CJC-1295

Overview

CJC-1295 is a synthetic analog of the first 29 amino acids of human growth hormone-releasing hormone (GHRH 1-29), the bioactive fragment of native GHRH. It was developed in the early 2000s by ConjuChem Biotechnologies as part of a program exploring albumin-binding "Drug Affinity Complex" (DAC) technology to extend peptide half-life. CJC-1295 is a growth hormone secretagogue: it acts on the pituitary to stimulate the release of growth hormone (GH), which in turn raises circulating insulin-like growth factor 1 (IGF-1).

The name "CJC-1295" is a frequent source of confusion because two distinct molecules circulate under closely related names:

• CJC-1295 with DAC (also written DAC:GRF): the long-acting, albumin-binding form characterized in the published human study.
• CJC-1295 without DAC: the unconjugated tetrasubstituted GRF (1-29) peptide, almost always sold and discussed under the name Modified GRF (1-29) or "Mod GRF 1-29." It is short-acting.

Chemistry and structure (DAC vs non-DAC)

Native GHRH is rapidly degraded in plasma, principally by the enzyme dipeptidyl peptidase-4 (DPP-4), giving sermorelin (unmodified GRF 1-29) a half-life of only minutes. CJC-1295 builds stability in two stages.

Stage 1 — the tetrasubstituted backbone (the part shared by both forms). Four amino acids of GRF (1-29) are substituted, conventionally summarized as D-Ala2, Gln8, Ala15, Leu27. The D-alanine at position 2 blocks DPP-4 cleavage; the other substitutions reduce other routes of enzymatic and chemical degradation. This tetrasubstituted peptide is the molecule sold as Modified GRF (1-29) / "CJC-1295 without DAC." Its reported core sequence is:

H-Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu-Ser-Arg-NH2

Stage 2 — the Drug Affinity Complex (DAC), unique to "CJC-1295 with DAC." A reactive maleimido group (an N-epsilon-maleimidopropionyl-lysine moiety) is attached. After injection this group forms a covalent bond with the free thiol of cysteine-34 (Cys34) on circulating serum albumin. Because albumin itself has a half-life of weeks, the peptide is effectively shielded from clearance and acts as a slow-release depot. This single chemical addition is the entire difference between the multi-day-acting and the minutes-acting forms.

Reported molecular weights and CAS identifiers vary across vendor and database sources, in part because of the with-DAC/without-DAC ambiguity; the figures above reflect the most commonly cited values and should be treated as approximate.

Mechanism of action

Both forms act as agonists at the GHRH receptor (GHRHR), a G-protein-coupled receptor expressed on the somatotroph cells of the anterior pituitary. Receptor binding activates adenylate cyclase, raising intracellular cAMP and triggering synthesis and pulsatile release of GH. Elevated GH then acts mainly on the liver to increase production of IGF-1.

The DAC modification does not change how strongly the peptide activates the receptor; it changes how long the peptide remains available to do so. The without-DAC form produces brief GH pulses that are cleared quickly; the with-DAC form maintains a low, continuous level of GHRH-receptor stimulation for days, raising mean GH and IGF-1 over an extended window.

Because GHRH agonists and ghrelin-receptor agonists drive GH release through different, complementary pathways, GHRH analogs are frequently studied alongside ghrelin mimetics such as Ipamorelin in comparative secretagogue research. CJC-1295 is also often discussed next to Tesamorelin, a related but separately developed, FDA-approved GHRH (1-44) analog.

Research and evidence (human vs animal)

Human data is limited and dated. The principal human reference is:

• Teichman et al. (2006), J Clin Endocrinol Metab. Two randomized, placebo-controlled, double-blind ascending-dose trials in healthy adults (28- and 49-day designs). A single subcutaneous injection of CJC-1295 (with DAC) produced dose-dependent increases in mean plasma GH of about 2- to 10-fold for 6 days or more, and in mean IGF-1 of about 1.5- to 3-fold for 9–11 days. The estimated half-life was 5.8–8.1 days, and repeated dosing produced a cumulative effect, with mean IGF-1 staying above baseline for up to 28 days. Doses such as 30 and 60 micrograms per kilogram were described as relatively well tolerated. These study doses are reported here only as historical fact, not as guidance.

