch-all (BPC-157, Selank, DSIP) is sanctioned less severely by default than a positive for an explicitly named S2 peptide (Ipamorelin, MK-677, TB-500). The distinction does not affect whether a violation occurred, only the magnitude of the sanction.

The three classes that capture the peptide corpus are S0, S2, and S4.

S0 — Non-Approved Substances

The S0 catch-all is the regulatory backstop that captures research peptides without explicit naming. The 2026 List defines S0 as:

Any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use (e.g. drugs under pre-clinical or clinical development or discontinued, designer drugs, substances approved only for veterinary use) is prohibited at all times.

The List explicitly names BPC-157 as an S0 example. The general implication for the corpus: any peptide without FDA / EMA / equivalent regulator approval that is also not specifically named in S1–S5 falls under S0. This includes most research peptides accessed through the gray-market channel.

The "no current approval" test is global: approval by any major regulator removes a substance from S0 (it may still be captured by S1–S5, but not by the catch-all). This is why Tesamorelin (FDA-approved for HIV lipodystrophy) is S2 rather than S0, why FDA approval of Elamipretide in September 2025 changed its regulatory profile, and why the bremelanotide situation is complicated.

S2 — Peptide Hormones, Growth Factors, Related Substances, and Mimetics

The S2 class is the primary peptide-targeting class. The 2026 List enumerates five subsections:

• S2.1 — Erythropoietins (EPO) and agents affecting erythropoiesis (EPO, darbepoetins, CERA, EPO-Fc, EPO-mimetics including CNTO-530, peginesatide, pegmolesatide; HIF activators; innate repair receptor agonists including asialo EPO and carbamylated EPO).
• S2.2 — Peptide hormones and their releasing factors (gonadotrophins, corticotrophins, growth hormone analogues including AOD-9604 and hGH 176-191, GHRH analogues including CJC-1293, CJC-1295, sermorelin, and tesamorelin; growth hormone secretagogues including anamorelin, capromorelin, ibutamoren/MK-677, ipamorelin, lenomorelin/ghrelin, macimorelin, tabimorelin; GH-releasing peptides including alexamorelin, examorelin/hexarelin, GHRP-1, GHRP-2/pralmorelin, GHRP-3, GHRP-4, GHRP-5, GHRP-6).
• S2.3 — Growth factors and growth factor modulators (FGFs, HGF, IGF-1/mecasermin, MGFs, PDGF, Thymosin-β4 and its derivatives e.g. TB-500, VEGF; plus the open-ended catch-all "other growth factors or growth factor modulators affecting muscle, tendon or ligament protein synthesis/degradation, vascularisation, energy utilization, regenerative capacity or fibre type switching").

All S2 substances are non-Specified — the default sanction is four years for a first violation. The class is the most consequential for the peptide audience because it captures the largest portion of the GH-axis and tissue-repair compounds that biohacker protocols routinely deploy.

S4 — Hormone and Metabolic Modulators

S4 covers aromatase inhibitors, anti-estrogens, agents preventing activin receptor IIB activation (myostatin inhibitors), and metabolic modulators including AMPK activators (with MOTS-c explicitly named in the 2026 List as "mitochondrial open reading frame of the 12S rRNA-c") and PPARδ agonists (GW1516). S4.1 and S4.2 substances are Specified; S4.3 and S4.4 are non-Specified.

The Monitoring Program

WADA maintains a separate 2026 Monitoring Program for substances not currently prohibited but tracked for patterns of misuse. The 2026 program includes "Markers of Semaglutide and Tirzepatide" in- and out-of-competition; the explanatory note clarifies that "the urine monitoring of semaglutide includes also the monitoring of tirzepatide." Monitoring is not prohibition — a positive marker does not trigger a violation — but the surveillance signals where future prohibitions might land. The GLP-1 class is in this position as of 2026.

Therapeutic Use Exemptions

The Therapeutic Use Exemption (TUE) process, governed by the International Standard for Therapeutic Use Exemptions, permits use of a prohibited substance when four criteria are met: a clearly diagnosed medical condition requires the substance; therapeutic use will not enhance performance beyond the athlete's return to normal health; no reasonable permitted alternative exists; and the necessity is not the consequence of prior prohibited-substance use. Applications are reviewed by a committee of at least three independent physicians.

For research-only peptides (S0 class), TUE pathways are essentially closed — by definition, no regulator has approved the substance for any indication, so the second and third criteria cannot be met. For explicitly named S2 peptides used for off-label biohacker indications (anti-aging, recovery, muscle preservation), TUE pathways are also closed: the indication is not a recognized medical condition. For FDA-approved peptides used for their approved indications by athletes with the corresponding diagnosis — semaglutide for genuine type 2 diabetes, tesamorelin for HIV lipodystrophy — TUE pathways are realistic, with appropriate documentation. The realistic-TUE column in the tables below distinguishes these cases.

