Answered from the record, or marked unanswerable and explained

What does BPC-157 do in the body?

In animals, it accelerates the repair of injured tissue. The best-characterised route is angiogenesis: it up-regulates the VEGFR2 receptor and promotes its internalisation, activating downstream Akt and endothelial nitric-oxide signalling ^[4]. In rats it reduced gastric ulcer area and accelerated ulcer healing ^[5]. Additional reported routes include the FAK-paxillin complex governing cell migration and sensitisation of growth-hormone-receptor signalling in tendon fibroblasts.

What it does in a human body is a separate question with a separate answer, which is that nobody has published a study designed to find out. The human record consists of three small pilot reports, and a 2025 review describes the compound as investigational on exactly that basis ^[2].

Is BPC-157 a growth hormone?

No. BPC-157 is a fifteen-amino-acid peptide derived from a partial sequence of a protein found in gastric juice. It is not a hormone, it is not produced by the pituitary, and it does not act on the growth-hormone axis in the way a secretagogue does.

One finding causes the confusion: in cultured tendon cells BPC-157 increased growth-hormone-receptor signalling, which is a claim about receptor sensitivity in a dish rather than about circulating hormone. The compound on this site that genuinely acts on that axis is CJC-1295, which binds the growth-hormone-releasing hormone receptor and raises circulating growth hormone and IGF-1 for days ^[21].

Does BPC-157 damage the liver?

There is no published evidence of liver injury, and the size of the evidence base is the important part of that sentence.

The first-in-human intravenous safety pilot administered up to 20 mg to two healthy adults and recorded no adverse events and no measurable change in cardiac, hepatic, renal, thyroid or glucose biomarkers ^[1]. That is a genuine result and it involves two people over a short window.

A 2025 review states that human data are extremely limited and that rigorous large-scale trials are lacking ^[2]. Absence of a signal in a study that small is not evidence of absence, and a hepatic safety question is answered by an adequately powered trial with prespecified liver endpoints, not by the reassuring silence of a two-person pilot.

What does the MOTS-c peptide do?

MOTS-c is a sixteen-amino-acid peptide encoded inside the mitochondrial 12S ribosomal RNA gene. Cells produce it themselves, and exercise increases its expression in skeletal muscle and in circulation ^[9].

Its characterised action is metabolic: it inhibits the folate cycle and de novo purine biosynthesis, raising AICAR and activating AMP-activated protein kinase, which improves glucose handling chiefly in muscle ^[11]. Under metabolic stress it moves into the nucleus and regulates gene expression there, including antioxidant-response genes through NRF2 ^[10]. A 2024 study identified casein kinase 2 as a direct binding target ^[6].

All of that describes what the peptide the body already makes does. What administering extra MOTS-c does to a person is undetermined, because no human interventional study has been published.

What are the negative side effects of MOTS-c?

This question currently has no evidentiary basis, and saying so is the accurate answer rather than an evasive one.

No human interventional study of MOTS-c has been published, so there is no adverse-event table, no discontinuation rate and no tolerability profile in the literature. This digest also carries no compiled set of community reports for MOTS-c, and it will not assemble one to fill the space.

The published human evidence is observational: a cohort of 94 haemodialysis patients in which naturally circulating MOTS-c was associated with mortality and cardiovascular events ^[7]. Nobody in that study was given anything, so it cannot report side effects. Any side-effect list circulating for MOTS-c is extrapolated from rodent experiments, and rodent tolerability does not transfer.

How often do you inject MOTS-c?

No interval appears anywhere on this site, and the reason is specific rather than cautious. No published human study has administered MOTS-c to anyone, so no human schedule exists in the literature to report.

The rodent work used per-kilogram amounts on schedules designed around rodent physiology, and there is no published measured human half-life, bioavailability or exposure-response relationship to convert them with. Any frequency circulating outside the literature was not derived from a human study, because no human study exists to derive it from.

The study that would have to come first is a phase 1 pharmacokinetic and tolerability trial. Until that is run and published, the honest answer to a question about frequency is that the field does not know.

What is tirzepatide?

Tirzepatide, marketed as Mounjaro and Zepbound, is a linear 39-amino-acid synthetic peptide based on the sequence of glucose-dependent insulinotropic polypeptide, carrying a C20 fatty diacid that binds albumin and gives it a half-life long enough for weekly administration. It appears in the literature as LY3298176.

