Evidence

FLGR-242: we searched nine indexes and found nothing at all

Q: Is there any published research on FLGR-242?

None that we could find. Searching PubMed, Europe PMC (which indexes preprints and patents), OpenAlex, Crossref, PubChem's compound and substance databases, ClinicalTrials.gov, UniProt and DailyMed in September 2026 returned zero records in every one, and a re-run on 16 October 2026, including a patent search and the FLGR232 spelling, found no record of it either. The seller's 17 references are about follistatin or a different protein, not this product.

Q: Searching FLGR returns results. Doesn't that mean it exists?

Those results are a different subject. In the scientific literature flgR is a sigma-54-dependent transcriptional activator controlling flagellar assembly in bacteria such as Campylobacter and Helicobacter. It has no connection to peptides or muscle. Read the titles before treating hits as evidence.

Q: What does the seller claim, and what is the evidence?

The seller says it blocks myostatin without binding activin, stays active for 19 days (its guide also says 14–15), binds albumin under 20 nM, reaches skeletal muscle directly and preserves lean mass, and it lists 17 references. None of those claims has published data on this product: the binding figure was measured in a patent on a different construct, the half-life is a patent's assertion, and the 17 papers are about follistatin or a different protein, FSTL1. The certificates we read do report 99.71–99.79% purity.

Q: Is FLGR-242 a form of follistatin?

Nothing published establishes that. The seller describes it as a modified fragment of follistatin-344 with an albumin-binding tail, but publishes only the tail's sequence, not the follistatin part. Other descriptions have called it follistatin itself or an FSTL3-derived analogue. Follistatin (UniProt P19883, 344 amino acids) and follistatin-related protein 3 (UniProt O95633, 263 amino acids) are different proteins.

Q: The seller says it contains a patented albumin binder. Is that true?

Partly. The 29-amino-acid tail the seller lists is sequence 4 of US patent 12,377,158 B1, granted in August 2025 to an individual inventor, and its core is SA21, an albumin-binding peptide Genentech published in 2002. But the patent covers only the tail and a version attached to alpha-Klotho; it does not mention activin, myostatin or FLGR. Its 'under 20 nM' binding figure is measured in the patent only for its alpha-Klotho version (7.94 nM against human albumin by surface plasmon resonance), never for a follistatin one, and the original peer-reviewed measurement of SA21, the tail's core peptide without the linker, is 467 nM against human albumin, about 23 times weaker.

Q: Does FLGR-242 bind activin?

Nobody outside the seller can say. The seller states that it does not, but publishes no binding data and does not disclose the follistatin sequence. Natural follistatin binds activin more tightly than myostatin, in one published measurement. A published activin-sparing variant, FS I-I, exists, but in its published animal tests it was a gene in mice, and it is not FLGR-242. The seller's own page also lists activin neutralization assays as a use.

Q: What is the molecular weight of FLGR-242?

The seller states about 40 kDa. None of the certificates we have read states any molecular weight, so the figure cannot be checked against them. By sequence, the working form of human follistatin weighs about 34.8 kDa before sugars and the disclosed tail about 2.95 kDa, so 40 kDa fits nearly the whole follistatin protein plus the tail, not a small fragment.

Q: What do the seller's 17 references show?

They are real papers, mostly about follistatin in mice, rats or cells, plus three about a different protein, FSTL1, and one retracted paper cited by its retraction notice. None mentions FLGR-242, and in none was a person given follistatin. At least six credit follistatin's effects partly to blocking activin, which the seller says its product does not do.

Q: Where does the long half-life figure come from?

From a 2025 US patent on the albumin-binding tail the seller discloses. The patent takes albumin's own 19-day half-life in people and asserts that proteins carrying the tail get about the same; it reports no measurement in people. The 2002 paper that introduced this tail peptide extended a fused antibody fragment's half-life to 32.4 hours in rabbits and 10.4 hours in mice, which its authors describe as 25 to 43 percent of the albumin half-life in those animals. No pharmacokinetic study of FLGR-242 exists in any species.

Q: The seller says injection-site redness is not an allergic reaction. Is that right?