Detection: mass spectrometry and the biological passport

Two parallel detection systems operate. Direct detection via liquid chromatography–tandem mass spectrometry (LC-MS/MS) of urine or blood targets the parent compound or its metabolites. Detection windows vary by peptide — most synthetic peptides clear urine within 24–48 hours, but metabolite fragments often extend the window to days. Hair testing (used in some sport-specific protocols) can extend detection further but is not the primary WADA-accredited method.

The Athlete Biological Passport (ABP) adds longitudinal indirect detection. The hematological module tracks markers of blood doping (hemoglobin concentration, reticulocyte counts, OFF-score) over time, with deviations triggering targeted testing. The endocrine module — launched in the lead-up to Paris 2024 in collaboration with the International Testing Agency — tracks markers of GH and IGF-1 axis modulation longitudinally. The endocrine module is the indirect detection pathway that catches GH secretagogues (GHRPs, GHRH analogues, MK-677) by their downstream IGF-1 elevation rather than by detecting the secretagogue itself, which clears the system within hours. A protocol using a short-half-life secretagogue with strategic timing relative to known testing windows can evade direct detection but cannot evade ABP because the IGF-1 elevation persists for weeks.

The Essendon precedent

The case study that anchors WADA enforcement of peptides is the Essendon Football Club supplements saga, a 2012 Australian Football League (AFL) program that became the most consequential peptide-doping case in WADA history. The program was supervised by sports scientist Stephen Dank, who administered subcutaneous injections of AOD-9604, an unspecified "thymosin," and a range of other supplements to Essendon players across the 2012 preseason and season (Essendon Football Club supplements saga, Wikipedia).

WADA's position, communicated publicly to the Australian Sports Anti-Doping Authority on 22 April 2013, was that AOD-9604 had been prohibited under S0 since 2011 — the substance had never received regulatory approval, and as a GH fragment also fell under the S2 framework. ASADA declined to pursue cases for AOD-9604 use before 22 April 2013 on the grounds that the substance had not been explicitly listed by name on the Prohibited List prior to clarification. The Court of Arbitration for Sport later concluded that the "thymosin" administered was thymosin-β4 (the S2.3 substance, the parent of TB-500), and 34 Essendon players were ultimately sanctioned for thymosin-β4 use, with bans imposed in early 2016. Stephen Dank received a lifetime ban from association with AFL.

The case is the operating precedent for several enforcement principles still in force in 2026. The S0 catch-all is enforceable even when a substance is not specifically named, provided WADA can demonstrate non-approval and the substance was administered for performance-relevant purposes. Vague labeling ("thymosin") is not protective when CAS can establish the actual substance from program records and the substance falls under a prohibited class. Sports scientists and physicians who administer prohibited substances bear personal regulatory exposure independent of the athletes. And finally — most relevant to the peptide corpus — the gray-market peptide channel, with its informal labeling and ambiguous documentation, does not insulate athletes from sanction; the substance is detected analytically, not labeled.

Peptide-by-peptide registry

BPC-157

BPC-157 is S0 (Non-Approved Substances), explicitly named in the 2026 Prohibited List as an example: "This class covers many different substances including but not limited to BPC-157, 2,4-dinitrophenol (DNP), ryanodine receptor-1-calstabin complex stabilizers...". The naming is recent — BPC-157 received explicit citation in the WADA list circa 2022, formalizing what had previously been captured under the general S0 catch-all. The status is Specified-Substance under S0, meaning sanctions are subject to fault-based reduction.

Detection is by LC-MS/MS targeting the intact 15-amino-acid peptide and its plasma metabolites. The peptide's stability is unusual for its size — BPC-157 resists gastric proteolysis better than typical 15-mers, which is part of why oral formulations have been studied — but plasma half-life is short and urine clearance windows are estimated at 24–48 hours for intact peptide, longer for metabolites. Athletes who use BPC-157 in the off-season and stop weeks before competition still bear out-of-competition testing exposure.

TUE pathway: closed. BPC-157 has no regulator-approved indication anywhere, so the "no permitted alternative" criterion is unmeetable — by definition any approved tissue-repair therapy is the alternative. The BPC-157 critic response addresses adjacent claims about the molecule's safety profile.

TB-500

TB-500 is S2.3 (Growth Factors), explicitly named in the 2026 List as an example: "Thymosin-β4 and its derivatives e.g. TB-500." TB-500 is the 17-amino-acid synthetic fragment corresponding to a putative active region of thymosin-β4; its derivative relationship to the parent compound is the basis for the listing. Sanction default: four years (non-Specified).

