Research and informational content only. Not medical advice. Many peptides discussed on this site are not approved for human use.
CJC-1295 with DAC
Research PeptideAlso known as: CJC-1295 DAC · DAC:GRF · DAC-GRF · CJC1295 · Drug Affinity Complex:GRF
Animal Only
The compound's mechanism and pharmacokinetics are established in animal models: Jetté 2005 (ConjuChem-sponsored, all-rat work) confirmed albumin conjugation within 15 minutes of injection, a 4-fold increase in GH AUC versus hGRF(1-29), and plasma detection beyond 72 hours. The GHRH-KO mouse study showed normalization of growth in severely GH-deficient animals. Both studies are animal-only; neither generalizes to GH-sufficient subjects. The evidence base is limited to animal and in vitro studies; a large-scale study was halted before reporting efficacy data and those results are permanently unavailable. No independent academic replication of any finding exists for this compound.
"CJC-1295" is ambiguous, and only mass spec can tell which one you have
Every published early-phase study of a compound labeled "CJC-1295" (Teichman 2006, Ionescu 2006 pulsatility, Sackmann-Sala 2009 proteomics, the terminated NCT00267527 study n=192) studied this compound, CJC-1295 WITH DAC: a 30-amino-acid peptide that covalently binds serum albumin and has a 6–8 day half-life. In the research-peptide market, "CJC-1295" is also used as shorthand for CJC-1295 NO DAC (Modified GRF 1-29), the 29-residue core without the albumin-binding extension, which has a half-life of approximately 30 minutes. The two are chemically distinct (differ by approximately 280 Da) and behave differently in the body, but they can co-elute on standard UV-HPLC. Mass spectrometry is the only reliable way to tell a vial labeled "CJC-1295" apart from one labeled "CJC-1295 DAC" apart from one that is actually no-DAC mislabeled as the DAC form.
The largest CJC-1295 DAC study was halted after a participant death, and its remaining participants' results were never published
ConjuChem's multi-centre visceral obesity study of CJC-1295 DAC (NCT00267527, n=192, North and South America) was TERMINATED in July 2006 after a participant in Argentina died of acute myocardial infarction approximately 3 hours after their eleventh dose. The attending physician attributed the death to pre-existing asymptomatic coronary artery disease, but no independent causality adjudication was ever published. ConjuChem halted development entirely and the company dissolved shortly thereafter. The body-composition, metabolic, and safety endpoints from the remaining approximately 191 participants, the largest pool of multi-dose CJC-1295 DAC safety data ever collected, were NEVER reported. This termination is routinely omitted from online content citing the early-phase GH/IGF-1 data as support for the compound; any honest summary of CJC-1295 DAC's research history should include both the Teichman 2006 surrogate-biomarker data AND the study whose endpoints remain permanently unavailable.
For laboratory research use only. Not for human or animal consumption.
Evidence Tier
Animal Only
Mol. Weight
3647.28 Da
Last Reviewed
Apr 22, 2026
Claimed benefits by evidence tier
Column header colour matches the tier
Anecdotal4
- Increases lean body mass
- Reduces body fat / visceral adipose tissue
- Improves sleep quality / increases slow-wave sleep
- Accelerates injury recovery / connective tissue repair
Unsupported2
- Anti-aging / longevity effects
- Cognitive enhancement / neuroprotection
About this peptide
Plain English
The pituitary gland releases growth hormone in pulses, triggered by a natural messenger called GHRH that degrades within minutes. CJC-1295 DAC is a lab-made, re-engineered version of GHRH designed to stay active far longer. Four amino acid swaps make it resistant to the enzymes that normally break it down, and a chemical handle on one end, the Drug Affinity Complex, or DAC, grabs hold of a long-lived blood protein called albumin within minutes of injection, turning the peptide into a slow-release reservoir. Animal and early-phase research indicates it keeps nudging the pituitary to release growth hormone for roughly six to eight days. It was developed in the early 2000s by a Canadian biotech, ConjuChem, as an investigational compound, and early-phase research was halted in 2006 and never resumed. Today it is available only as a research-use-only material, not for human or animal consumption, with no regulatory authorization from any major agency for any indication.
