SS-31

Dosing from the Literature

Published for longevity: nothing approved; Forzinity's 40 mg a day is for Barth syndrome. Not published: a trial of off-label doses for aging or fatigue.

The last column of each row names where its figures come from.

What It Is

SS-31 is a synthetic tetrapeptide (a chain of 4 amino acids) with the sequence D-Arg-Dmt-Lys-Phe-NH₂ (where Dmt is 2',6'-dimethyl-L-tyrosine). It is one of the Szeto-Schiller (SS) family of mitochondria-targeting peptides; Hazel Szeto's group designed it, and it entered clinical development in 2010 (Szeto & Birk, Clin Pharmacol Ther 2014; PMID 25188726). Under the clinical name elamipretide, it was developed by Stealth BioTherapeutics through a multi-indication clinical program culminating in FDA accelerated approval on September 19, 2025 as Forzinity^®, which FDA called the first treatment for Barth syndrome (FDA, September 19, 2025), a rare X-linked mitochondrial disorder caused by TAFAZZIN gene mutations affecting cardiolipin remodeling. It is approved to improve muscle strength in adults and children with Barth syndrome who weigh at least 30 kg (Forzinity label).

What distinguishes SS-31 from nearly every other peptide in the Kalios database is the novelty of its mechanism: it selectively accumulates in the inner mitochondrial membrane — not via receptor binding, but through physical affinity for cardiolipin, the signature phospholipid of the inner mitochondrial membrane, which is present at extremely low concentration elsewhere in the cell. SS-31 carries a net positive charge at physiological pH and is lipophilic enough to cross both the outer and inner mitochondrial membranes and concentrate in the cardiolipin-rich inner leaflet at 1,000–10,000× its cytoplasmic concentration. Once bound to cardiolipin, SS-31 stabilizes the inner membrane structure, preserves cristae architecture, protects cardiolipin from peroxidation, and improves electron-transport-chain efficiency (Birk et al., J Am Soc Nephrol 2013; PMID 23813215).

Clinically, SS-31 has been studied across a broader range of indications than its Barth syndrome approval suggests: heart failure (PROGRESS-HF), ischemia-reperfusion injury (EMBRACE-STEMI), dry age-related macular degeneration (ReCLAIM), primary mitochondrial myopathy (MMPOWER-3), and aged-muscle fatigue. Most of these Phase 2/3 programs produced mixed results — sometimes meeting exploratory endpoints while failing primary endpoints. Barth syndrome was the indication where the cardiolipin-specific mechanism converged with the disease biology, and where the 168-week open-label extension TAZPOWER data ultimately supported accelerated FDA approval.

Its approved use (Barth syndrome) is rare and narrowly defined, while its mechanism (cardiolipin stabilization, mitochondrial protection) is proposed for many diseases involving mitochondrial dysfunction. Off-label community use for anti-aging, heart failure support, skeletal-muscle fatigue and macular degeneration rests on that mechanism and on Phase 2 results, often mixed, and is not within the approved label.

Mechanism of Action

The Forzinity label describes elamipretide as a mitochondrial cardiolipin binder that localizes to the inner mitochondrial membrane and improves mitochondrial morphology and function (Forzinity label). The findings below come from cell, isolated-mitochondria and animal studies unless a line says otherwise.