The Essendon case anchors enforcement: thymosin-β4 was the substance for which 34 AFL players were ultimately sanctioned, with the Court of Arbitration for Sport accepting analytical evidence supporting thymosin-β4 administration even where labels read only "thymosin." Detection methods for thymosin-β4 and TB-500 metabolites in urine have matured since the Essendon investigation; LC-MS/MS protocols target the parent peptide and characteristic fragment ions (Esposito et al., Anal Bioanal Chem 2012, 402:2789–2796, abstract-confirmed). Urine detection windows are reported at multiple days for the intact peptide and longer for metabolites.

TUE pathway: closed. No approved indication for thymosin-β4 or TB-500 in any major regulatory jurisdiction.

GHK-Cu

GHK-Cu — copper tripeptide-1, GHK bound to Cu(II) — is not explicitly named on the 2026 WADA Prohibited List under any class. The compound's cosmetic-grade use is widespread (topical formulations are sold globally as anti-aging skincare). The injectable formulation is the regulatory question: a peptide that affects "regenerative capacity" arguably falls within the S2.3 catch-all language ("other growth factors or growth factor modulators affecting muscle, tendon or ligament protein synthesis/degradation, vascularisation, energy utilization, regenerative capacity or fibre type switching"), but GHK-Cu's documented mechanism is principally on collagen synthesis and copper modulation in skin / fibroblast contexts rather than skeletal-muscle protein turnover, and WADA has not invoked the catch-all against it in any published decision found through May 2026.

Practical position: athletes using topical GHK-Cu in anti-aging cosmetic formulations face negligible regulatory exposure. Injectable GHK-Cu use for systemic effect is in a gray zone — not explicitly named, plausibly captured under the S2.3 catch-all if WADA elected to invoke it. [unverified — confirm against any WADA technical document or decision specifically addressing GHK-Cu].

TUE pathway: practically irrelevant given the ambiguous prohibited status.

KPV

KPV is the C-terminal tripeptide of α-melanocyte-stimulating hormone (lysine-proline-valine), studied for anti-inflammatory activity. The compound is S0 (Non-Approved Substances) by default — no regulator approval anywhere, no specific naming in S1–S5. Detection is by LC-MS/MS targeting the intact tripeptide, with short urine clearance characteristic of small peptides. The literature is rodent-dominated and human evidence is thin; the regulatory landscape reflects that KPV is essentially unknown to mainstream sports medicine.

TUE pathway: closed.

Ipamorelin

Ipamorelin is S2.2 (Peptide Hormones and Their Releasing Factors), explicitly named in the 2026 List under "growth hormone secretagogues (GHS) and their mimetics": "e.g. anamorelin, capromorelin, ibutamoren (MK-677), ipamorelin, lenomorelin (ghrelin), macimorelin and tabimorelin." Sanction default: four years (non-Specified).

Detection is well-characterized. Direct detection of ipamorelin in urine has historically been challenging because the parent compound is rapidly metabolized; ipamorelin (1-4) free acid is the metabolite that extends the detection window after the parent has cleared (Semenistaya et al., Drug Test Anal 2015, 7:919–925). Detection windows after a single subcutaneous dose are reported in the low days for the metabolite. Dried-blood-spot LC-MS methods have been validated and reduce the burden on urine collection (Thomas et al., J Pharm Biomed Anal 2021, 195:113853, abstract-confirmed).

More important than direct detection: ipamorelin's central mechanism — pulsatile endogenous GH release, downstream IGF-1 elevation — is exactly what the Endocrine Module of the Athlete Biological Passport is designed to catch. An ipamorelin protocol that respects direct-detection windows but produces sustained IGF-1 elevation triggers ABP anomalies that persist for weeks.

TUE pathway: closed for biohacker indications. The "no permitted alternative" criterion fails because growth hormone deficiency, if genuinely diagnosed, has established somatotropin replacement protocols.

CJC-1295

CJC-1295 is S2.2, explicitly named in the 2026 List under growth hormone-releasing factors: "growth hormone-releasing hormone (GHRH) and its analogues (e.g. CJC-1293, CJC-1295, sermorelin and tesamorelin)." The listing covers both the with-DAC variant (with the Drug Affinity Complex extending half-life to days) and the without-DAC variant (modified GRF 1-29). Sanction default: four years (non-Specified).

Detection is by LC-MS/MS of the intact peptide and characteristic metabolites; the long-half-life DAC variant has the longest direct-detection window of the GHRH analogues. Endocrine Module surveillance applies for the same reason as ipamorelin — sustained or pulsatile downstream IGF-1 elevation triggers indirect detection regardless of whether the parent compound is detected directly.

TUE pathway: closed for biohacker indications. The molecule has no approved indication anywhere.