Technical
CJC-1295 DAC is a 30-residue, C-terminally amidated synthetic peptide analog of hGRF(1-29) incorporating four point mutations (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) that confer DPP-IV resistance and reduce methionine oxidation, plus a C-terminal Lys³⁰ bearing an Nε-maleimidopropionyl (MPA) group, the Drug Affinity Complex. The electrophilic maleimide undergoes a Michael addition reaction with the free thiol of Cys-34 on endogenous serum albumin, forming a stable thioether bond. The resulting peptide-albumin conjugate has an extended plasma half-life of approximately 6–8 days (vs ~30 min for the no-DAC form and ~3–5 min for native hGRF(1-29)), because albumin avoids renal filtration and is protected from enzymatic clearance. Pharmacodynamically, CJC-1295 DAC is a GHRH receptor (GHRHR) agonist on anterior pituitary somatotrophs, signaling through Gαs → adenylyl cyclase → cAMP → PKA → CREB to drive GH gene transcription and secretory granule exocytosis. Preserved pulsatile GH release with increased pulse amplitude has been observed in early-phase research; downstream hepatic IGF-1 synthesis follows. Molecular formula C₁₆₅H₂₆₉N₄₇O₄₆; MW 3,647.28 g/mol (free base). The evidence base traces entirely to ConjuChem-sponsored research or the Frohman group; no independent academic replication exists.
Mechanism of action
GHRH receptor (GHRHR) agonism → cAMP/PKA → GH secretion
CJC-1295 DAC binds and activates the pituitary GHRHR, a class B GPCR. Receptor activation couples through Gαs → adenylyl cyclase → cAMP → PKA → CREB phosphorylation, driving GH gene transcription and vesicular GH release from anterior pituitary somatotrophs. The Jetté 2005 rat study established the mechanism with a 4-fold increase in GH AUC over 2 hours versus hGRF(1-29) and plasma detection beyond 72 hours in animal models.
Covalent albumin conjugation → extended plasma half-life
The signature mechanism distinguishing CJC-1295 DAC from all other GHRH analogs. The Nε-maleimidopropionyl group on Lys³⁰ is an electrophilic warhead that reacts with the single free thiol of Cys-34 on endogenous serum albumin via Michael addition, forming a stable thioether bond within approximately 5–15 minutes. The resulting peptide-albumin conjugate has a plasma half-life of approximately 6–8 days, roughly 200 times longer than the no-DAC form (~30 min) and roughly 2,000 times longer than native hGRF(1-29) (~3–5 min), because albumin is both too large for renal filtration and largely shielded from enzymatic clearance. Critical QC corollary: if the maleimide ring hydrolyzes before albumin conjugation (which can occur in aqueous solution), the resulting ring-opened form cannot conjugate and the extended half-life is lost entirely. Standard UV-HPLC does not distinguish intact vs ring-opened maleimide; only high-resolution MS does.
Preservation of pulsatile GH secretion
Unlike exogenous GH replacement (which suppresses endogenous pulsatility) or continuous GHRH infusion (which desensitizes the receptor), CJC-1295 DAC maintains physiological pulsatile GH release while increasing the amplitude of individual pulses. This was observed in early-phase research using deconvolution analysis of frequent GH sampling. Mechanistically important because pulsatile GH patterns are required for many downstream physiological effects (hepatic IGF-1 synthesis, lipolysis, anabolism). CAVEAT: the Ionescu & Frohman 2006 study is the sole source for this specific claim; no independent replication exists; whether preserved pulsatility translates to any meaningful outcome has never been tested in a controlled study.
