CJC-1295 reviewed: the human pharmacokinetics, the DAC distinction, and the anti-doping detection record.

A Review of the CJC-1295 Research Literature

CJC-1295 raised mean plasma growth hormone 2- to 10-fold for six days or more and IGF-1 1.5- to 3-fold for nine to eleven days in healthy adults, after a single subcutaneous dose, with an estimated half-life of 5.8 to 8.1 days ^[1]. That one sentence is the reason CJC-1295 is studied at all, and the reason it is on the WADA Prohibited List. This site reads the record that produced that sentence — in sequence, the way the evidence actually accrued.

CJC-1295 is a synthetic long-acting analog of growth-hormone-releasing hormone (GHRH), built on the first 29 residues of human GH-releasing factor, hGRF(1-29), and carrying four amino-acid substitutions that block the enzymes that would otherwise clear it within minutes ^[2]. The long-acting DAC variant adds one more thing: a chemical handle that covalently binds the peptide to serum albumin already circulating in the blood, dragging its half-life toward that of albumin itself ^[2]. The short-acting form — Modified GRF 1-29, the no-DAC version — keeps the four substitutions but drops the albumin handle, so it clears in minutes to hours.

Keeping those two variants distinct is the single most useful thing a CJC-1295 review can do, because marketing and forums conflate them constantly. We give the distinction its own page.

The evidence is a chronology. The 2005 rat study identified CJC-1295 as the lead albumin-bioconjugate and measured a four-fold increase in GH exposure over the unconjugated peptide ^[2]. The 2006 human studies pinned the multi-day half-life and, importantly, showed that the natural pulsing rhythm of GH survives continuous stimulation ^[1][3]. A 2009 study mapped the serum-protein changes the compound leaves behind ^[5]. In 2010, analysts identified CJC-1295 by mass spectrometry inside a black-market vial ^[6] — the moment the research compound became an anti-doping target. From there the story is a detection arms race, surveyed most recently by a 2025 Nature Reviews Endocrinology review of the whole GHRH-analog class ^[11].

CJC-1295 is not approved for human use by the FDA or any major regulator, and it is prohibited at all times in tested sport ^[4]. This is a digest of what the published studies measured — not medical guidance, and not a place to obtain anything. The findings are organized across the published research, the DAC and no-DAC pharmacokinetics, the CJC-1295 side effects literature, and a full reference list.

What is CJC-1295?

CJC-1295 is a synthetic long-acting analog of growth-hormone-releasing hormone, built on hGRF(1-29) with four protease-resistant substitutions; the DAC variant adds covalent serum-albumin conjugation for a multi-day half-life, while the no-DAC form is short-acting ^[2]. It is an unapproved research chemical, handled by suppliers for laboratory use only.

Mechanistically it does one thing. It binds the GHRH receptor on the pituitary's growth-hormone cells, triggers the Gs/cAMP/PKA signaling cascade those cells use, and prompts them to synthesize and release growth hormone in pulses; the liver responds to that GH by producing IGF-1 ^[2]. The four substitutions — D-Ala at position 2, plus changes at 8, 15 and 27 — exist to stop dipeptidylpeptidase-IV and oxidation from destroying the molecule before it reaches the receptor ^[2].

What does CJC-1295 do?

It binds the GHRH receptor on pituitary somatotrophs and stimulates pulsatile growth-hormone release, which raises hepatic IGF-1. In healthy adults, single 30-60 ug/kg doses produced dose-dependent multi-fold GH increases and 1.5- to 3-fold IGF-1 increases lasting days ^[1].

What it does not do is flatten the body's own GH rhythm. A single 60 or 90 ug/kg dose in healthy young men raised basal GH roughly 7.5-fold and left the frequency and size of natural GH pulses unchanged a week later ^[3]. That preserved pulsatility is the finding that distinguished CJC-1295 from a constant GH infusion and is why the GHRH-analog approach drew interest in the first place. The measured effects, the comparator analogs, and the open questions are all covered in the published research.

Reading the record honestly

The human evidence base is small and short. The studies that matter most are early Phase I pharmacokinetic trials in healthy volunteers; they established how GH and IGF-1 move after a dose, not whether long-term use is safe or does anything a person would notice ^[12]. A ConjuChem Phase 2 trial of the DAC compound in HIV-associated visceral obesity (NCT00267527) was discontinued, and the long-acting program did not advance ^[12].

So this review holds two things at once. The pharmacokinetics are real, replicated, and quantified — we lead with them. The long-term safety and efficacy data in healthy adults do not exist — we mark that gap as plainly as we mark the numbers, on the CJC-1295 side effects page and throughout. The frequently asked questions page answers the most common specific questions directly.