Tesamorelin

Tesamorelin is S2.2, explicitly named in the 2026 List in the same GHRH analogue line as CJC-1295. The molecule is FDA-approved (as Egrifta) for HIV-associated lipodystrophy — the regulatory approval does not remove tesamorelin from S2, because the S2 class captures the substance by chemistry and mechanism regardless of approval status. Sanction default: four years (non-Specified).

Detection is by LC-MS/MS plus Endocrine Module surveillance. The Egrifta dosing protocol produces measurable IGF-1 elevation that is detectable through ABP monitoring even when parent-compound direct detection windows are missed.

TUE pathway: realistic for athletes with a documented HIV lipodystrophy diagnosis using tesamorelin for its approved indication. This is one of the few peptides in the corpus where a TUE pathway is genuinely available — the molecule has an approved indication, a recognized clinical population, and no permitted alternative for visceral adipose tissue reduction in HIV lipodystrophy specifically. The TUE would not extend to off-label use for body composition, anti-aging, or athletic recovery — those uses route back through the S2 default.

MK-677 (Ibutamoren)

MK-677 is S2.2, explicitly named in the 2026 List as a growth hormone secretagogue: "ibutamoren (MK-677)." The compound is an orally-bioavailable nonpeptide ghrelin receptor agonist — not technically a peptide, but functionally a GH secretagogue and captured by the GHS framework. Sanction default: four years (non-Specified).

Direct detection of MK-677 is by LC-MS/MS targeting the parent compound; oral dosing produces sustained plasma concentrations with urine windows in the days. The more critical detection vector is the Endocrine Module: MK-677 produces the largest and most sustained IGF-1 elevation of any peptide-class GH secretagogue in clinical use, with effects on IGF-1 that persist for weeks after discontinuation. An MK-677 protocol that ends weeks before in-competition direct testing still produces ABP signal anomalies. The MK-677 long-cycle taper playbook and the GH secretagogue discontinuation playbook discuss the long-tail IGF-1 dynamics; for drug-tested athletes the implication is that even multi-month withdrawal windows do not guarantee ABP clearance.

TUE pathway: closed for non-medical indications. The compound has no marketed indication and is investigational; failed clinical development programs (most notably for sarcopenia) eliminate the "indicated treatment" pathway.

Semaglutide

Semaglutide is NOT prohibited on the 2026 WADA Prohibited List. The molecule is, however, on the 2026 Monitoring Program: "Markers of Semaglutide and Tirzepatide" are monitored in- and out-of-competition. Monitoring is surveillance, not prohibition — a positive marker does not constitute a doping violation. The placement signals WADA's interest in usage patterns; whether semaglutide moves to a Prohibited class in future years is an open question and may turn on whether evidence accumulates for ergogenic effect distinct from the weight-loss and metabolic indications.

For competitive athletes prescribed semaglutide for an approved indication (type 2 diabetes; chronic weight management in obesity), the molecule's monitoring status means the use can be disclosed on the doping-control form without triggering an adverse analytical finding; the body composition effects are part of an approved therapy. The picture changes if WADA reclassifies in a future update.

The relevant context is the broader GLP-1 discontinuation playbook — for athletes, the discontinuation timing question intersects with both the monitoring status and the possibility of future prohibition.

TUE pathway: not applicable while the substance is on the monitoring program rather than prohibited.

Tirzepatide

Tirzepatide is NOT prohibited on the 2026 WADA Prohibited List. The 2026 Monitoring Program explicitly captures it: the urine monitoring of semaglutide also includes monitoring of tirzepatide per the 2026 Summary of Major Modifications and Explanatory Notes. Same framing as semaglutide — surveillance, not prohibition.

TUE pathway: not applicable.

Liraglutide

Liraglutide is NOT prohibited on the 2026 WADA Prohibited List. The molecule is not explicitly named in the 2026 Monitoring Program, though the broader "Markers of Semaglutide and Tirzepatide" language may capture some shared metabolites incidentally. As of the 2026 list, liraglutide is unrestricted for athletes.

TUE pathway: not applicable.

Retatrutide

Retatrutide is NOT explicitly named on the 2026 WADA Prohibited List or the 2026 Monitoring Program. The molecule remains investigational (Phase 3 program ongoing as of early 2026 with no regulatory approval); the GLP-1/GIP/glucagon triple agonism is mechanistically novel and the metabolic effects on energy expenditure raise an ergogenic-effect question that WADA's pharmacology committee will likely consider in future cycles.

Default status: arguably captured by S0 (no current regulatory approval anywhere). The molecule has not been the subject of a published WADA enforcement decision through May 2026. [unverified — confirm against any WADA technical document specifically addressing retatrutide once the molecule reaches regulatory approval].

TUE pathway: closed for investigational use.