GH → hepatic IGF-1 axis activation → downstream anabolic/metabolic effects
Sustained GH elevation drives hepatic IGF-1 synthesis via JAK2/STAT5b signaling. IGF-1 promotes protein synthesis via PI3K/AKT/mTOR, increases glucose uptake in muscle, promotes lipolysis in adipose tissue, and has anabolic effects on bone and connective tissue. Early-phase research documented IGF-1 elevation lasting 9–11 days after a single injection, and cumulative elevation above baseline for up to 28 days with multiple doses. Sackmann-Sala 2009 confirmed proteomic serum changes consistent with GH/IGF-1 axis activation in a small animal and in vitro context. Whether these biochemical changes translate into meaningful outcomes in adequately powered preclinical or controlled studies has not been tested.
All four mechanisms above are supported by a narrow and non-independent evidence base: Jetté 2005 was authored entirely by ConjuChem employees; Teichman 2006 was five-of-six ConjuChem-affiliated authors with Frohman (UIC) as the one non-sponsor academic; Ionescu 2006 and Sackmann-Sala 2009 also include Frohman; the ConjuChem development program was halted in 2006 and body-composition results from the Phase II work were never published. There is no independent academic replication of the foundational PK/PD findings. The GHRH-KO mouse work (Norstedt 2006) is often over-cited as if it supported efficacy in GH-sufficient subjects; it does not, because GHRH-KO mice model severe genetic GH deficiency. The rat pharmacology (Jetté 2005) established mechanism and half-life, but rats have different baseline GHRH kinetics and pituitary feedback dynamics, so translation is qualitative, not quantitative. No adequately powered controlled study has assessed any meaningful endpoint (lean mass, fat loss, bone density, recovery, cognition).
Key studies
Independence warning: most research for this peptide originates from a single research group. Replication by independent groups is limited.
Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog (2005)
Jetté L, Léger R, Thibaudeau K, Benquet C, Robitaille M, Pellerin I, Paradis V, van Wyk P, Pham K, Bridon DP · Endocrinology 146(7):3052–3058
- Participants
- Male Sprague-Dawley rats plus cultured rat anterior pituitary cells
- Methodology
- In vitro GRF receptor assay plus in vivo rat pharmacokinetics/pharmacodynamics. Western blot confirmation of albumin conjugation within 15 min of injection.
- Result
- CJC-1295 produced 4× GH AUC versus hGRF(1-29) in rats; plasma half-life extended beyond 72 hours; albumin conjugation confirmed within 15 minutes of SC dosing.
Honest read
Animal model only. All ten authors were affiliated with ConjuChem Inc., the compound's developer. No independent replication of these pharmacokinetic findings in animals. Translation to humans was confirmed qualitatively by Teichman 2006 (half-life + GH elevation) but not quantitatively. Conflict of interest: direct sponsor; the entire paper is, effectively, the ConjuChem development team characterizing their own lead compound.
Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse (2006)
Alba M, Fintini D, Bowers CY, Parlow AF, Salvatori R (ref.) / Norstedt group · American Journal of Physiology, Endocrinology and Metabolism
- Participants
- GHRH-knockout mice (severe GH deficiency model)
- Methodology
- Once-daily SC CJC-1295 WITH-DAC versus controls; growth normalization assessed.
- Result
- CJC-1295 normalized growth and IGF-1 levels in GH-deficient mice.
Honest read
Animal model. GHRH-KO mice represent severe genetic GH deficiency, a condition entirely different from the wellness/anti-aging use case or even subclinical GH decline in aging humans. Evidence of rescue in a deficiency model does not predict meaningful benefit in GH-sufficient adults. Routinely over-cited in pro-CJC-1295 content as if it supported human efficacy in the predominant real-world use case, it does not.
Research timeline
- 2000
ConjuChem Biotechnologies (Montreal) develops the Drug Affinity Complex (DAC) platform for extending peptide half-lives via covalent albumin conjugation in the early 2000s. CJC-1295 (DAC:GRF) identified as the lead candidate from a library of maleimido-hGRF(1-29) bioconjugates.