It is the first approved dual incretin agonist, activating both the GIP and the GLP-1 receptor. The FDA approved it in May 2022 for type 2 diabetes mellitus ^[14], with later approvals covering chronic weight management and moderate-to-severe obstructive sleep apnoea in adults with obesity. It is prescription-only and is not approved for type 1 diabetes ^[14].

How does tirzepatide work?

It activates two incretin receptors with a single molecule. Engaging both the GIP and the GLP-1 receptor enhances glucose-dependent insulin secretion, suppresses glucagon, slows gastric emptying, and reduces appetite and food intake.

Glucose dependence is the detail that governs its safety profile: insulin release scales with circulating glucose, so on its own the agent carries low risk of driving blood sugar too low, and that risk returns when it is combined with insulin or a sulfonylurea.

Whether two receptors beat one was not settled by the mechanism but by direct comparison. Against semaglutide (Ozempic, Wegovy) it produced larger reductions in glycated haemoglobin and weight in type 2 diabetes ^[17] and larger weight reduction in obesity, -20.2% against -13.7% at 72 weeks ^[13].

What is tirzepatide used for?

Its first approval, in May 2022, was for type 2 diabetes mellitus ^[14]. Later approvals cover chronic weight management in adults with obesity or with overweight plus a weight-related condition, and moderate-to-severe obstructive sleep apnoea in adults with obesity.

The weight-management evidence is the largest body of trial data attached to any compound on this site. In SURMOUNT-1, 2539 adults with obesity and without diabetes were followed for 72 weeks, with mean weight change of -15.0%, -19.5% and -20.9% across three doses against -3.1% on placebo ^[16]. Gastrointestinal adverse events were the most common and were concentrated during dose escalation ^[16].

What is CJC-1295?

CJC-1295 is a synthetic analog of growth-hormone-releasing hormone, built on the first 29 residues of human growth-hormone-releasing factor with four substitutions that resist enzymatic breakdown. The DAC variant additionally binds covalently to circulating albumin, which extends its plasma half-life toward that of albumin itself; the no-DAC form, modified GRF 1-29, omits that group and is short-acting.

The two forms are routinely treated as one thing and are not. In healthy adults the DAC form had an estimated half-life of 5.8 to 8.1 days ^[21], while the no-DAC form lasts minutes to hours. Any statement about the compound that does not specify which form it means is unreadable.

It is not approved for human use by any major regulator and is distributed as a research chemical. It is prohibited in sport at all times.

Is CJC-1295 safe?

The published human studies were small, short and designed to measure hormone kinetics rather than to detect harm, so the literature cannot answer a safety question in the sense the question intends ^[21][22].

What is on record: the compound has no approval for human use anywhere and its human evidence is limited to early pharmacology work ^[21]. Immunogenicity, meaning an immune response raised against the peptide, was among the safety concerns cited in the 2024 FDA advisory-committee briefing materials for this class ^[18].

Carried in this digest without an attached citation, and reported as such: an epidemiological association between higher circulating IGF-1 and modestly increased risk of certain cancers, which matters because the DAC form keeps IGF-1 elevated for extended periods; fluid retention, swelling and nerve-compression effects from growth-hormone-driven sodium and water retention; and reduced insulin sensitivity, since growth hormone is glucose-sparing.

A safety answer requires a trial with prespecified safety endpoints and enough accumulated exposure-time to detect an uncommon event. No such trial has been published.

How much CJC-1295 should I take?

No figure is given here, and the reason is structural rather than squeamish. Dose-finding is a study design, and a dose-finding study requires an endpoint to optimise against. No clinical endpoint was ever chosen for this compound, so no dose-finding programme was ever run, so no dosing standard exists to report.

What the record contains instead is exposure descriptions from pharmacology experiments: administrations calculated per kilogram of body weight, given to volunteers under supervision so that growth hormone and IGF-1 could be measured over the following days ^[21][22]. Those are measurements of an experiment. They were never scaled to an individual, they were never tested against any outcome, and this site does not perform the conversion that would turn them into guidance.

A further problem sits underneath the question. Because the DAC and no-DAC forms differ in duration by orders of magnitude ^[21], a quantity that does not name the form is not merely unsafe, it is uninterpretable.