Selank

Selank is S0 (Non-Approved Substances). The compound is approved as a prescription anxiolytic in Russia, but no other major regulator has approved it; Russian approval does not satisfy the S0 test, which requires approval by any governmental regulatory health authority and is interpreted by WADA in practice as referring to major international regulators (FDA, EMA, Health Canada, TGA, PMDA, equivalent). The Russian approval has been argued historically as satisfying the test in the abstract — the question has not been litigated specifically for Selank at CAS so the position is unsettled — but the operating assumption for drug-tested athletes outside Russia should be S0.

Detection is by LC-MS/MS targeting the seven-amino-acid intact peptide; urine windows are short (hours) given the molecule's metabolic profile. The clinical literature on Selank is dominated by Russian-language sources with limited Western replication; the Selank peptide page addresses the evidence-quality limitations.

TUE pathway: closed outside Russia. Within Russia, the molecule's approved anxiolytic indication would in principle support a TUE for an athlete with documented anxiety disorder — though anxiolytic medications with more established TUE precedents (benzodiazepines, SSRIs, generally not prohibited substances) make the necessity test difficult to clear.

Semax

Semax is S0 by the same logic as Selank — Russian approval, no FDA/EMA/equivalent approval. The compound is a seven-amino-acid analogue of ACTH(4-10) studied for nootropic effects; the Russian approval covers stroke recovery and cognitive disorders. Western evidence is thin and replication is limited.

The S0 designation has a secondary consideration: as a melanocortin-pathway peptide, Semax could in principle be argued under a future S2-style framework, though the current S2 melanocortin language is narrow and Semax does not match a named subsection. The operating position for 2026 is S0.

TUE pathway: closed outside Russia.

Dihexa

Dihexa is S0. The compound is a six-amino-acid analogue of angiotensin IV with hepatocyte growth factor / c-Met activity, studied investigationally for cognitive applications. No regulatory approval anywhere. Detection by LC-MS/MS of intact peptide with short urine clearance. The HGF mechanism overlaps with S2.3 ("Hepatocyte growth factor (HGF)" is an explicitly listed S2.3 example, and "other growth factor modulators" extends the language), and a regulatory argument could be made that Dihexa is captured by S2.3 as an HGF modulator. The conservative position for athletes is to treat Dihexa as at minimum S0 and potentially S2.3. [unverified — WADA has not published a position specifically addressing Dihexa].

TUE pathway: closed.

Thymosin α-1 (Thymalfasin / Zadaxin)

Thymosin α-1 is NOT explicitly named on the 2026 WADA Prohibited List under any class. The compound is structurally distinct from thymosin-β4 (the S2.3-listed substance) despite the shared "thymosin" name — α-1 is a 28-amino-acid peptide derived from thymic prothymosin-α and acts on immune cells, particularly T-cell maturation, rather than on the muscle/tendon/ligament axis that S2.3 catch-all language captures.

Approval status: thymalfasin (Zadaxin) is approved in 35+ countries for chronic hepatitis B, hepatitis C, and adjunctive cancer indications; it is not FDA-approved. The international approvals are sufficient to satisfy the S0 "any governmental regulatory health authority" test, removing thymosin α-1 from S0 coverage.

The conclusion: as of the 2026 list, thymosin α-1 is not prohibited under any explicit class. This position rests on (a) the molecule not being named, (b) the mechanism not falling within S2.3's muscle/tendon/ligament catch-all, and (c) the international regulatory approvals exiting S0. The position is defensible but not formally adjudicated. [unverified — confirm by checking WADA's response to any specific federation inquiry regarding thymosin α-1].

TUE pathway: not currently required given non-prohibited status.

MOTS-c

MOTS-c is S4.4.1 (Metabolic Modulators), explicitly named in the 2026 List as an AMPK activator: "Activators of the AMP-activated protein kinase (AMPK), e.g. 5-N,6-N-bis(2-fluorophenyl)-[1,2,5]oxadiazolo[3,4-b]pyrazine-5,6-diamine (BAM15), AICAR, mitochondrial open reading frame of the 12S rRNA-c (MOTS-c)." The 16-amino-acid mitochondrial-encoded peptide is captured by name. Sanction default: four years (non-Specified, per S4.4 designation).

The placement under S4.4 rather than S2 reflects the mechanism — MOTS-c's effects on AMPK and mitochondrial energy utilization are categorized as metabolic modulation rather than peptide-hormone signaling. This is consistent with the placement of AICAR (the same S4.4.1 line) as a small-molecule AMPK activator.

Detection is by LC-MS/MS; the mitochondrial peptides dossier covers the molecular biology. Like other small peptides, urine windows are short and direct detection requires sample timing.

TUE pathway: closed. No approved indication.

Epitalon

Epitalon is S0. The four-amino-acid synthetic tetrapeptide (Ala-Glu-Asp-Gly) is studied for telomerase induction and pineal-axis effects in primarily Russian-language gerontology literature, with no regulator approval anywhere. The mechanism — telomerase induction, pineal modulation — does not match any S2 or S4 subsection cleanly, so the S0 catch-all applies.