There is no data on this product either way, so a reaction cannot be assumed harmless. Widespread hives, swelling of the lips or tongue, or trouble breathing after an injection can be signs of a severe allergic reaction (anaphylaxis) and need urgent care, according to the World Allergy Organization's 2020 guidance.

No published research, in every scientific literature index and registry we could query — re-checked on 16 October 2026. So what is said about FLGR-242 comes from the seller. Below, each of the seller's claims sits beside what has been published or measured on that point, followed by what the certificates and the safety data sheet in circulation do and do not show.

We looked for published research on FLGR-242 and found none. This page sets out what we searched, what the seller says about the product, and what the published record and the paperwork show on each point.

What we searched, and what came back

First run 6 September 2026, re-run in full on 11 September 2026, and run again on 16 October 2026, against three spellings each: FLGR-242, FLGR242 and FLGR 242 — and, in October, the FLGR232 spelling printed on one certificate. Every run returned the same thing.

PubMed — 0 records, all three spellings

Europe PMC (includes preprints and patents) — 0 records, all three spellings

OpenAlex — 0 works

Crossref — no matching work

PubChem, compound database — no such name

PubChem, substance database — no such name

ClinicalTrials.gov — 0 registered studies

DailyMed — 0 entries (checked in September)

UniProt — 0 entries

Google Patents, exact phrase — 0 results (October)

goodtides, re-checked 16 October 2026

One search does return a number. PubMed Central, searched for the two loose tokens FLGR 242 rather than the exact phrase, returns nine records. We opened all nine: every one is bacterial genetics — Campylobacter, Helicobacter, Salmonella, Arcobacter — matching the gene name plus an unrelated numeral. Searched as an exact phrase, the same database returns zero.

The indexes are working. The bare token FLGR returns forty PubMed records, thirty-four of them about flgR, a gene that controls how bacteria such as Campylobacter and Helicobacter build their flagella; the other six merely share the letters. None has anything to do with peptides or muscle.

What the seller says, and the data

BioLongevity Labs, the seller whose certificates we read, describes the product on its own page, which we read in full on 16 October 2026 — an Internet Archive copy from 9 November 2025 carries the same description, which our September report missed — and in a two-page printed usage guide. Both label it for research use only. Below, each claim sits beside what has been published or measured on that point. Quoted words are the seller's.

The seller says	The data
It “does not bind to the protein activin”, so there are “no unwanted cellular growth signals”	No published data. No binding measurement has been made public, and the follistatin sequence is undisclosed.
An extended half-life: “active 19 days per injection” (guide), and 14–15 days elsewhere in the same guide	Not measured. No half-life has been published for this product in any species; the 19-day figure is a patent's assertion, reasoned from albumin's own half-life.
Albumin binding of “<20 nM”	Measured in the patent only on a different construct, its alpha-Klotho version (7.94 nM); none has been published for this product. The peer-reviewed figure for the tail's core peptide is 467 nM.
A “novel fragmented, modified version” of follistatin-344, about 40 kDa	Not disclosed or independently confirmed. Only the tail's sequence is published, and no certificate states a molecular weight or a sequence.
“Superior tissue distribution”: it reaches skeletal muscle directly (guide)	No published data on this product. No distribution study has been published in any species.
Lean-mass preservation; it is “anabolic — aggressively so” (guide)	No published data on this product. No study of its effect on muscle or body composition has been published in any species.
≥99% purity, US GMP manufacture, “third-party verified” certificates	Purity and quantity, not identity. The three certificates we read report 99.71–99.79% purity and about the labelled amount. GMP manufacture is the seller's statement; the certificates say nothing about it.
17 research references	Real papers, none on FLGR-242. 13 are on follistatin, mostly in mice, rats or cells; 3 are on FSTL1, made from a different gene; 1 is a retracted paper, cited by its retraction notice.
Redness or swelling at the injection site “is not an allergic reaction” (guide)	No data. A reaction to this product cannot be assumed harmless. Widespread hives, swelling of the lips or tongue, or trouble breathing need urgent care (World Allergy Organization guidance, 2020).

The product page heads the product “10mg”; that is a pair of 5 mg vials (its page title says 5mg, its stock code 5MG-2PK), and all three certificates we read are for 5 mg vials.