• Cardiolipin binding at inner mitochondrial membrane — SS-31 binds cardiolipin, a lipid found only in the inner mitochondrial membrane, and this binding accounts for its concentration there; from fluorescence and NMR studies, the developers propose that its two basic residues bind the lipid's phosphate head groups electrostatically while its aromatic residues sit among the lipid's fatty-acid tails (Szeto & Birk, Clin Pharmacol Ther 2014; PMID 25188726). The SS peptides concentrate more than 1,000-fold in that membrane (Szeto, AAPS J 2006; PMID 16796378), and the developers describe them as the first compounds known to target a membrane lipid rather than a protein (Szeto & Birk, 2014).
• Cristae-structure preservation — Cardiolipin's cone shape curves membranes; it is needed to form the inner membrane's folds (cristae), and on them it lets the respiratory complexes pack into supercomplexes (Szeto & Birk, 2014; PMID 25188726). In rats, SS-31 protected cristae during kidney ischemia (Birk et al., J Am Soc Nephrol 2013; PMID 23813215).
• Cardiolipin peroxidation protection — Cytochrome c bound too tightly to cardiolipin turns into a peroxidase that oxidizes it; oxidized cardiolipin makes the cristae lose their curvature and, with calcium, opens the permeability transition pore, releasing cytochrome c to trigger apoptosis (programmed cell death) (Szeto & Birk, 2014; PMID 25188726). Bound to cardiolipin, SS-31 blocked that peroxidase activity in lab tests (Birk et al., 2013; PMID 23813215). Whether it also scavenges free radicals is disputed: the developers' early work describes the SS peptides as scavengers of hydrogen peroxide (Szeto, 2006; PMID 16796378), while a 2014 study found no scavenging in cell-free tests (Brown et al., J Cardiovasc Pharmacol Ther 2014; PMID 24288396).
• Electron-transport-chain efficiency — Cardiolipin holds cytochrome c, which carries electrons from complex III to complex IV, close to both complexes (Szeto & Birk, 2014; PMID 25188726). In lab studies SS-31 raised state 3 respiration and the ATP made per unit of oxygen (Szeto & Birk, 2014), and in rats it sped ATP recovery after kidney ischemia (Birk et al., 2013).
• Reduced ROS generation at source — Less efficient electron transport leaks more electrons and makes more ROS; the developers propose that by speeding electron transfer at cytochrome c, the SS peptides reduce that leak (Szeto & Birk, 2014; PMID 25188726). SS-31 lowered ROS levels in isolated heart mitochondria without scavenging ROS in cell-free tests, and the authors conclude it likely reduces their generation (Brown et al., 2014; PMID 24288396).
• Mitochondrial membrane potential preservation — Preserves ΔΨ_m, the proton gradient that drives ATP synthase. Relevant in ischemia-reperfusion, where ΔΨ_m collapse triggers mitochondrial permeability transition pore opening and apoptosis (Zhao et al., J Biol Chem 2004; PMID 15178689).
• Anti-apoptotic signaling — The SS peptides prevented cytochrome c release in isolated mitochondria and reduced oxidant-induced cell death in neuronal cells (Zhao et al., J Biol Chem 2004; PMID 15178689); in rats, SS-31 reduced apoptosis after kidney ischemia (Birk et al., 2013; PMID 23813215).
• Receptor binding — The SS peptides grew out of work on an opioid peptide, but SS-31 has negligible affinity for opioid receptors (Szeto & Birk, 2014; PMID 25188726). In lab tests it did inhibit one drug transporter, MATE1 (Forzinity label).
• Tissue distribution — In animals given an injection under the skin, it reached the kidney, heart, liver, skeletal muscle and lung within 30 minutes, with the highest levels in the kidney and little in fat (Szeto & Birk, 2014; PMID 25188726). In people it spreads through total body water (Forzinity label).
• Pharmacokinetics in humans — After an injection under the skin, blood levels peak within 0.5 to 1 hour, about 92% of the dose is absorbed, and nearly all of it is recovered in the urine within 48 hours, as the drug or its breakdown products, with little build-up on daily dosing (Forzinity label). Phase I studies in healthy volunteers found an elimination half-life of about 4 hours; in rats, dogs and monkeys it was about 2 hours, which the developers note was enough for once-daily dosing to work in those species (Szeto & Birk, 2014; PMID 25188726).

What the Research Shows

SS-31 has been studied in multiple Phase 2 programs in addition to TAZPOWER, the Barth syndrome trial behind its approval.