- 2005
Jetté et al. publish the first preclinical pharmacology paper identifying CJC-1295 as a long-lasting GRF analog in rats. Establishes the DAC albumin-binding mechanism (within 15 min of injection), 4× GH AUC versus hGRF(1-29), and plasma detection beyond 72 hours. All authors ConjuChem-affiliated, direct sponsor COI; no independent replication.
- 2006
Teichman et al. publish early-phase dose-escalation studies in JCEM documenting 5.8–8.1 day half-life, 2–10× GH elevation for at least 6 days, and 1.5–3× IGF-1 elevation for 9–11 days. Five of six authors ConjuChem-affiliated.
- 2006
Ionescu & Frohman publish mechanistic pulsatility study (JCEM) confirming GH pulsatility is preserved despite sustained CJC-1295 WITH-DAC stimulation in early-phase research.
- 2006
GHRH-KO mouse study demonstrates once-daily CJC-1295 normalizes growth in severely GH-deficient animals (Norstedt 2006, Am J Physiol). Animal model of severe genetic deficiency; findings do not generalize to GH-sufficient subjects.
- 2006
July 2006, ConjuChem TERMINATES its multi-centre visceral obesity study (NCT00267527, n=192 across North and South American sites) after a participant in Argentina dies of acute MI approximately 3 hours after their eleventh dose. The attending physician attributes the death to pre-existing asymptomatic coronary artery disease; no formal independent causality adjudication is ever published. Efficacy endpoints from the remaining approximately 191 participants are NEVER reported. ConjuChem halts development entirely and the company ultimately dissolves.
- 2009
Sackmann-Sala et al. publish exploratory serum proteomics in a small cohort: decreased ApoA1 and transthyretin isoforms, increased beta-hemoglobin and C-terminal albumin fragments. Hypothesis-generating only; no control arm for the proteomic analysis; the reduced-ApoA1 signal (potential cardiovascular relevance) is never followed up.
- 2010
Henninge et al. publish forensic LC-MS identification of CJC-1295 in a seized injectable pharmaceutical preparation (Drug Test Anal), first analytical confirmation in a real-world (non-clinical) sample and establishment of doping-control methodology.
- 2013
CJC-1295 becomes central to Australian sports-doping investigations, ASADA and the Cronulla Sharks NRL case; AFL investigation of Stephen Dank. Several players receive suspensions. Establishes the compound's profile as a performance-enhancement substance in the doping-enforcement literature.
- 2019
Equine doping-control LC-HRMS/MS methodology published for CJC-1295 detection in horse plasma, reinforcing that distinguishing DAC from no-DAC forms requires mass spectrometry, not UV-HPLC.
- 2023
FDA places CJC-1295 and CJC-1295 DAC (all salt forms) on Category 2 of the interim 503A bulks list, the "significant safety risks" category.
- 2024
September/October 2024, FDA removes CJC-1295 and CJC-1295 DAC (free base, acetate, and TFA salt forms) from Category 2 following nominator withdrawal and a legal settlement. Removal does NOT add the compound to Category 1; it enters the evaluation queue.
- 2024
December 4, 2024, FDA Pharmacy Compounding Advisory Committee (docket FDA-2024-N-4777) votes AGAINST recommending CJC-1295 and CJC-1295 DAC for inclusion on the 503A Bulks List.
- 2026
February 27, 2026, HHS Secretary Robert F. Kennedy Jr. announces on the Joe Rogan Experience (Episode #2461) an intent to move approximately 14 peptides, reportedly including CJC-1295, from Category 2 restrictions back to Category 1. Not a formal Federal Register action; no immediate regulatory effect.
- 2026
April 15, 2026, FDA publishes 503A Categories Update for April 2026, removing 12 peptide substances from Category 2 effective April 22, 2026. Whether CJC-1295 DAC is among the 12 is NOT CONFIRMED (primary FDA document not directly accessible during this research pass). Multiple secondary sources suggest the April action does NOT include CJC-1295, already removed from Category 2 in September 2024, and that it remains in post-PCAC-"no-vote" limbo.