What we checked

The tail is real, published and patented

The last 18 amino acids of the tail the seller lists, RLIEDICLPRWGCLWEDD, are a peptide called SA21. Genentech scientists found it by screening for albumin binders and published it in 2002 (Dennis and colleagues, Journal of Biological Chemistry, PMID 12119302). The first 11, GGSGGSGGSGG, are a common flexible linker made of the amino acids glycine and serine. Albumin is the most common protein in blood plasma, and a tail that grips it is meant to make a drug last longer in the body.

The whole 29-amino-acid tail appears, letter for letter, as sequence 4 of US patent 12,377,158 B1, “Enhanced peptide constructs for albumin binding”, granted on 5 August 2025 to an inventor, Michael Farber; Google Patents lists the assignee as an individual rather than a company. Whether the seller owns or licenses it is not public, and we make no claim either way. The patent's claims are about the tail and a version of it attached to a different protein, alpha-Klotho. The words activin and myostatin do not appear in it, and neither does FLGR. Follistatin comes up in two sentences: once as a possible use, and once in a bare statement, with no data, that a follistatin made this way has a 7-day half-life in dogs. So “patented” describes the tail, not the follistatin part.

The albumin-binding figure

The seller's “<20 nM” matches the patent's wording. The patent states it for human albumin and reports one measurement behind it: a surface-plasmon-resonance run, carried out by an outside company, KMD Bioscience, in which its mouse alpha-Klotho construct bound immobilised human albumin at 7.94 nM. Its other albumin figures — about 8 nM, and under 19 nM — are against dog albumin, Klotho again. The original peer-reviewed measurement of SA21 itself, without the linker, was 467 nM against human albumin (266 nM for rat, 320 nM for rabbit); a lower number means tighter binding, so that is about 23 times weaker than the seller's figure. The patent credits the linker for the difference. No published measurement isolates the linker's effect.

The half-life

The roughly 19-day figure traces to the same patent. It starts from albumin's own half-life in people, 19 days, and asserts that proteins carrying the tail get about the same; it reports no measurement in people. In the 2002 paper that introduced this tail peptide, an albumin-binding peptide fused to an antibody fragment extended that fragment's half-life 37-fold, to 32.4 hours in rabbits, and 26-fold, to 10.4 hours in mice — which its authors describe as 25 to 43 percent of the albumin half-life in those animals. No half-life has been published for FLGR-242 in any species.

Activin

Follistatin binds activin more tightly than myostatin: 1.72 nM, against 12.3 nM, in one published measurement (Nakatani and colleagues, FASEB Journal 2008, PMID 17893249). That paper also describes a follistatin variant that spares activin, FS I-I. It kept its grip on myostatin, but about four times more weakly, and in its published animal tests it was a gene switched on inside mouse muscle, not an injected protein. FS I-I is not FLGR-242. A follistatin that does not bind activin would need a change to the follistatin part, and the seller has not described one. Its page also lists activin neutralization assays as a research use.

The seller gives activin as the cause of unwanted cell growth when myostatin is blocked. We found no published support for that. The published reason for sparing activin is that activin works in many organs, so blocking it could affect tissues besides muscle (the FS I-I paper). In a human trial of a broad blocker of this pathway — ACE-031, given to boys with Duchenne muscular dystrophy — the problems that stopped the trial were nosebleeds and small widened blood vessels (telangiectasias) (Campbell and colleagues, Muscle & Nerve 2017, PMID 27462804). And the seller's first reference (Lee and colleagues, 2010) reports that myostatin only partly explains follistatin's effect on muscle, with genetic evidence suggesting activin A may be one of the other ligands involved.

About 40 kDa

Follistatin-344 is the full-length form cells first make. They cut off a 29-amino-acid signal piece, leaving the working protein: 315 amino acids, weighing about 34.8 kDa before sugars are attached. (We computed this from its sequence in UniProt, P19883.) Add the 29-amino-acid tail, about 2.95 kDa, and the total is about 37.7 kDa — and follistatin carries two sugar chains, which add more.

