BIO101
BIO101, pharmaceutical-grade 20-hydroxyecdysone and MAS receptor activator
Written by Aaron CuhaReviewed Sep 2026
Also known as: Sarconeos, 20-hydroxyecdysone pharmaceutical grade, BIO-101
A 233-person phase 2b in sarcopenia that missed its primary endpoint in the full analysis set and hit it per-protocol, with COVID-19 destroying 55 percent of its final assessments.
Overview
BIO101 is the pharmaceutical development of the same molecule sold as an ecdysterone supplement, and its trial is the most informative thing on any of these three pages.
SARA-INT randomised 233 community-dwelling older adults with sarcopenia, mean age 75.5, to two BIO101 doses or placebo for six to nine months. The primary endpoint was change in gait speed on a 400-metre walk, which is a genuine functional outcome rather than a biomarker.
The result needs both halves. At the higher dose, gait speed improved by 0.07 metres per second against placebo in the full analysis set, which was not significant, and by 0.09 metres per second in the per-protocol population at p equal to 0.008. The pandemic cost the trial 55 percent of its on-site end-of-treatment assessments, which reduced its power.
So: primary endpoint missed on the analysis that counts everyone, hit on the analysis that counts only those who completed as intended, with a genuine external reason for the missing data.
Mechanism of action
Pharmaceutical-grade 20-hydroxyecdysone, developed as an activator of the MAS receptor, the receptor for angiotensin 1-7 and part of the protective counter-regulatory arm of the renin-angiotensin system. Activating that arm opposes the muscle wasting, fibrosis and inflammation driven by angiotensin II signalling through the AT1 receptor. That is a different proposed mechanism from the estrogen receptor beta and Akt route usually cited for ecdysterone in sports contexts, and the two have not been reconciled for this molecule.
Human evidence
One properly designed 233-person randomised double-blind phase 2b with a functional primary endpoint, damaged by the pandemic, which missed on intention to treat and hit per-protocol.
- 233 randomised, three arms, six to nine months, in community-dwelling older adults meeting formal sarcopenia criteria.
- Primary endpoint gait speed on a 400-metre walk: 0.07 m/s against placebo in the full analysis set, not significant.
- Per-protocol population: 0.09 m/s, p = 0.008, which approaches the 0.1 m/s generally treated as the minimal clinically important difference in sarcopenia.
- COVID-19 caused loss of 55 percent of on-site end-of-treatment efficacy assessments, reducing statistical power.
- Predefined higher-risk subgroups showed 0.047 to 0.066 m/s with a trend toward dose response.
- Safety was good, with related adverse events no more common on drug than on placebo.
- The authors' own conclusion describes strong trends consistent with a clinically relevant effect, which is careful language for a missed primary endpoint.
What this does not tell you: The distinction between the two analyses is the whole story and it matters. A per-protocol analysis includes only participants who completed treatment as intended, which systematically removes people who stopped for side effects or lack of benefit, so it is more prone to overstating an effect than an intention-to-treat analysis. The pandemic explanation for the missing data is genuine and it does not make the full analysis set result significant. Conflicts are extensive: several authors are employees or former employees of the sponsor and many more are advisers or consultants.
Reading the research record
This is a good page for practising the reading this site is built for. There is a real trial here, properly randomised and double-blind, with a functional endpoint that matters, in a condition with no approved treatment anywhere. That is worth respecting.
The result is a miss on the analysis that counts everyone and a hit on the analysis that counts completers, and the honest interpretation sits between the two framings you will encounter elsewhere. The sponsor's framing emphasises the per-protocol significance and the pandemic. A dismissive framing says the primary endpoint failed. Both leave something out. What can be said is that no sarcopenia drug exists, that this trial produced an effect close to the clinically meaningful threshold in completers, that its intention-to-treat result was not significant, and that a confirmatory trial is the only thing that will settle it.
