CJC-1295 Peptide

## What it is CJC-1295 is a synthetic analog of growth-hormone-releasing hormone (GHRH 1-29) developed by Conjuchem in the early 2000s as a sustained-release GH secretagogue. Two distinct variants are sold under the same name and frequently confused: the DAC (Drug Affinity Complex) version carries a maleimide group that covalently bonds to a cysteine residue on serum albumin, extending plasma half-life to roughly 7 days. The non-DAC variant, often called Mod GRF 1-29 or CJC-1295 no-DAC, lacks the albumin tether and clears in approximately 30 minutes. The compound was originally pursued for adult GH deficiency and AIDS-related lipodystrophy. Conjuchem advanced it through phase 1/2 (Teichman 2006) before discontinuing development. Today it is sold exclusively in the research-peptide grey market and is not approved as a drug in any major jurisdiction. Users are predominantly anti-aging clinic patients, body-composition-focused athletes, and biohackers chasing subjective sleep and recovery effects. WADA bans CJC-1295 under S2 (peptide hormones, growth factors). ## Mechanism of action CJC-1295 binds the GHRH receptor on pituitary somatotrophs, stimulating endogenous growth-hormone synthesis and pulsatile release. Because it acts on the pituitary rather than supplying exogenous GH, the negative feedback architecture of the GH-IGF-1 axis remains partially intact, theoretically reducing the risk of pituitary atrophy seen with chronic exogenous GH administration. The DAC modification is the pharmacokinetic hinge. By tethering the peptide to circulating albumin, plasma residence is extended from minutes to days, producing sustained rather than pulsatile GH elevation. The non-DAC variant retains the modifications that resist DPP-4 cleavage but clears quickly, generating a brief receptor activation that more closely mimics physiologic GHRH pulses. Many anecdotal protocols pair non-DAC CJC-1295 with Ipamorelin, a ghrelin/GHS-R agonist, on the rationale that the two pathways converge on somatotrophs and produce a larger pulsatile response than either alone. ## Evidence base Human trial evidence is dominated by a single phase 1/2 study. Teichman 2006 (n=65 healthy adults) administered single ascending doses of CJC-1295 with DAC at 60, 125, 250, and 500 mcg/kg subcutaneously. Mean serum GH increased 2 to 10 fold over baseline and remained elevated for approximately 6 days at the higher doses. IGF-1 rose 1.5 to 3 fold and remained elevated for 9 to 11 days, consistent with the long albumin-tethered half-life. A subsequent multiple-dose study reported sustained IGF-1 elevation across weekly dosing for 28 days with no acute safety signals. No phase 3 RCT has been completed for either variant. The non-DAC variant has even less direct human trial data; most published GHRH-analog evidence in humans relies on tesamorelin (an FDA-approved structural cousin), which has demonstrated reductions in visceral adipose tissue of around 15 to 18% in HIV-associated lipodystrophy across LIPO-026 and related trials. Body-composition outcomes for CJC-1295 specifically are inferred from IGF-1 axis activation rather than directly measured. Anecdotal user reports describe modest fat loss, improved sleep depth, and faster recovery from training, with effects typically appearing after 4 to 6 weeks. None of these claims are supported by controlled human trials specific to CJC-1295. The honest reading is that the Teichman trial established proof of pharmacology, but downstream clinical outcomes remain extrapolation. ## Dosage and administration The DAC variant is dosed 1 to 2 mg subcutaneously weekly to twice weekly. The non-DAC variant is dosed 100 mcg 1 to 3 times daily, typically pre-bed and post-workout to align with endogenous GH pulse windows. Anecdotal cycling protocols run 8 to 12 weeks on, then 4 weeks off, on the assumption that continuous stimulation could blunt pituitary responsiveness. There is no controlled human data on optimal cycle length. A typical 2 mg vial reconstituted with 2 mL bacteriostatic water gives 1 mg/mL (1000 mcg/mL). A 100 mcg dose equals 10 units on a U100 insulin syringe. Injection rotates between abdomen, thigh, and deltoid. Many users injecting non-DAC dose pre-bed, sometimes 30 minutes before lights-out to align peak GH with the early-night pulse. Label confusion is endemic in the research-peptide market: the same vial is sometimes sold as CJC-1295, CJC-1295 DAC, and Mod GRF 1-29 by different vendors. Confirm with the supplier which variant is in the vial before dosing, as the dosing schedules differ by orders of magnitude. ## Side effects and safety Reported adverse effects are generally mild: injection-site reactions (numbness, tingling, transient flushing), water retention, vivid dreams, and mild head pressure or transient headache. The DAC variant produces sustained supraphysiologic GH, which can induce insulin resistance over weeks. Fasting glucose and HbA1c monitoring are advisable for users on continuous protocols, particularly those with metabolic risk factors. Contraindications include active malignancy (GH and IGF-1 are mitogenic and a theoretical concern for tumor progression), diabetic retinopathy (theoretical worsening), prior pituitary tumor, and pregnancy. Drug interactions include synergistic GH release with Ipamorelin (commonly co-administered), GH-induced insulin resistance that can shift glycemic control over weeks, and blunting of GH-axis response by corticosteroids. Athletes should know CJC-1295 is detectable on WADA-accredited testing and the GH-axis fingerprint it produces is distinguishable from baseline endogenous activity. ## Practical notes Lyophilized vials are stable at room temperature but are best refrigerated. Once reconstituted, refrigerate and use within 2 to 4 weeks. The DAC variant binds albumin within minutes of injection, so the choice of injection site does not meaningfully alter pharmacokinetics; the non-DAC variant clears too quickly for site selection to matter. Expect subjective changes (sleep depth, recovery quality) within 2 to 4 weeks on either variant. Fat-loss and lean-mass changes, if any, accumulate over 8 to 12 weeks and require concurrent training and nutrition for any effect to be detectable. Users tracking outcomes should baseline IGF-1 before starting and recheck at 6 to 8 weeks; absence of IGF-1 elevation suggests the vial is inactive or under-dosed, a recurring problem in unregulated supply chains.