This single published pharmacology study, plus a small number of related early-phase reports, represents the bulk of the controlled human evidence. Subsequent decades did not produce large, peer-reviewed efficacy or long-term safety trials, and there is no published high-quality evidence supporting the performance, body-composition, or anti-aging claims commonly attached to the compound in non-scientific sources.

Analytical / forensic literature. Henninge et al. (2010, Drug Testing and Analysis) identified CJC-1295 in an unknown pharmaceutical preparation using high-resolution tandem mass spectrometry, noting that the peptide was being manufactured illicitly and was believed to be in use in the bodybuilding community despite incomplete clinical development. Later analytical work focused on detecting CJC-1295 and its DAC form in anti-doping testing.

Animal / preclinical data. GHRH-analog research, including studies of tetrasubstituted GRF (1-29), has used rodent and other animal models to characterize GH pulse dynamics and receptor pharmacology. This preclinical literature should be kept separate from the human findings above: animal GH responses do not establish human efficacy or safety.

Clinical and regulatory status

CJC-1295 reached early clinical trials under ConjuChem for indications that reportedly included growth hormone deficiency and lipodystrophy. According to secondary sources, clinical development was discontinued following the death of a trial subject; the attending physician reportedly attributed the death to pre-existing coronary artery disease rather than to the compound, but development did not continue. This account is widely repeated but rests on limited public documentation and should be treated with appropriate caution.

The compound was never approved by the FDA, EMA, or comparable authorities, and there is no marketed pharmaceutical product. It exists today only as a "research use only" chemical not intended for human administration. By contrast, the related GHRH analog Tesamorelin was approved (FDA, 2010) for HIV-associated lipodystrophy, illustrating that a GHRH-analog mechanism can reach approval, but that CJC-1295 specifically did not.

Safety and reported effects

Because controlled human data is so limited, the safety profile of CJC-1295 is not well established. Points that can be stated factually:

• In the Teichman 2006 trials, doses around 30–60 micrograms per kilogram were described as relatively well tolerated, with no serious adverse reactions reported in that small, short-term setting.
• Theoretical and class-level concerns for any agent that sustains elevated GH and IGF-1 include fluid retention, joint discomfort, effects on glucose metabolism/insulin sensitivity, and the general concern that chronically elevated IGF-1 is biologically active in tissues. None of these has been characterized for CJC-1295 in adequate long-term human studies.
• The reported termination of clinical development after a trial-subject death (above) is part of the compound's history regardless of attributed cause.

The absence of large safety studies is itself the most important safety fact: long-term human risk is genuinely unknown.

Legal status (including anti-doping)

• Drug/medicine status: Not an approved drug anywhere; not a dietary supplement. Material on the market is sold as a research chemical labeled "not for human consumption." Selling or marketing it for human use is generally unlawful in major jurisdictions.
• Anti-doping: CJC-1295 is prohibited at all times (in- and out-of-competition) under the World Anti-Doping Agency (WADA) Prohibited List, Section S2 — "Peptide Hormones, Growth Factors, Related Substances and Mimetics," which covers growth hormone secretagogues and GHRH/GH-releasing factors. Athletes in WADA-compliant sport are subject to sanction for its use.

How it compares

CJC-1295 is one of several growth-hormone peptides documented here, differing mainly by mechanism and, importantly, by regulatory status:

• Ipamorelin, GHRP-2 and GHRP-6 act on the ghrelin receptor (a complementary pathway); GHRP-2/6 also raise cortisol and prolactin, while ipamorelin is more selective.
• Sermorelin is a shorter-acting GHRH analog that was formerly FDA-approved (now discontinued/compounded).
• Tesamorelin is a GHRH analog that is FDA-approved, but only for HIV-associated lipodystrophy.

CJC-1295 itself is not approved anywhere. Of this group, only Tesamorelin holds a current approval (narrow indication), and only Sermorelin has a prior approval history, a useful frame when weighing evidence quality. See the Muscle & growth hormone overview.