Ecdysteroids are steroid hormones that control moulting in insects and appear in some plants, notably spinach, quinoa and Ajuga turkestanica. They are structurally unrelated to androgens and do not bind the androgen receptor, which is the basis of the claim that they build muscle without steroid side effects. Read the family together rather than one at a time. 20-hydroxyecdysone, also called ecdysterone, has a controlled human trial reporting increased muscle mass and bench press performance, and a 233-person pharmaceutical phase 2b in sarcopenia that missed its primary endpoint in the full analysis set. Turkesterone, the one that dominates supplement marketing, has no human trial of any kind. Evidence within this family does not transfer between members, and the member with the most evidence is not the member being sold hardest.
The evidence, charted
Fig. 1 · evidence composition
2of 2 citations (100%) are in people
Every citation cited here is Human work; no other study type is cited on this page. This count is of our own citation list and understates any literature larger than the sources we cite.
Fig. 2 · evidence over time
Citations here span just two years, 2019 and 2025.
Too few distinct publication years on this page to plot as a timeline.
Fig. 3 · legal status at a glance
US
Not approved
UK
Approved
AU
Approved
CA
Not approved
Approved in 2 of 4, prescription route in 0, not approved in 2. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.
Fig. 4 · dose response
No human dose response curve exists
We draw this figure where the data supports it. For this compound in humans it does not, so the panel stays empty rather than borrowing an animal curve and implying it transfers.
Key studies & citations
- Human2025
BIO101 in sarcopenic seniors at risk of mobility disability: results of a double-blind randomised interventional phase 2b trial
SARA-INT. 233 randomised, mean age 75.5, 54.3% female, three arms at 175 mg twice daily, 350 mg twice daily or placebo, planned six months and up to nine in 50 subjects. Eligibility required meeting FNIH sarcopenia criteria and a Short Physical Performance Battery score of 8 or less out of 12. Primary endpoint was change in gait speed on the 400-metre walk test. At 350 mg twice daily, gait speed improved 0.07 m/s against placebo in the full analysis set, not significant, and 0.09 m/s in the per-protocol population, p = 0.008. COVID-19 cost 55% of on-site end-of-treatment efficacy assessments, reducing power. Predefined higher-risk subpopulations showed effects of 0.047 to 0.066 m/s with a trend toward dose response. Safety was good, with related treatment-emergent adverse events in 16.0%, 13.3% and 13.5% of the placebo, 175 mg and 350 mg groups. Many authors are employees, former employees, advisory board members or consultants of the sponsor, Biophytis.
Journal of Cachexia, Sarcopenia and Muscle - Human2019
Ecdysteroids as non-conventional anabolic agent: performance enhancement by ecdysterone supplementation in humans
The same molecule in a sports context, where a controlled human trial found increased muscle mass and bench press performance. Included because the contrast between a positive strength result in trained young people and a missed functional endpoint in sarcopenic older adults is the central fact about this compound.
Archives of Toxicology
Frequently asked questions
Did BIO101 work for sarcopenia?
Its phase 2b missed the primary endpoint in the full analysis set, improving gait speed by 0.07 metres per second against placebo without reaching significance, and hit it in the per-protocol population at 0.09 metres per second with p equal to 0.008. The pandemic destroyed 55 percent of final assessments, which reduced the power to detect an effect.
Why does per-protocol versus full analysis matter?
Because per-protocol counts only the people who completed treatment as intended, which quietly removes those who stopped for side effects or lack of benefit. That makes it more likely to overstate an effect. The full analysis set is the honest test, and in the full analysis set this trial did not reach significance.
Is this the same as buying ecdysterone?
The molecule is the same. The formulation, dose certainty and manufacturing are not, and oral bioavailability of this compound is poor enough that those differences plausibly matter. A supplement product has not been tested in sarcopenia and this trial does not transfer to it.
Is there any approved drug for sarcopenia?
No, anywhere, which is why this programme is worth following despite the missed endpoint. Current treatment is resistance training and adequate protein, both of which this site covers in the training and diet sections and both of which have better evidence than any drug in this space.