• Szeto-Schiller peptide design (Szeto, 2006, AAPS J; PMID 16796378) — Foundational design paper establishing the SS-peptide family and the cardiolipin-targeting mechanism.
• Cardiolipin binding mechanism (Birk et al., JASN 2013; PMID 23813215) — Demonstration that SS-31 re-energizes ischemic mitochondria by interacting with cardiolipin.
• TAZPOWER Phase 2/3 Barth syndrome, 28-week randomized portion (Thompson et al., Genet Med 2021; PMID 33077895) — Initial randomized placebo-controlled phase in 12 patients; primary endpoint missed at 28 weeks but set up the open-label extension.
• TAZPOWER 168-week extension (Thompson et al., Genet Med 2024; PMID 38602181) — 8 patients reached 168 weeks. 6-minute walk distance improved by a cumulative 96.1 m from the extension's baseline at week 168; improvements in Barth Syndrome Symptom Assessment fatigue score and muscle strength. Basis for FDA accelerated approval.
• Heart failure, one infusion (Daubert et al., Circ Heart Fail 2017; PMID 29217757) — Randomized, placebo-controlled, ascending-dose trial of a single 4-hour IV infusion in 36 patients with heart failure with reduced ejection fraction (EF ≤35%). No serious adverse events; at the highest dose, left-ventricular end-diastolic and end-systolic volumes fell (−18 mL and −14 mL versus placebo) at the end of the infusion.
• Heart failure, 4 weeks — PROGRESS-HF Phase 2 (Butler et al., J Card Fail 2020; PMID 32068002) — 71 patients with heart failure with reduced ejection fraction (EF ≤40%) randomized to placebo, 4 mg or 40 mg SubQ once daily for 28 days. Well tolerated; neither dose changed left-ventricular end-systolic volume or ejection fraction versus placebo.
• Heart failure — canine HF (Sabbah et al., Circ Heart Fail 2016; PMID 26839394) — Improved LV and mitochondrial function in dogs with advanced HF. Foundational preclinical cardiac data.
• Primary mitochondrial myopathy — Phase 1 crossover (Karaa et al., Neurology 2018; PMID 29500292) — Dose-escalation, single-dose pharmacodynamic evidence of 6-minute walk improvement.
• Primary mitochondrial myopathy — MMPOWER-3 Phase 3 (Karaa et al., Neurology 2023; PMID 37268435) — In 218 people with primary mitochondrial myopathy, 40 mg a day for 24 weeks missed both primary endpoints, the 6-minute walk and fatigue. In an analysis by genotype, participants with nuclear-DNA defects walked farther than on placebo.
• EMBRACE-STEMI (ST-elevation MI) — Phase 2 in STEMI, an IV infusion during primary angioplasty. Infarct size, its primary endpoint, measured by the CK-MB enzyme in blood, was similar on the drug and placebo, as was infarct size on MRI at 30 days (ClinicalTrials.gov NCT01572909). In rabbits, the drug (as Bendavia) cut infarct size by about half when started 20 minutes before blood flow returned, but not when started 10 minutes after (Brown et al., J Cardiovasc Pharmacol Ther 2014).
• ReCLAIM dry AMD — Phase 2 in dry age-related macular degeneration; functional visual endpoint improvement in subsets.
• Aged muscle energetics (Roshanravan et al., PLoS One 2021) — Single-dose elamipretide improved in-vivo mitochondrial ATP production in older adult skeletal muscle in a randomized study; the rise was measured right after the infusion and was gone a week later, and fatigue resistance did not change.
• Aged kidney (Sweetwyne et al., Kidney Int 2017; PMID 28063595) — SS-31 rescued age-related glomerular (pertaining to the kidney's filtering units) architecture changes in aged mice. Preclinical support for mitochondrial-related chronic-kidney-disease applications.
• Human failing heart ex vivo (Chatfield et al., JACC Basic Transl Sci 2019) — Improved mitochondrial function in ex-vivo tissue from failing human hearts. Direct human cardiac mechanistic confirmation.
• Barth-syndrome mouse model mitophagy (Sci Rep 2024; DOI 10.1038/s41598-024-64368-y) — SS-31 ameliorates cardiac mitochondrial morphology and defective mitophagy in a Barth syndrome murine model.

Human Data

The record of SS-31 / elamipretide in people:

• Phase 1 PK/safety (multiple) — Established pharmacokinetics, once-daily SubQ dosing, clean safety profile. Urva and Stealth BioTherapeutics publications.
• TAZPOWER (NCT03098797) — Barth syndrome, 28 weeks placebo-controlled + 168 weeks open-label. Basis for FDA accelerated approval in September 2025.
• MMPOWER-3 — Primary mitochondrial myopathy Phase 3 in 218 people. Missed both primary endpoints at 24 weeks (Karaa et al., 2023).
• EMBRACE-STEMI — Acute STEMI Phase 2. Primary endpoint missed; mechanistic substudies informative.
• PROGRESS-HF — Phase 2 in heart failure with reduced ejection fraction (71 patients, 28 days). Well tolerated; no change in left-ventricular volumes or ejection fraction versus placebo (Butler et al., 2020).
• ReCLAIM-1, ReCLAIM-2 — Phase 2 dry AMD studies. Some functional visual endpoint improvement.
• Leber hereditary optic neuropathy (LHON) — Exploratory and compassionate-use cases described.
• Aged-muscle energetics (Roshanravan et al., 2021) — In a randomized trial in 39 older adults, one infusion raised ATP production in a hand muscle right after it, not a week later; fatigue resistance did not change.
• Forzinity accelerated approval (September 2025) — FDA accelerated approval based on TAZPOWER extension under Stealth BioTherapeutics.
• Required confirmatory trial — As a condition of the accelerated approval, FDA requires a randomized, double-blind, placebo-controlled trial to confirm that the gains in knee muscle strength translate into a benefit to patients (FDA, September 19, 2025).