What we don't know
- Long-term safety. The longest published early-phase research was approximately 49 days; no published data exists on CJC-1295 DAC safety at 3 months or beyond. A larger study was conducted but those results are permanently unavailable.
- Efficacy for any meaningful endpoint. No completed, published controlled study has measured body composition, lean mass, fat mass, bone density, exercise performance, sleep architecture, recovery time, cognitive function, or any other outcome specific to this compound.
- Safety in GH-sufficient subjects. Early-phase research used subjects with normal GH status. The consequences of chronically elevated GH and IGF-1 in this context, particularly carcinogenesis risk, have not been studied.
- Carcinogenesis risk. Elevated IGF-1 has been associated in epidemiological literature with increased risks for colorectal, breast, and prostate cancers. Whether the IGF-1 elevations CJC-1295 DAC produces for extended periods would increase cancer incidence is completely unknown.
- Drug interactions. No published data on interactions with insulin, exogenous GH, glucocorticoids, anti-diabetic medications, or any other drug.
- DAC maleimide hydrolysis in vivo. The maleimide ring can hydrolyze in aqueous solution before albumin conjugation occurs, producing a ring-opened form that cannot conjugate and has no extended half-life. The in vivo proportion of injected CJC-1295 DAC that successfully conjugates to albumin vs degrades to the ring-opened form has not been characterized under clinical injection conditions.
- Pharmacokinetics in non-healthy populations. Low albumin states (liver disease, malnutrition, nephrotic syndrome) would theoretically reduce DAC binding and alter half-life dramatically. No data exists.
- Antibody formation. Whether repeated dosing induces anti-CJC-1295 or anti-CJC-1295-albumin antibodies has not been characterized beyond the reported early-phase study durations.
- Optimal administration interval. The 6–8-day half-life is well established in animal models, but the relationship between administration interval, cumulative IGF-1 load, and any safety or biological outcome is uncharacterized.
- Effects in aging models. Age-related GH decline is a common mechanistic rationale for interest in this compound. No study has been conducted in aged animal models or any other aging context.
- Reproductive and endocrine effects. Chronic GHRH agonism could affect the HPG axis (GH → IGF-1 interacts with sex hormone production), LH/FSH dynamics, and thyroid function. Unstudied.
- Independent replication of any foundational finding. The entire published evidence base traces to ConjuChem-sponsored or Frohman-group research; no independent academic replication of the GH, IGF-1, pulsatility, or proteomic findings exists.
Stability & handling
- Lyophilized shelf life
- Estimated 24 months sealed and protected from moisture/light at −20°C (secondary/compounding guidance; no peer-reviewed stability study specific to CJC-1295 DAC identified).
- Lyophilized storage
- Freeze at −20°C (long-term) or 2–8°C (short-term). Avoid room-temperature long-term storage, thermal degradation and moisture uptake accelerate. Do not open cold vials until equilibrated to room temperature; moisture condensation is a primary degradation pathway.
- Reconstitution diluents
- Bacteriostatic water for injection (0.9% benzyl alcohol in sterile water), standard, Sterile water for injection (single-use only)
- Reconstituted (refrigerated)
- Commonly cited 14–28 days at 2–8°C. CRITICAL CAVEAT: the DAC maleimide ring can hydrolyze slowly in aqueous solution over this window, producing a ring-opened form that no longer binds albumin. Standard UV-HPLC does not detect this silent potency loss.
- Reconstituted (room temp)
- Degradation accelerates sharply above 8°C. Secondary sources report 15–20%/week potency losses at room temperature for reconstituted solution; avoid.