Working follistatin (315 amino acids) — about 34.8 kDa

Disclosed tail (29 amino acids) — about 2.95 kDa

Together, before sugars — about 37.7 kDa

The seller's stated weight — about 40 kDa

Average masses computed from the UniProt P19883 sequence and the disclosed tail; sugars not included.

So about 40 kDa fits nearly the whole working follistatin protein plus the tail, not a small piece of it. If “fragmented” means only that the signal piece is gone, that is the ordinary working form of follistatin, which binds activin tightly. The patent describes making these constructs in living cells (hamster ovary, human kidney or insect cells), which yields a protein with sugars attached. None of the three certificates we read states a molecular weight, so the figure cannot be checked against them.

Other descriptions

Not every description agrees with the seller's. Its own one-line summary calls the product a “High-purity Follistatin glycoprotein”; another seller, Paramount Peptides, describes its FLGR242 as “Supplied as a lyophilized blend for laboratory research”; and it has been described elsewhere as an analogue of FSTL3. Follistatin is UniProt P19883, gene FST, 344 amino acids; follistatin-related protein 3 is UniProt O95633, gene FSTL3, 263 amino acids — a different gene product with a similar name. A fragment of a protein is not the protein.

The seller's 17 references

The seller's page carries a list of 17 papers under the heading of follistatin research. We looked up every one in PubMed and checked the title, authors and identifier against the seller's list. All 17 are real papers. None mentions FLGR-242 or an albumin-binding tail. They are summarized below in our own words, labelled by what was studied and in what — background on a related protein, not evidence about this product.

17 references checked · 0 about FLGR-242

13 about follistatin itself (its gene, its mRNA or the protein, including the forms FST288 and FST315) — 1 of them a review

3 about FSTL1, a different protein from a different gene

1 retracted — the seller's identifier is the retraction notice itself

0 in which a person was given follistatin

goodtides, checked against PubMed on 16 October 2026

Two patterns run through the list. In at least six of these papers the authors credit follistatin's effects at least partly to blocking activin. And almost everything here was done in mice, rats or cells; the only human data are measurements of people's own follistatin, never a dose of it.

Muscle

Lee and colleagues, Molecular Endocrinology 2010 — mouse genetics · follistatin gene. Mice with one working copy of the follistatin gene instead of two had smaller muscles. Part of that effect remained in mice with no myostatin at all, so the authors conclude follistatin also works through other targets, possibly including activin A. Nobody was given follistatin. PMID 20810712
Gangopadhyay, Scientific Reports 2013 — mice · FST288 protein made in bacteria. Daily injections under the skin for 13 weeks raised lean mass and lowered fat, with larger muscle fibres at the highest dose. Six mice per group; a single author. PMID 23942549
Zhu and colleagues, American Journal of Pathology 2011 — mice and cells · follistatin, bred-in over-production. Mice bred to make extra follistatin regrew more muscle fibres and formed less scar tissue after injury. The authors put the effect in mice down to blocking myostatin and to new blood-vessel growth; the activin A and TGF-β1 part is their account of follistatin's effect on muscle-cell differentiation in culture. PMID 21689628
Han and colleagues, Journal of Cachexia, Sarcopenia and Muscle 2019 — mice, gene transfer · FST288; people measured only. Extra FST288 made inside mouse muscle enlarged it and raised insulin-driven sugar uptake by 75%. The authors describe FST288 as an activin A blocker. In people, the study only measured their own follistatin, which doubled a week after gastric bypass surgery. PMID 31402604
Schumann and colleagues, Theranostics 2018 — mice · follistatin mRNA delivered to the liver. After eight weeks of injections, lean mass was about 10% higher than in mice given saline. The authors say follistatin works by blocking myostatin and activin A. PMID 30555546