Reconstitution & Storage

Forzinity is a ready-to-use solution, 280 mg in 3.5 mL (80 mg/mL), in single-patient-use vials (Forzinity label). SS-31 sold as a research chemical comes as a powder to be mixed with bacteriostatic water; the rows below show the arithmetic for 10 mg and 40 mg vials.

• Reconstitution (research vial) — Online reconstitution guides describe adding the bacteriostatic water slowly down the vial wall at a 45° angle, then swirling gently rather than shaking.
• Storage — The Forzinity label says to keep vials refrigerated at 2–8°C and not to freeze them; after the first dose, an opened vial can be kept refrigerated or at room temperature (20–25°C) and is thrown away 8 days after first opening (Forzinity label).
• Injection sites — The Forzinity label describes injection under the skin of the abdomen, at least 2 inches from the navel, or the outer thigh, rotating the site daily (Forzinity label).
• Timing — The Forzinity label gives the dose at the same time each day (Forzinity label).
• Inspection — The Forzinity label says not to use the solution if it is cloudy, discolored or contains particles (Forzinity label).

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Side Effects & Risks

In its trials elamipretide was reported as well tolerated (Daubert et al., 2017; Butler et al., 2020; Karaa et al., 2023; Thompson et al., 2024). In the trials of daily injections, most adverse events were mild to moderate (Thompson et al., 2021; Karaa et al., 2023). The Forzinity label adds a warning for allergic reactions (Forzinity label).

• Injection-site reactions — The most common adverse events in the trials of daily injections (Karaa et al., 2023; Thompson et al., 2024). In the Barth syndrome trial, redness at the site affected all 12 patients on the drug versus 3 of 12 on placebo, and hardening, itching, pain, bruising and hives were also more common on the drug (Forzinity label); 2 of 10 patients left the open-label extension because of these reactions (Thompson et al., 2021).
• Headache — Reported in the trials, but no more often than on placebo: 1 of 12 on the drug versus 3 of 12 on placebo in the Barth syndrome trial (Thompson et al., 2021), and 2 of 9 at the top dose versus 2 of 9 on placebo in a 5-day infusion trial (Karaa et al., 2018).
• Stomach upset — No more common than on placebo in the Barth syndrome trial: gastrointestinal complaints in 1 of 12 on the drug versus 4 of 12 on placebo, nausea in 1 of 12 on each (Thompson et al., 2021).
• Blood counts and heart rhythm — Eosinophil counts often rose in studies of 30 days or more, peaking around 90 days and returning to baseline after 6 to 12 months or after stopping, without symptoms; no clinically significant QTc prolongation was seen at three times the peak concentration of the 40 mg dose (Forzinity label).
• Allergic reactions — The label warns of hypersensitivity reactions, including serious allergic reactions that needed emergency treatment, with rash, raised or eczema-like skin lesions, or cough, appearing within minutes to months of starting; serious hypersensitivity to elamipretide or its ingredients is its one contraindication (Forzinity label).
• Drug interactions — In lab tests elamipretide did not inhibit or induce the main CYP liver enzymes but did inhibit the drug transporter MATE1; it is broken down from its C-terminal end into inactive fragments, not by the liver. Given with aspirin or clopidogrel it did not change their blood levels or effects, nor heparin's effect on clotting tests (Forzinity label).
• Pregnancy / lactation — No human data, because Barth syndrome rarely affects females; in rat and rabbit studies it caused no harm to development (Forzinity label).
• Pediatric use — Approved for children with Barth syndrome who weigh at least 30 kg, at the same 40 mg dose; the extension study behind the approval included seven children aged 12 and older. It is not established below 30 kg, and it is not approved for newborns: its preservative, benzyl alcohol, has caused serious and fatal reactions in premature and low-birth-weight newborns given benzyl-alcohol-containing drugs intravenously (Forzinity label).
• Long-term (168-week TAZPOWER extension) — Elamipretide was well tolerated through the extension, in which 8 of 10 patients reached week 168; injection-site reactions were the most common adverse events (Thompson et al., 2024).
• Purity (gray-market research-chemical supply) — Forzinity is FDA-approved (Drugs@FDA, NDA 215244); SS-31 sold as a research chemical is a different, unapproved product, unregulated for quality.
• WADA status — Not named on the Prohibited List. Elamipretide is FDA-approved (Forzinity, 2025), so S0, which covers substances with no government approval, does not apply (WADA Prohibited List 2026).

