SHAPE is the Study of Healthy Aging and Physical function with Elamipretide (SS-31), the Marcinek lab’s XPRIZE Healthspan pilot

#1

Saw this mention of the pilot study here:

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So had Claude find and summarize the data:

SHAPE Study

SHAPE is the Study of Healthy Aging and Physical function with Elamipretide, the Marcinek lab’s XPRIZE Healthspan pilot. The trial is real and well documented, but I could not find any public source for the N=23 or the efficacy numbers: no abstract, preprint, paper, or posted registry results.

What the trial is

  • Registration: NCT07275424, an open-label, single-arm Phase 2a pilot of daily subcutaneous elamipretide in older adults.
  • People: David Marcinek (University of Washington) is sponsor-investigator, with Stealth BioTherapeutics as collaborator. Suman Jayadev is co-investigator, and visits ran at the Fred Hutchinson Cancer Center Prevention Center. Stealth is now Mighty Therapeutics.
  • Design: 4 weeks of daily injections, a midpoint phone check, post-intervention visits mirroring baseline, and a 2-week follow-up, with planned enrollment of 30.
  • Dose: the registry gives no milligram dose, only an 80 mg/mL multi-dose vial. The 40 mg/day used in earlier trials is likely, but that is my inference.
  • Population: ages 65 to 80, with VO2peak at or below 37.3 mL/kg/min (men) or 25.7 (women), no exercise routine, and no CoQ10, creatine, or L-carnitine.
  • Primary endpoint: treatment-related adverse events and completion of 4 weeks of injections.
  • Secondary endpoints: BDNF, VEGF, IGF-1, IL-6, and TNF-alpha; six-minute walk; MoCA, Trail Making A and B, and Stroop; one-rep-max knee extension.

Peak VO2 is an inclusion criterion but not a registered outcome, so any VO2 result is outside the prespecified endpoint list.

Timeline and what has been disclosed

  • November 2025: the trial started on November 26, with primary completion estimated for March 15, 2026.
  • April 2026: Marcinek said data collection had just finished, and findings were expected at the American Aging Association meeting in June. I found no abstract from that meeting.
  • May 2026: David Brown of Stealth presented SHAPE data at a Reagan-Udall Foundation meeting, reported only as encouraging open-label functional gains over 30 days.
  • August 2026: the team won a $1 million XPRIZE Milestone 2 award premised on the pilot data. The press release has no numbers, and Marcinek calls the results feasibility data.
  • Registry today: still listed as recruiting, last updated December 2025, no results posted.

The XPRIZE landscape report says 9 of 10 awardees submitted small randomized trials and one submitted a single-arm open-label study, which matches SHAPE’s design. That report’s awardee lookbook (page 78) is the most likely origin of your summary line, but I could not extract that page.

How much weight the claims can bear

  • Evidence level: uncontrolled pre-post data from a small, sponsor-partnered pilot, with no public effect sizes, confidence intervals, completer counts, or adverse event data. High confidence the direction was reported as positive; low confidence in magnitude or causality.
  • Regression to the mean: participants were selected for low VO2peak, so some rebound in that measure is expected without any drug effect.
  • Practice and effort effects: six-minute walk, one-rep max, Trail Making, Stroop, and MoCA all improve on retest, and open-label participants may push harder.
  • Enrollment: if 23 is correct, the trial fell short of its planned 30. Whether 23 means enrolled or completers is unknown.
  • Controlled history: a single-dose randomized trial in 39 older adults improved mitochondrial ATP production. But in the Phase 3 mitochondrial myopathy trial, week-24 walk gains were about 15 m on drug versus 17 m on placebo, and an earlier trial found VO2 changes no different from placebo.
  • Conflict of interest: Marcinek has been a paid scientific advisor to Stealth.

What comes next

A Phase 2 double-blind, placebo-controlled trial will test one year of treatment on muscle, cognition, and immune health, running through 2029. Under XPRIZE rules, a team must show at least 20% more participants than control achieving meaningful improvement across all three domains.