Common misconceptions

• "CJC-1295 and Mod GRF 1-29 are the same thing." They share the same tetrasubstituted GRF (1-29) backbone, but "CJC-1295" in the published human literature refers to the DAC-conjugated, multi-day-acting molecule. "Mod GRF 1-29" (often mislabeled "CJC-1295 without DAC") is the unconjugated, ~30-minute peptide. Treating the days-long half-life data as if it applied to the without-DAC form is a common and significant error.
• "The 5.8–8.1 day half-life applies to whatever I'm reading about." That figure is specific to the with-DAC form. The without-DAC peptide is cleared in well under an hour.
• "It's an approved or clinically validated GH therapy." It is not. Human evidence is essentially one small pharmacology study; development was halted.
• "Approval of Tesamorelin means CJC-1295 is safe/approved." They are different molecules with different development histories; only Tesamorelin was approved.

Community claims & recent evidence

These points address claims circulating in the peptide community — including popular video "masterclasses" — checked against the primary sources we were able to reach. CJC-1295 is a real GHRH analog with a genuine but very thin published human record, and popular talks often attach data from other compounds to it. A caution on method: where we say a claim "could not be traced," that reflects the limits of the literature we can access — much relevant work (regional and non-English journals, paywalled papers, clinical practitioner experience, conference abstracts, and unpublished or proprietary data) is not indexed in the sources we searched. Not finding a citation here is not proof that a claim is false; it means we could not confirm it, and it should be read as unverified rather than disproven.

Verified additions

• [Human] The GHRH + ghrelin-pathway synergy is real and predates these peptides: in healthy men a growth hormone-releasing peptide (GHRP) given together with GHRH released more GH than either agent alone — a genuine supra-additive effect (Bowers et al., J Clin Endocrinol Metab 1990). This validates the mechanism behind pairing a GHRH analog with a ghrelin mimetic, but it was shown with GHRP-6 + GHRH, not with CJC-1295 + ipamorelin.
• [Animal] Dosing frequency matters even for the long-acting DAC form: once-daily CJC-1295 normalized body weight and length in GHRH-knockout mice, while the same dose was less effective when spaced to every 48 or 72 hours (Alba et al., Am J Physiol Endocrinol Metab 2006).
• [Human] After a single subcutaneous dose, CJC-1295 (with DAC) raised mean IGF-1 roughly 1.5–3× for 9–11 days, with an estimated 5.8–8.1-day half-life; repeat dosing kept IGF-1 above baseline for up to 28 days (Teichman et al., J Clin Endocrinol Metab 2006) — the concrete basis for "roughly weekly" dosing.

Claims we could not verify

• "The combo gives 40% more GH than either peptide alone (2018 European Journal of Endocrinology, humans)." → We found no human trial of CJC-1295 + ipamorelin in the accessible literature, and we could not trace the specific 40% figure to any identifiable published study — which is not proof it does not exist. GHRH + ghrelin synergy is real in principle (Bowers et al. 1990) but was demonstrated with different compounds; for this pair the number remains [Hypothesis] until a primary source is located.
• "A 2013 JCEM study showed with-DAC beat without-DAC for consistent IGF-1." → The date and attribution do not match what we could confirm. The human study we can point to is Teichman et al. 2006, which tested only the with-DAC form — we found no head-to-head with-DAC vs without-DAC trial, and no 2013 JCEM CJC-1295 study in the sources we searched. Absence here reflects what is indexed and reachable, not a demonstration that no such work exists.
• "One injection lasts over a week, up to two weeks." → This runs ahead of the measured figures. Reported human half-life is 5.8–8.1 days and single-dose IGF-1 elevation lasts about 9–11 days (Teichman et al. 2006) — consistent with roughly weekly, rather than two-week, dosing in the data available to us.
• "CJC-1295 rebuilds immunity, cognition (BDNF +45%), telomerase activity, kidney and heart function, and lowers cancer risk." → These appear to describe general GH/IGF-1 biology, and in several cases studies of injected recombinant human GH — e.g., the "1990 NEJM" result cited is Rudman et al., N Engl J Med 1990, which used biosynthetic human GH, not a GHRH analog. In the accessible literature, CJC-1295 itself has essentially one small human study, measuring only GH and IGF-1 levels (Teichman et al. 2006); we found no human trial measuring muscle, cognition, immune, cancer, or longevity outcomes for CJC-1295 specifically — which is a gap in the published record we can reach, not evidence that CJC-1295 lacks such effects. What can be said is narrower: GH-therapy and IGF-1 mechanistic findings are not, on their own, CJC-1295 outcomes, and treating them as such is not supported by any CJC-1295 study we located.