Fat, metabolism and the liver

Braga and colleagues, Journal of Lipid Research 2014 — cells, plus expression measured in mouse tissue · follistatin protein. Follistatin added to mouse fat-precursor cells switched on “browning” genes, which make fat cells burn energy as heat, and raised the cells' energy use. No animal was treated. PMID 24443561
Tao and colleagues, Molecular Metabolism 2023 — mouse genetics · FST315 made by the liver. In mice whose liver insulin signalling was switched off, the liver's own follistatin raised energy use, and extra liver follistatin reduced fat gain on a high-fat diet. No protein was injected. PMID 36906067
Tong and colleagues, Diabetes, Metabolic Syndrome and Obesity 2022 — human liver cells and mice, gene transfer · follistatin; human liver samples measured only. More follistatin meant less fat build-up in liver cells, and follistatin gene transfer reduced weight gain and liver fat in mice on a high-fat diet. In human liver samples, follistatin was higher in people with fatty liver disease. PMID 36325432
Pervin and colleagues, Frontiers in Endocrinology 2021 — a review, no new data. A review of follistatin and myostatin in fat “browning”, written by three of Braga 2014's authors. It treats follistatin for obesity as something to study, not a result. PMID 33897620

Repair, bone and skin

Antsiferova and colleagues, Laboratory Investigation 2009 — mouse genetics · follistatin removed from skin cells. Mice without follistatin in their skin cells regrew skin over wounds sooner, with no change in scarring. The seller cites it for the claim that follistatin regulates keratinocyte proliferation and migration during repair; the result itself points the other way from the idea that adding follistatin speeds wound closure. PMID 19079322
Fahmy-Garcia and colleagues, Frontiers in Bioengineering and Biotechnology 2019 — cells and rats · FST288 and FST315 protein. In cells, follistatin helped cells move and form vessel-like tubes, and helped bone-forming cells lay down mineral. In rats with a skull defect, neither form improved bone healing compared with controls. PMID 30881954

Reproduction and development (basic biology)

Yao and colleagues, Developmental Dynamics 2004 — mouse embryos · follistatin gene. The follistatin gene is needed for the ovary to develop normally before birth. PMID 15162500
Kirk and colleagues, Endocrinology 1994 — rats · the body's own follistatin. How often the brain releases pulses of the hormone GnRH changes how much follistatin the pituitary gland makes. PMID 8070381

Not follistatin: three papers about FSTL1

Follistatin-like 1 (FSTL1) has a similar name but is a different protein, made from a different gene on a different chromosome: FSTL1 sits on chromosome 3, and follistatin's gene, FST, on chromosome 5. Three of the seller's references are about FSTL1. They are the only support for its heart and brain-protection claims. Under its heart-and-blood-vessel heading they are two of the three references; the third is Fahmy-Garcia, a follistatin paper whose vessel findings are in cells. None is evidence about follistatin, let alone FLGR-242.

Ouchi and colleagues, Journal of Biological Chemistry 2008 — mice and cells. FSTL1 delivered by a virus sped blood-flow recovery in mouse legs with a blocked artery. PMID 18718903
Oshima and colleagues, Circulation 2008 — mice and rat heart cells. FSTL1 delivered by a virus reduced heart damage in mice after blood flow to the heart was stopped and restored. PMID 18519848
Liang and colleagues, Stroke 2014 — rats. FSTL1 injected into the brain after a stroke reduced the damaged area. PMID 25139876

Retracted

One reference is to Pisconti and colleagues in the Journal of Cell Biology. The identifier the seller gives is not the paper: it is the journal's 2013 retraction notice (PMID 23341472). The original 2006 paper (PMID 16401724) was retracted after the editors found duplicated image panels and an apparently erased band in its figures, and the authors could not find the original data. The notice says no data in the paper should be cited, so we have not summarized it.

Follistatin has reached human testing as gene therapy: a small 2015 study in Becker muscular dystrophy delivered the follistatin gene with a virus (Mendell and colleagues, Molecular Therapy, PMID 25322757). It is not on the seller's list, and it is not a study of an injected protein, let alone FLGR-242.

A citation that points at a different paper

One citation circulating in support of FLGR-242 attributes a 2015 Science Translational Medicine paper, volume 7, issue 287, page 287ra74, to Mendell and colleagues. Those coordinates match one paper in PubMed: PMID 25972006, first author Cao, about myelin-reactive T cells in multiple sclerosis — nothing to do with follistatin, muscle or peptides. Jerry Mendell did publish follistatin work in 2015: the gene-therapy trial above, in Molecular Therapy, volume 23, pages 192 to 201, which delivered the follistatin gene with a virus and is not a study of FLGR-242.

