Frequently Asked Questions

What is CJC-1295?

A synthetic analogue of growth-hormone-releasing hormone, built on the first 29 residues of human growth-hormone-releasing factor and carrying four amino-acid substitutions that block enzymatic cleavage. The DAC variant adds a linker that bonds covalently to serum albumin; the no-DAC variant, sold as Modified GRF (1-29), does not and is short-acting ^[7]. It is not approved for human use anywhere and is sold as a research chemical ^[4].

What is the half-life of CJC-1295?

In healthy adults given single subcutaneous doses of 30 or 60 micrograms per kilogram, the estimated half-life was 5.8 to 8.1 days ^[4]. That is a human figure, and it applies to the DAC form. The no-DAC form is short-acting and the two are routinely confused ^[7]. In rats, the albumin conjugate remained detectable in plasma beyond 72 hours ^[7] — a different species and a different measurement, quoted here as such.

How much CJC-1295 should I take?

This desk does not answer that question, and the reason is not caution for its own sake.

CJC-1295 has no approved human indication anywhere, no established therapeutic dose, and a published human evidence base limited to a handful of early pharmacology studies ^[4]. There is no trial-derived dose to report, and the amounts used in those studies were administered under research conditions to healthy volunteers for pharmacokinetic measurement, not as a treatment for anything.

More generally, a dose and an interval are clinical decisions made against an indication, a specific person and a monitoring plan. A half-life figure is an input to that decision, not a substitute for it. Reporting the measurement is this desk's job. Making the decision is not.

Is CJC-1295 safe?

The honest answer is that nobody knows, because the studies that would establish it have not been done. Published human evidence is limited to a small number of early pharmacology studies, with no large or long-term trials in healthy adults ^[4]. Immunogenicity was among the safety concerns cited in 2024 FDA briefing materials for the Pharmacy Compounding Advisory Committee, as part of the basis for not recommending it for the 503A compounding bulks list ^[1]. Mechanism-based concerns in the record — sustained IGF-1 elevation, fluid retention with nerve-compression effects, and reduced insulin sensitivity — rest on sources outside this digest's reference set and are reported on the CJC-1295 page without citation numbers for that reason.

What is ipamorelin?

A synthetic pentapeptide, Aib-His-D-2-Nal-D-Phe-Lys-NH2, that selectively activates the ghrelin receptor GHS-R1a on pituitary somatotrophs and triggers a pulse of growth-hormone release. Its distinguishing feature is selectivity: unlike the earlier growth-hormone-releasing peptides it does not meaningfully raise ACTH, cortisol or prolactin. It has never been approved as a drug anywhere, and its only published Phase 2 trial missed its primary endpoint ^[10].

What is the half-life of ipamorelin?

Approximately 2 hours terminal half-life in healthy male volunteers, measured after five 15-minute intravenous infusions, with clearance of 0.078 litres per hour per kilogram and a steady-state volume of distribution of 0.22 litres per kilogram ^[11]. The growth-hormone response peaked at about 0.67 hours, roughly 40 minutes after dosing, as a single discrete pulse ^[11].

The route matters as much as the number. That figure was measured intravenously, and subcutaneous injection introduces an absorption step that can dominate the observed curve. An intravenous half-life does not transfer to a subcutaneous one without being measured again.

What are the risks of ipamorelin?

Long-term human safety is uncharacterised. The controlled human data amount to one Phase 2 trial over a short perioperative window ^[10] and one acute single-dose pharmacokinetic study ^[11]; there is no Phase 3 trial and no approved indication. A 28-day preclinical safety study of a different GHS-R1a agonist found dose-dependent myocardial degeneration and necrosis in rats, with elevated heart-type fatty-acid-binding protein but no troponin elevation — a class-level signal in rats rather than a finding about ipamorelin itself ^[9]. Community reports describe flushing, tingling, water retention, increased hunger and a diminishing response over months; those are anecdotal, not clinical evidence. Most material sold is research-grade of variable purity from unregulated suppliers.