Detection by LC-MS/MS of intact tetrapeptide; short urine windows. The Russian-dominant literature has limited Western replication; the anti-aging decision guide addresses the evidence-quality questions.

TUE pathway: closed.

PT-141 (Bremelanotide)

PT-141 — bremelanotide — is NOT explicitly named on the 2026 WADA Prohibited List under any class. The molecule is FDA-approved as Vyleesi (2019) for hypoactive sexual desire disorder in premenopausal women, satisfying the S0 "any governmental regulatory health authority" test. The molecule's mechanism — melanocortin-4 receptor agonism — does not match any explicitly named S2 subsection in the 2026 List. S2.2 covers gonadotrophins and corticotrophins but not melanocortin agonists generally.

The conclusion: PT-141 is not prohibited as of 2026. The position is well-supported by the explicit absence from the 2026 List index. [unverified — secondary sources occasionally claim PT-141 is "captured under S2"; this is not supported by the 2026 List text and appears to be erroneous restatement; the position here is based on direct reading of the 2026 List].

TUE pathway: not currently required.

DSIP

DSIP — delta sleep-inducing peptide — is S0. The nine-amino-acid peptide has no regulator approval anywhere and the mechanism does not match an S2 or S4 subsection. The clinical literature is limited and dated (peak research interest in the 1970s–1980s); the sleep quality decision guide places DSIP in evidence-poor territory relative to peptide alternatives.

Detection by LC-MS/MS; short urine windows characteristic of small peptides.

TUE pathway: closed.

SS-31 (Elamipretide)

SS-31 — elamipretide — was historically S0 (investigational, no approval) but the regulatory status changed in September 2025: FDA granted accelerated approval for elamipretide (brand name Forzinity, Stealth BioTherapeutics) for the treatment of Barth syndrome in patients weighing at least 30 kg (FDA accelerated approval announcement, September 2025).

The FDA approval removes elamipretide from S0 coverage. The molecule does not match any explicitly named S2 or S4 subsection in the 2026 List — SS-31's mechanism (cardiolipin stabilization, mitochondrial inner-membrane targeting) is not captured by S2.3 muscle/tendon/ligament catch-all language, nor by S4.4 AMPK or PPARδ subsections.

Conclusion for 2026: elamipretide is NOT prohibited under any explicit class, by virtue of (a) FDA approval exiting S0 and (b) no match to S2 or S4 explicit subsections. This represents a status change from 2025 when SS-31 was unambiguously S0. [unverified — confirm against any WADA-issued clarification on elamipretide following the 2025 FDA approval; this position rests on direct reading of the 2026 List text without WADA-issued clarification].

TUE pathway: realistic for athletes with documented Barth syndrome. Practically irrelevant for biohacker indications given the rarity of Barth syndrome (approximately 150 diagnosed individuals in the United States).

AOD-9604

AOD-9604 is S2.2.3, explicitly named in the 2026 List as a growth hormone fragment: "growth hormone fragments, e.g. AOD-9604 and hGH 176-191." The compound is the 15-amino-acid C-terminal fragment of human growth hormone, originally developed for obesity by Metabolic Pharmaceuticals (failed Phase III), subsequently used in off-label and gray-market contexts. Sanction default: four years (non-Specified).

The historical case study is the Essendon Football Club supplements saga (covered in detail above). WADA's position that AOD-9604 was prohibited under S0 since 2011 was clarified to ASADA on 22 April 2013; the molecule was subsequently moved to S2 by name. The Essendon program's use of AOD-9604 was one of the two pillars of the sanctions investigation, with thymosin-β4 the other.

Detection methods for AOD-9604 in urine have been validated with limits of detection in the 50 pg/mL range using LC-MS/MS with solid-phase extraction (Cox et al., Drug Test Anal 2015, 7:31–38, abstract-confirmed). Six metabolites have been characterized in vitro, extending the effective detection profile beyond the parent compound.

TUE pathway: closed. No approved indication exists for AOD-9604 anywhere.

Sermorelin

Sermorelin is S2.2, explicitly named in the 2026 List as a GHRH analogue: "growth hormone-releasing hormone (GHRH) and its analogues (e.g. CJC-1293, CJC-1295, sermorelin and tesamorelin)." The compound is the 29-amino-acid synthetic version of human GHRH(1-29), historically approved by FDA (Geref) for pediatric GH deficiency, with that approval discontinued. Current US availability is through compounding pharmacies. Sanction default: four years (non-Specified).

The historical FDA approval is no longer current — the brand product Geref was discontinued — so the S0 question does not apply, and S2 applies by mechanism. Detection is by LC-MS/MS plus Endocrine Module surveillance, with the same caveats as CJC-1295 and tesamorelin regarding ABP capture of downstream IGF-1 elevation.