The certificates: purity and quantity, not identity

Three certificates of analysis for this product, issued by MDx BioAnalytical Laboratory, Inc. for BioLongevity Labs, were in circulation when we read them on 11 September 2026. MDx is a real laboratory — founded in 2008, based in the United States, with a public certificate-search page — and the certificates are professionally produced, with chromatography and mass-spectrometry traces, a photograph of the vial and a named signatory. Nothing suggests the laboratory did anything other than measure what it was sent.

COA 261543 — labeled identity FLGR-242 · determined identity FLGR-242 · 5.24 mg against a 5 mg label · purity 99.71% · endotoxin pass

COA 261001 — labeled identity FLGR232, with CAS 3108438-94-1 · determined identity FLGR232 · 5.09 mg · purity 99.74% · endotoxin pass

COA 260085 — labeled identity FLGR242 · determined identity FLGR242 · 5.18 mg · purity 99.79% · endotoxin pass · batch number: FLGR

What they establish is real: a single dominant peak, purity above 99.7 percent, and about 5 mg of material where 5 mg was labelled. What they cannot establish is identity. A mass-spectrometry identity check compares the measured mass against the expected mass of a declared compound, and with the follistatin part undisclosed and no registry entry, there is nothing external to compare against — so in each certificate the determined identity restates the identity written on the vial that was sent. None of the three states a molecular weight. Our COA guide covers why an identity line needs an external standard.

Read together, they also disagree. The middle certificate is headed FLGR232 and carries CAS 3108438-94-1, while the mass-spectrometry trace printed on the same page is captioned FLGR242. That CAS number has a valid check digit, which is easy to construct; we found no matching record in PubChem's compound or substance databases or in Europe PMC, and CAS's own registry needs an API key we do not hold, so we record it as unresolved rather than absent. The other two certificates carry no CAS number. The third records its batch number as the string FLGR — a product code, not a lot — and dates receipt 7 January 2025 and reporting 9 January 2026, more likely a typing error than a year-long analysis.

An endotoxin pass is not a sterility test and not a safety clearance: it looks for one class of bacterial breakdown product, against a threshold, and says nothing about what else is in the vial. Each certificate says it is searchable on the laboratory's site; that search sits behind a cookie-consent gate, and we did not accept terms on anyone's behalf, so we could not complete the check. Anyone holding a vial can.

The safety data sheet is partly about oxytocin

The fourth document in circulation, from Paramount Peptides, is a safety data sheet: a hazard-communication document written by the supplier, not a laboratory result. We read all six pages on 11 September 2026. It names FLGR242 throughout, but in three places its hazard text is about oxytocin: a section 2 classification that reasons from an oxytocin LD50 (rat, under the skin, over 20,520 mg/kg); a section 2 note that oxytocin “may induce uterine contractions”, warning women of childbearing potential; and a section 11 pharmacological note on oxytocin as a hormone.

Section 2 carries each of its entries twice — an oxytocin version with a generic research-compound version beneath it — which reads as an oxytocin template only partly rewritten. That is evidence about the paperwork, not the powder: nothing suggests the vials contain oxytocin. The sheet also contradicts itself on toxicology: section 2 reasons from a specific LD50, while section 11 says no acute toxicity data is available for this compound.

Its identity section defers to the certificates for what the certificates do not contain:

CAS Number — "Proprietary / research compound"

Molecular Formula — "Proprietary peptide (MF undisclosed)"

Molecular Weight — "Research compound (see COA for batch-specific MW)"

Amino Acid Sequence — "Proprietary peptide sequence (see COA)"

Number of Amino Acids — "Proprietary"

“Proprietary” is a normal thing for a supplier to write. But the sheet's CAS line cannot be squared with the CAS printed on the other seller's certificate, and the molecular weight and sequence it defers to the certificate of analysis appear on none of the three we read.

What we are not saying

We are not saying FLGR-242 does not exist as a physical substance. Vials exist; something is in them. We are saying that nothing in the public scientific record establishes what.

We are not saying it is dangerous. There is no toxicology to cite in either direction — an absent safety record is not a clean safety record, and the two are often confused.

And we are not saying it will never have a literature. Compounds do emerge, and the list below is what would change this page.