Sources:

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#2

u know, I saw this earlier today; I was studying ss31 a bit. I see people using this and idk why with the 5mg dose three times a week, or whatever they are claiming. It’s a pretty expensive peptide as far as peptides go. I tried a short cycle and found no change. After reading about the 40mg used SC each day forever (not cycled) and it’s only been found to help those with cardiolipin dysfunction (Barth Syndrome), I’m not sure it’s helpful (for me)… It didn’t improve scores in the other trials either. lemme see, still in the brave history…

A few additional points:

  • No efficacy data exists below 40 mg in any published human trial. The TAZPOWER trial (Barth syndrome) and MMPOWER-3 (mitochondrial myopathy) both used 40 mg SC daily. The only lower-dose arm ever studied was a 4 mg/day group in a 28-day heart failure trial, and that trial was terminated.
  • The FDA label itself notes that elamipretide exposure is dose-proportional from 2 to 80 mg , meaning 2 mg gives you roughly 5% of the studied exposure. Whether that produces any meaningful mitochondrial effect in a healthy person is purely speculative.
  • The “start low, titrate up” framing on community sites is borrowed from general peptide culture, not from any SS-31-specific safety data. There’s no known reason to fear 40 mg in a healthy adult that wouldn’t also apply to the lower doses.

So the short version: 2–10 mg is a budget compromise , not a pharmacological choice.

in practice it’s a chronic, indefinite daily injection . The data supports this:

  • The TAZPOWER open-label extension ran for up to 192 weeks (~3.7 years) , and the Barth Syndrome Foundation notes that more than half of the original trial patients are still on it 8+ years after starting.
  • There’s no defined “course length” or taper protocol in the label. It’s a progressive mitochondrial disease with no cure, so the intent is continuous daily dosing.
  • The 168-week OLE data showed sustained (not waning) improvements in 6MWT distance, fatigue scores, and cardiac volumes across the entire extension — suggesting the benefit doesn’t plateau off-treatment or require “re-charging” cycles.

So for a Barth patient, it’s the same as taking a daily statin or insulin — you don’t stop.

Is there any benefit for a healthy person?

No. The data is actually quite clear on this, and it cuts against the community narrative:

The closest human data point is a 39-person RCT in older adults (60–85) who were specifically enrolled because they had impaired mitochondrial function. A single IV infusion raised in vivo ATP capacity acutely versus placebo — but there was no improvement in muscle fatigue resistance and no difference at day 7. It’s a transient biochemical blip with no functional consequence.

The preclinical data makes the mechanism explicit: in the aging muscle studies, SS-31 restored aged animal muscle to young-adult profiles. Young animals showed no effect. As one analysis puts it: “This is a repair tool for dysfunctional mitochondria, not an enhancement tool for healthy ones.” A 25-year-old with normal cardiolipin and normal ETC coupling has nothing to repair.

The large trial that should have shown a general benefit didn’t: MMPOWER-3 (n=218, primary mitochondrial myopathy) missed both co-primary endpoints — 6MWT difference was −3.2 m (p=0.69) and fatigue score showed no benefit (p=0.37). Even in people with actual mitochondrial disease, the drug didn’t reliably improve the outcomes that matter.

What doesn’t exist:

  • No trial showing improved training recovery, performance, or stress tolerance in healthy exercising people
  • No cognitive benefit in healthy adults
  • No longevity or healthspan data in any species beyond lifespan-extension in progeria mouse models (which is a disease model, not aging per se)
  • A Phase 2a pilot in healthy adults 65+ (NCT07275424) is recruiting since late 2025, but its endpoint is safety/tolerability only, not performance

So the honest summary: the community is paying for a plausible mechanism in the wrong population. The drug fixes a specific molecular defect (cardiolipin disorganization). If you don’t have that defect, there’s no target to act on.

Now, epitalon, on the other hand, that’s a very interesting peptide. I am thinking of ordering 500mg… and yes, you need 5mg dosing at least, but that’s another story.

#3

If you are new to SS-31 you should definitely read this thread first and not just follow a generic LLM overview in the topic.

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#4

yes i see you’ve been discussing it for a long while now.
and it still seems like 40mg daily (!)