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for off-label use of SS-31. For Forzinity, the label tells prescribers to watch for allergic (hypersensitivity) reactions throughout treatment and sets the dose by kidney function, halving it in adults with an eGFR under 30 mL/min who are not on dialysis (Forzinity label). The Barth syndrome trial measured the 6-minute walk, a fatigue score, knee-extensor strength, heart structure and function by echocardiography, and the monolysocardiolipin-to-cardiolipin ratio in dried blood spots (Thompson et al., 2021).

What to Expect — Timeline

No trial has followed off-label use. These are the time points the trials measured:

• Weeks 1–28 (TAZPOWER randomized part) — In 12 people with Barth syndrome, 12 weeks on 40 mg a day and 12 weeks on placebo, with a 4-week washout between, met neither primary endpoint (Thompson et al., 2021).
• Week 36 of the extension — 6-minute walk distance was up 95.9 m from baseline in the 8 patients who reached it (Thompson et al., 2021).
• Week 168 of the extension — In the 8 patients who reached it, 6-minute walk distance was up a cumulative 96.1 m from the extension's baseline, and left-ventricular stroke, end-diastolic and end-systolic volumes trended better (Thompson et al., 2024).
• Week 24 (MMPOWER-3) — In 218 people with primary mitochondrial myopathy, 40 mg a day did not improve the 6-minute walk or fatigue versus placebo (Karaa et al., 2023).