What would change this page

We will update it for any of the following, and each is checkable by anyone:

A published sequence or structure in a peer-reviewed source, a preprint, or a patent.
An entry in PubChem, ChEMBL, the FDA substance registry, or any equivalent registry, with a CAS number or INN.
A named originating laboratory with a traceable publication record for this compound.
A registered study of any phase, in any jurisdiction.
Third-party mass-spectrometry results checked against a declared theoretical mass — with the theoretical mass stated, so the comparison can be seen.

One of those partly exists: the August 2025 patent covers the albumin-binding tail, but it does not name FLGR-242 or describe the follistatin part, so it does not meet the first condition.

The short version

FLGR-242 has no published research in any index we could search. The seller discloses a short albumin-binding tail, borrowed from published and patented work, and a weight of about 40 kDa; the follistatin part, which decides what the molecule is and what it binds, is undisclosed. The seller's claims about activin, half-life, albumin binding, tissue distribution and lean mass have no published data on this product, and its 17 references are about follistatin or a different protein, FSTL1. The certificates in circulation measure purity and quantity, not identity, and the safety data sheet is partly about oxytocin.

Compounds sold under research code names are not FDA-approved medicines, and nothing here is a recommendation to take any amount of anything. If you track what you use, our free app works from tested milligrams on a certificate rather than the number printed on a label.

Guide

How to read a peptide COA

Why an identity line needs an external standard to mean anything.

Evidence

MID-35: five papers, all in mice

What a compound with a real literature — and no human data — looks like.

Frequently asked

Is there any published research on FLGR-242?

None that we could find. Searching PubMed, Europe PMC (which indexes preprints and patents), OpenAlex, Crossref, PubChem's compound and substance databases, ClinicalTrials.gov, UniProt and DailyMed in September 2026 returned zero records in every one, and a re-run on 16 October 2026, including a patent search and the FLGR232 spelling, found no record of it either. The seller's 17 references are about follistatin or a different protein, not this product.

Searching FLGR returns results. Doesn't that mean it exists?

Those results are a different subject. In the scientific literature flgR is a sigma-54-dependent transcriptional activator controlling flagellar assembly in bacteria such as Campylobacter and Helicobacter. It has no connection to peptides or muscle. Read the titles before treating hits as evidence.

What does the seller claim, and what is the evidence?

The seller says it blocks myostatin without binding activin, stays active for 19 days (its guide also says 14–15), binds albumin under 20 nM, reaches skeletal muscle directly and preserves lean mass, and it lists 17 references. None of those claims has published data on this product: the binding figure was measured in a patent on a different construct, the half-life is a patent's assertion, and the 17 papers are about follistatin or a different protein, FSTL1. The certificates we read do report 99.71–99.79% purity.

Is FLGR-242 a form of follistatin?

Nothing published establishes that. The seller describes it as a modified fragment of follistatin-344 with an albumin-binding tail, but publishes only the tail's sequence, not the follistatin part. Other descriptions have called it follistatin itself or an FSTL3-derived analogue. Follistatin (UniProt P19883, 344 amino acids) and follistatin-related protein 3 (UniProt O95633, 263 amino acids) are different proteins.

The seller says it contains a patented albumin binder. Is that true?

Partly. The 29-amino-acid tail the seller lists is sequence 4 of US patent 12,377,158 B1, granted in August 2025 to an individual inventor, and its core is SA21, an albumin-binding peptide Genentech published in 2002. But the patent covers only the tail and a version attached to alpha-Klotho; it does not mention activin, myostatin or FLGR. Its 'under 20 nM' binding figure is measured in the patent only for its alpha-Klotho version (7.94 nM against human albumin by surface plasmon resonance), never for a follistatin one, and the original peer-reviewed measurement of SA21, the tail's core peptide without the linker, is 467 nM against human albumin, about 23 times weaker.

Does FLGR-242 bind activin?

Nobody outside the seller can say. The seller states that it does not, but publishes no binding data and does not disclose the follistatin sequence. Natural follistatin binds activin more tightly than myostatin, in one published measurement. A published activin-sparing variant, FS I-I, exists, but in its published animal tests it was a gene in mice, and it is not FLGR-242. The seller's own page also lists activin neutralization assays as a use.