TUE pathway: theoretically available for documented adult GH deficiency, though the indication is more commonly served by direct somatropin replacement under TUE — which is itself a documented but uncommon pathway. The "no permitted alternative" criterion is difficult to satisfy because somatropin TUEs exist as the standard pathway for genuine GHD.

Hexarelin

Hexarelin is S2.2, explicitly named in the 2026 List as a GH-releasing peptide: "GH-releasing peptides (GHRPs) [e.g. alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, GHRP-5 and GHRP-6]." The compound is a six-amino-acid synthetic GHRP studied in the 1990s for GH-deficiency indications, never advancing to regulatory approval. Sanction default: four years (non-Specified).

Detection is well-established. Hexarelin and its metabolites have been characterized in urine LC-MS/MS protocols since the early 2010s (Thomas et al., Anal Bioanal Chem 2011, 401:507–516, abstract-confirmed); the parent peptide and characteristic fragments are routinely targeted in WADA-accredited laboratory panels. ABP Endocrine Module surveillance applies for the same downstream-IGF-1 reasons as ipamorelin.

TUE pathway: closed. No approved indication.

ARA-290 (Cibinetide)

ARA-290 is captured by S2.1.5 (Innate Repair Receptor Agonists). The 2026 List explicitly enumerates: "Innate repair receptor agonists, e.g. asialo EPO; carbamylated EPO (CEPO)." ARA-290 is the prototypical innate-repair-receptor (IRR) agonist — the 11-amino-acid synthetic peptide derived from the EPO B-helix, engineered specifically to activate the IRR heteromer (EPOR/βcR / CD131) while lacking the erythropoietic signaling that prohibits EPO under S2.1.1.

The S2.1.5 listing language is open-ended ("Innate repair receptor agonists, e.g. ...") and the regulatory intent — captured by the inclusion of carbamylated EPO and asialo EPO as examples of non-erythropoietic EPO derivatives — covers ARA-290 by mechanism even though the molecule is not named. Sanction default: four years (non-Specified). [unverified — confirm by any WADA technical document specifically addressing ARA-290; the position here rests on direct mechanistic match to S2.1.5 wording rather than explicit naming].

The substance is investigational (Phase 2 completed for sarcoidosis-associated neuropathy with FDA orphan designation; no approved indication as of 2026). Detection is by LC-MS/MS targeting the intact 11-amino-acid peptide.

TUE pathway: closed in absence of approved indication.

Cerebrolysin

Cerebrolysin is NOT explicitly named on the 2026 WADA Prohibited List. The product is a complex peptide mixture (low-molecular-weight peptides and amino acids derived from porcine brain tissue), approved in 50+ countries primarily for neurological indications (stroke, traumatic brain injury, vascular dementia) but not FDA-approved. The international approvals satisfy the S0 "any governmental regulatory health authority" test, removing it from S0 coverage.

The mechanism — broad neurotrophic and neuroprotective effects, BDNF-pathway modulation — does not match any explicitly named S2 or S4 subsection. The S2.3 catch-all language covers "growth factors or growth factor modulators affecting muscle, tendon or ligament protein synthesis/degradation, vascularisation, energy utilization, regenerative capacity or fibre type switching" — cerebrolysin's neurotrophic effects do not cleanly fit this language, which is muscle/connective-tissue-axis focused.

Conclusion for 2026: cerebrolysin is not prohibited under any explicit class. [unverified — confirm by checking any WADA technical document specifically addressing cerebrolysin; the position rests on direct reading of the 2026 List].

TUE pathway: not currently required.

5-Amino-1MQ

5-Amino-1MQ — 5-amino-1-methylquinolinium — is a small molecule, not a peptide. The compound is an NNMT (nicotinamide N-methyltransferase) inhibitor in preclinical development for metabolic and body-composition applications. No regulator approval anywhere. The molecule is not explicitly named on the 2026 WADA Prohibited List.

Default status: S0 by catch-all (non-approved pharmacological substance, not addressed by any subsequent section). The NNMT mechanism is novel and does not match S2 or S4 explicit subsections; the AMPK/NAD pathway adjacency could in principle invoke S4.4.1 if WADA elected to extend the AMPK activator language, but no current technical document supports that interpretation. [unverified — confirm against any WADA technical document addressing NNMT inhibitors as a class once the molecule has clinical-development advancement].

TUE pathway: closed.

Class-level summary

The corpus splits cleanly into five regulatory exposure tiers.