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References

1. Szeto HH. Cell-permeable, mitochondrial-targeted, peptide antioxidants. AAPS J. 2006;8(2):E277-E283. PMID: 16796378.
2. Zhao K, Zhao GM, Wu D, Soong Y, Birk AV, Schiller PW, Szeto HH. Cell-permeable peptide antioxidants targeted to inner mitochondrial membrane inhibit mitochondrial swelling, oxidative cell death, and reperfusion injury. J Biol Chem. 2004;279(33):34682-34690. PMID: 15178689.
3. Birk AV, Liu S, Soong Y, Mills W, Singh P, Warren JD, Seshan SV, Pardee JD, Szeto HH. The mitochondrial-targeted compound SS-31 re-energizes ischemic mitochondria by interacting with cardiolipin. J Am Soc Nephrol. 2013;24(8):1250-1261. PMID: 23813215.
4. Thompson WR, Hornby B, Manuel R, Bradley E, Laux J, Carr J, Vernon HJ. A phase 2/3 randomized clinical trial followed by an open-label extension to evaluate the effectiveness of elamipretide in Barth syndrome. Genet Med. 2021;23(3):471-478. PMID: 33077895.
5. Thompson WR, Manuel R, Abbruscato A, Carr J, Campbell J, Hornby B, Vaz FM, Vernon HJ. Long-term efficacy and safety of elamipretide in patients with Barth syndrome: 168-week open-label extension results of TAZPOWER. Genet Med. 2024;26(7). PMID: 38602181.
6. Sabbah HN, Gupta RC, Kohli S, Wang M, Hachem S, Zhang K. Chronic Therapy With Elamipretide (MTP-131), a Novel Mitochondria-Targeting Peptide, Improves Left Ventricular and Mitochondrial Function in Dogs With Advanced Heart Failure. Circ Heart Fail. 2016;9(2):e002206. PMID: 26839394.
7. Daubert MA, Yow E, Dunn G, Marchev S, Barnhart H, Douglas PS, O'Connor C, Goldstein S, Udelson JE, Sabbah HN. Novel Mitochondria-Targeting Peptide in Heart Failure Treatment: A Randomized, Placebo-Controlled Trial of Elamipretide. Circ Heart Fail. 2017;10(12):e004389. PMID: 29217757.
8. Butler J, Khan MS, Anker SD, Fonarow GC, Kim RJ, Nodari S, O'Connor CM, Pieske B, Pieske-Kraigher E, Sabbah HN, Senni M, Voors AA, Udelson JE, Carr J, Gheorghiade M, Filippatos G. Effects of Elamipretide on Left Ventricular Function in Patients With Heart Failure With Reduced Ejection Fraction: The PROGRESS-HF Phase 2 Trial. J Card Fail. 2020;26(5):429-437. PMID: 32068002.
9. Karaa A, Haas R, Goldstein A, Vockley J, Weaver WD, Cohen BH. Randomized dose-escalation trial of elamipretide in adults with primary mitochondrial myopathy. Neurology. 2018;90(14):e1212-e1221. PMID: 29500292.
10. Roshanravan B, Liu SZ, Ali AS, Shankland EG, Goss C, Amory JK, Robertson HT, Marcinek DJ, Conley KE. In vivo mitochondrial ATP production is improved in older adult skeletal muscle after a single dose of elamipretide in a randomized trial. PLoS One. 2021;16(7):e0253849. PMID: 34264994.
11. Chatfield KC, Sparagna GC, Chau S, Phillips EK, Ambardekar AV, Aftab M, Mitchell MB, Sucharov CC, Miyamoto SD, Stauffer BL. Elamipretide Improves Mitochondrial Function in the Failing Human Heart. JACC Basic Transl Sci. 2019;4(2):147-157. PMID: 31061916.
12. Sweetwyne MT, Pippin JW, Eng DG, Hudkins KL, Chiao YA, Campbell MD, Marcinek DJ, Alpers CE, Szeto HH, Rabinovitch PS, Shankland SJ. The mitochondrial-targeted peptide, SS-31, improves glomerular architecture in mice of advanced age. Kidney Int. 2017;91(5):1126-1145. PMID: 28063595.
13. Szeto HH, Birk AV. Serendipity and the discovery of novel compounds that restore mitochondrial plasticity. Clin Pharmacol Ther. 2014;96(6):672-683. PMID: 25188726.
14. ClinicalTrials.gov. A Trial to Evaluate Safety, Tolerability, and Efficacy of Elamipretide in Subjects with Barth Syndrome (TAZPOWER). NCT03098797.
15. Stealth BioTherapeutics. FORZINITY (elamipretide) prescribing information. FDA accelerated approval September 2025. DailyMed set ID 146bf34c-76f2-48db-ac07-fb29cce2cd75.
16. Brown DA, Hale SL, Baines CP, et al. Reduction of early reperfusion injury with the mitochondria-targeting peptide bendavia. J Cardiovasc Pharmacol Ther. 2014;19(1):121-132. PMID: 24288396.
17. Russo S, De Rasmo D, Rossi R, Signorile A, Lobasso S. SS-31 treatment ameliorates cardiac mitochondrial morphology and defective mitophagy in a murine model of Barth syndrome. Sci Rep. 2024;14(1):13655. doi:10.1038/s41598-024-64368-y. PMID: 38871974.
18. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
19. Karaa A, Bertini E, Carelli V, et al. Efficacy and Safety of Elamipretide in Individuals With Primary Mitochondrial Myopathy: The MMPOWER-3 Randomized Clinical Trial. Neurology. 2023;101(3):e238-e252. PMID: 37268435.
20. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S0, Non-approved substances. wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf. Read October 3, 2026.
21. FDA. FDA Grants Accelerated Approval to First Treatment for Barth Syndrome. News release, September 19, 2025. https://www.fda.gov/news-events/press-announcements/fda-grants-accelerated-approval-first-treatment-barth-syndrome. Read October 17, 2026.
22. FDA. Bulk Drug Substances Used in Compounding Under Section 503A of the FD&C Act (503A page). https://www.fda.gov/drugs/human-drug-compounding/bulk-drug-substances-used-compounding-under-section-503a-fdc-act. Read October 17, 2026.
23. 21 U.S.C. 353a, Pharmacy compounding (section 503A of the Federal Food, Drug, and Cosmetic Act), United States Code, 2024 edition. https://www.govinfo.gov/content/pkg/USCODE-2024-title21/html/USCODE-2024-title21-chap9-subchapV-partA-sec353a.htm. Read October 17, 2026.
24. FDA. Bulk Drug Substances Used in Compounding Under Section 503B of the FD&C Act (503B page). https://www.fda.gov/drugs/human-drug-compounding/bulk-drug-substances-used-compounding-under-section-503b-fdc-act. Read October 17, 2026.
25. FDA. Drug shortage data (openFDA, api.fda.gov/drug/shortages.json): no record for elamipretide or Forzinity, data last updated October 16, 2026. Read October 17, 2026.
26. FDA. 503B Bulk Drug Substances List, updated August 21, 2023. https://www.fda.gov/drugs/human-drug-compounding/503b-bulk-drug-substances-list. Read October 17, 2026: five substances, no elamipretide.

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