What is the molecular weight of FLGR-242?

The seller states about 40 kDa. None of the certificates we have read states any molecular weight, so the figure cannot be checked against them. By sequence, the working form of human follistatin weighs about 34.8 kDa before sugars and the disclosed tail about 2.95 kDa, so 40 kDa fits nearly the whole follistatin protein plus the tail, not a small fragment.

What do the seller's 17 references show?

They are real papers, mostly about follistatin in mice, rats or cells, plus three about a different protein, FSTL1, and one retracted paper cited by its retraction notice. None mentions FLGR-242, and in none was a person given follistatin. At least six credit follistatin's effects partly to blocking activin, which the seller says its product does not do.

Where does the long half-life figure come from?

From a 2025 US patent on the albumin-binding tail the seller discloses. The patent takes albumin's own 19-day half-life in people and asserts that proteins carrying the tail get about the same; it reports no measurement in people. The 2002 paper that introduced this tail peptide extended a fused antibody fragment's half-life to 32.4 hours in rabbits and 10.4 hours in mice, which its authors describe as 25 to 43 percent of the albumin half-life in those animals. No pharmacokinetic study of FLGR-242 exists in any species.

The seller says injection-site redness is not an allergic reaction. Is that right?

There is no data on this product either way, so a reaction cannot be assumed harmless. Widespread hives, swelling of the lips or tongue, or trouble breathing after an injection can be signs of a severe allergic reaction (anaphylaxis) and need urgent care, according to the World Allergy Organization's 2020 guidance.

Does zero published evidence mean the compound is unsafe?

It means unknown, which is a distinct thing. There is no toxicology to cite either way. An absent safety record is not a clean safety record.

There are certificates of analysis for FLGR-242. Doesn't that prove it is what it says?

Those certificates establish purity and quantity, not identity. All three we read report a single dominant peak, roughly 5 mg of material against a 5 mg label, and an endotoxin pass — real measurements. But a mass-spectrometry identity check compares the measured mass against the expected mass of a declared compound, and FLGR-242 has no published sequence for its follistatin part and no registry entry, so in each certificate the determined identity restates the identity written on the vial the lab was sent.

Do the certificates agree with each other?

No. Of the three issued by the same laboratory for the same vendor, one is headed FLGR232 and carries CAS 3108438-94-1 while the mass-spectrometry trace inside it is captioned FLGR242; another has a batch number that is just the string FLGR and records receipt and reporting dates a year apart. The third is internally consistent.

The certificate lists a CAS number. Can I look it up?

We tried. CAS 3108438-94-1 has a valid check digit, so it is correctly formatted — but a valid checksum is trivial to construct and proves nothing about registration. We found no matching record in PubChem's compound or substance databases or in Europe PMC. CAS's own registry is the authoritative check and its public API requires a key we do not hold, so we record this as unresolved rather than definitively absent. Note also that the other two certificates for the same product carry no CAS number at all.

It passed an endotoxin test. Does that mean it is safe to inject?

No. Endotoxin testing looks for one class of bacterial breakdown product against a stated threshold. It is not a sterility test and it says nothing about what else may be present.

Why does the safety data sheet talk about oxytocin?

Three passages in it are about oxytocin: a section 2 classification that reasons from an oxytocin LD50, a section 2 warning to women of childbearing potential about uterine contractions, and a pharmacological note in section 11. Section 2 carries each of its entries twice, one oxytocin version and one generic version, which reads as an oxytocin sheet only partly rewritten for this product. That is evidence about the paperwork, not about what is in the vials; nothing suggests the material is oxytocin.

Does the safety data sheet give a CAS number or a sequence?

No. It records the CAS number as 'Proprietary / research compound', the molecular formula as 'undisclosed', the amino-acid count as 'Proprietary', and defers both the molecular weight and the sequence to the certificate of analysis — which carries neither. It also directly contradicts the other vendor's certificate, which prints CAS 3108438-94-1.

Sources

For research peptide users tracking their own protocol. Not medical advice. Peptides referenced here are research chemicals, not FDA-approved drugs. Consult a qualified clinician for medical decisions.