Explicitly named S2 (highest regulatory exposure): TB-500, Ipamorelin, CJC-1295, Tesamorelin, MK-677, AOD-9604, Sermorelin, Hexarelin. All are non-Specified with four-year default sanctions; all are direct-detection targets in WADA-accredited LC-MS/MS panels; all trigger Endocrine Module ABP surveillance through downstream IGF-1 elevation; TUE pathways are closed for biohacker indications and realistic only for Tesamorelin's specific HIV-lipodystrophy indication.

S0 catch-all (research-only peptides, lower default sanction): BPC-157 (explicitly named in S0 examples), KPV, Selank, Semax, Dihexa, Epitalon, DSIP, 5-Amino-1MQ. Specified-Substance status allows for reduced sanctions on no-significant-fault findings, but the violations themselves are still violations. Detection by direct LC-MS/MS of intact peptide or characteristic metabolites.

S2.1.5 — innate repair receptor agonists: ARA-290 (captured by mechanism if not by name).

S4.4.1 — explicitly named metabolic modulator: MOTS-c.

Not currently prohibited: GHK-Cu (topical/cosmetic clearly outside; injectable in S2.3 catch-all gray zone), Semaglutide (Monitoring Program), Tirzepatide (Monitoring Program), Liraglutide (unrestricted), Retatrutide (unrestricted but investigational so plausibly future S0), Thymosin α-1 (international approvals exit S0; mechanism does not match S2.3), PT-141 (FDA approval exits S0; mechanism not matched by named S2 subsection), SS-31/Elamipretide (FDA-approved September 2025 exits S0; mechanism not matched), Cerebrolysin (international approvals exit S0; mechanism not matched).

The "not currently prohibited" tier carries the most consequential regulatory uncertainty. WADA's annual review cycle can move substances onto the list in any year; the 2026 monitoring placement of semaglutide and tirzepatide signals that the GLP-1 class is being actively considered. Athletes whose protocols include any peptide in this tier should verify status before each season and watch for technical document updates.

The competitive-sport ethical framing

The brand position here, consistent across the corpus, is harm reduction. For peptide users in general, harm reduction includes practical pharmacology, evidence-quality honesty, and the gap between what the research says and what marketing claims. For athletes in drug-tested sport, harm reduction includes a regulatory-exposure dimension that other audiences do not face.

The framing is not that doping is acceptable when undetectable, nor that the WADA Code is unjust, nor that "everybody does it" makes individual use ethically neutral. The framing is that an athlete who takes a research peptide without understanding the prohibited-substance landscape bears a real risk of a four-year competition ban, retroactive disqualification of results, and reputational and financial consequences that exceed any plausible benefit from the peptide. Informed consent to that exposure is a meaningful ethical category. Uninformed consent is not.

The corollary: WADA's framework is imperfect, the science underlying some prohibitions is contested, and the regulatory pace lags ergogenic-compound development. Those critiques are legitimate. They do not change the operational reality that the Code is the regime within which competitive athletes operate, the testing infrastructure is well-funded and increasingly capable (the Endocrine Module is more sensitive than direct detection alone, and the ABP framework gets more powerful with each annual update), and sanctions are imposed on substance presence, not intent.

For the audience considering peptide use while subject to drug testing: the conservative position is to assume any research peptide is at minimum S0, treat any GH-axis peptide as detectable in-class even when timing seems to favor evasion, and consult an anti-doping organization's national-level guidance before adding any peptide to a protocol. The peptide vendors and clinicians who serve this market may not surface regulatory exposure in their consultations. The athlete bears strict liability under the Code regardless of vendor or practitioner advice.

For the audience outside drug-tested sport, the WADA framework is informational rather than operational, but the list itself is a useful pharmacology resource: WADA's pharmacology committee is one of the better-funded technical bodies surveying novel performance-enhancement compounds, and the inclusion or exclusion of a substance from the list often precedes (and occasionally drives) regulatory attention from FDA, EMA, and equivalent bodies.

Sources cited

• WADA 2026 Prohibited List — primary reference document
• WADA 2026 Monitoring Program — GLP-1 monitoring status
• WADA 2026 Summary of Major Modifications and Explanatory Notes — changes from 2025
• WADA International Standard for Therapeutic Use Exemptions — TUE framework
• WADA Endocrine Module Laboratory Guidelines — ABP framework for GH and IGF-1 surveillance
• Essendon Football Club supplements saga — historical case study
• FDA accelerated approval for elamipretide (Forzinity), September 2025 — SS-31 regulatory status change
• Semenistaya et al., Drug Test Anal 2015, 7:919–925 — GHRP and ipamorelin urinary metabolite detection
• Thomas et al., Anal Bioanal Chem 2011, 401:507–516 — GHRP urinary LC-MS/MS doping control method
• Cox et al., Drug Test Anal 2015, 7:31–38 — AOD-9604 detection and in vitro metabolism
• Thomas et al., J Pharm Biomed Anal 2021, 195:113853 — Ipamorelin dried blood spot detection