What is semaglutide, and how does it work?

A 31-amino-acid acylated analogue of GLP-1, marketed as Ozempic, Wegovy and Rybelsus, and an approved prescription medicine. It activates the GLP-1 receptor, potentiating glucose-dependent insulin secretion, suppressing glucagon release and slowing gastric emptying; its weight effect is mainly central, acting on hypothalamic and brainstem appetite circuits.

Kinetically it is the reference implementation of half-life extension in this set. An alpha-aminoisobutyric acid at position 8 blocks the enzyme that destroys native GLP-1 within minutes, and a C18 fatty di-acid on lysine 26 binds serum albumin strongly but reversibly, which protects the peptide from renal clearance. The large outcome trials all administered it once weekly by subcutaneous injection ^[14][15][16].

What is tesamorelin?

A synthetic 44-amino-acid analogue of growth hormone-releasing hormone with a trans-3-hexenoic acid group on the N-terminus, which blocks cleavage by dipeptidyl peptidase-IV. It was approved in the United States in 2010 to reduce excess abdominal fat in HIV-infected patients with antiretroviral-related lipodystrophy ^[19]. It stimulates the pituitary to release the body's own growth hormone rather than supplying growth hormone directly, and the resulting IGF-1 drives lipolysis preferentially in visceral fat.

Will tesamorelin help me lose belly fat?

This desk reports what the trials measured, in the populations they measured it in, and stops there.

In HIV-associated lipodystrophy, a meta-analysis of five randomised trials found a mean reduction in visceral adipose tissue of -27.71 square centimetres, alongside -1.18 kilograms of trunk fat and a -4.28 per cent change in hepatic fat fraction, all P<0.001 ^[18]. A six-month randomised trial in 50 antiretroviral-treated adults found a -42 square centimetre treatment effect on visceral fat, P=0.005 ^[20]. Over 52 weeks the reduction was sustained at -18 per cent, and visceral fat reaccumulated when treatment stopped ^[22].

Those results were obtained in HIV-positive adults on antiretroviral therapy, which is the only population in which the pivotal trials were run and the only indication for which the drug is approved ^[19]. Generalising them to anyone else is not something the cited evidence supports, and whether a prescription medicine is appropriate for a particular person is a question for a clinician.

Does a longer half-life mean fewer injections?

That inference is the one this desk exists to decline.

A half-life is a measured rate of disappearance. A dosing interval is a clinical decision that also depends on the indication, the target exposure, the shape of the effect, the tolerability profile and how the compound is monitored. The four compounds here show how loosely the two are coupled. CJC-1295 has an estimated half-life of 5.8 to 8.1 days in healthy adults, and IGF-1 stayed above baseline as long as 28 days after multiple doses ^[4]. Tesamorelin clears from plasma quickly and its measured effects run for a year ^[22]. Ipamorelin clears in about 2 hours and its growth-hormone response is a single 40-minute pulse ^[11].

Those are three different relationships, and no arithmetic converts any one of them into a schedule. Where a trial protocol is known it is reported on the relevant page as a fact about that trial. It is not a recommendation, and it is not transferable.

Why are these peptides injected instead of swallowed?

Because the digestive system is built to destroy them. Stomach acid and intestinal proteases break peptide bonds by design, and the gut wall does not pass molecules of this size intact. Oral administration therefore loses most of the material before absorption and absorbs little of what survives.

Every human study cited on this site used a route that bypasses the gut: subcutaneous injection for CJC-1295 ^[4][5], intravenous infusion for ipamorelin ^[11], weekly subcutaneous injection in the semaglutide trials ^[14][15][16], daily subcutaneous injection in the tesamorelin trials ^[20][21][22].

One oral peptide formulation appears in this set. Semaglutide has an oral form that depends on an absorption enhancer and must be taken fasted, with administration errors substantially reducing exposure — which is a measure of how narrow the oral route is even when it has been engineered for. Its bioavailability figures are outside this digest's reference set and are not quoted here.