- OK to refreeze
- No
- Light sensitive
- Yes, protect from light
CJC-1295 DAC-specific stability failure modes that matter for what's actually in the vial: (1) MALEIMIDE RING HYDROLYSIS is the single most insidious degradation pathway. The electrophilic maleimide on Lys³⁰ can undergo aqueous hydrolysis to a succinamic-acid-containing ring-opened form that is the same MW + 18 Da and cannot conjugate to albumin, completely eliminating the extended half-life. Standard UV-HPLC typically does NOT distinguish intact vs ring-opened. Only high-resolution mass spectrometry does. A "≥98% purity by HPLC" COA on an aqueous preparation provides no assurance the peptide is still DAC-functional. (2) SALT FORM MISREPRESENTATION, CJC-1295 DAC can be supplied as free base, acetate salt (+~59 Da/molecule), or trifluoroacetate salt (+~114 Da/molecule). Vendors selling by claimed peptide weight while the product is TFA salt systematically underdeliver actual peptide by 3–5%. The FDA's December 2024 PCAC materials explicitly listed all three salt forms as commercially relevant distinct entries. Ion chromatography or NMR confirms counter-ion identity; most consumer-facing COAs do not include this. (3) POSITION-8 DEAMIDATION, the engineered Gln⁸ residue is deamidation-prone; deamidation adds 0.984 Da (undetectable by UV-HPLC; detectable only by high-resolution MS) and may reduce receptor affinity. (4) DAC VS NO-DAC CROSS-CONTAMINATION, the two forms differ by ~280 Da and can co-elute on standard HPLC. Only mass spec can confirm the product sold as "DAC" actually contains the maleimide extension versus the no-DAC core.
Frequently asked questions
What is the difference between CJC-1295 with DAC and CJC-1295 without DAC, and does it matter?
Yes, substantially. These are different molecules. CJC-1295 WITH DAC (this compound) has a half-life of approximately 6–8 days because the DAC modification causes it to covalently bind serum albumin. CJC-1295 WITHOUT DAC (Modified GRF 1-29) is the same 29-residue core without the albumin-binding extension, with a half-life of approximately 30 minutes. The "without DAC" form was developed as a shorter-acting alternative after the DAC version, and the naming convention was borrowed to leverage brand recognition, a decision that created durable market confusion. Mass spectrometry is the only reliable way to confirm which form a vial actually contains.
Was the participant death in the CJC-1295 DAC NCT00267527 study caused by the compound?
The attending physician concluded the most likely cause was pre-existing, asymptomatic coronary artery disease, not the compound. However, no independent adjudication of causality was ever published, because ConjuChem halted development voluntarily and the compound never progressed further. The honest answer is that the death was most likely coincidental, but the data needed to formally confirm this (autopsy findings, full study safety database, independent adjudication) were never made public. It is a genuine unresolved safety signal even if the most plausible interpretation is non-causation, and the efficacy and safety data from the remaining approximately 191 participants was never reported either.
Is CJC-1295 DAC the same as sermorelin or tesamorelin?
No. Sermorelin is hGRF(1-29), the native 29-amino-acid N-terminal fragment of GHRH, with a half-life of approximately 30 minutes. CJC-1295 DAC is derived from sermorelin but incorporates four amino acid substitutions plus a 30th residue bearing the DAC maleimide group, extending the half-life to approximately 7 days. Tesamorelin is a different long-acting GHRH analog, a modified hGRF(1-44) rather than hGRF(1-29/30), that completed a formal development program. The comparison is instructive: tesamorelin demonstrates that GHRH analogs can complete the full development process. CJC-1295 DAC did not complete that process.
What should I look for on a CJC-1295 DAC COA?
Five items, separately reported: (1) MASS-SPEC CONFIRMATION of the DAC modification, intact maleimide on Lys³⁰. Intact and ring-opened forms differ by only 18 Da and can appear nearly identical on standard UV-HPLC; only high-resolution MS reliably distinguishes them, and a product whose DAC has hydrolyzed silently loses the extended half-life. (2) MASS-SPEC CONFIRMATION that the compound is DAC, not no-DAC; the two forms differ by approximately 280 Da and can co-elute on standard HPLC. (3) NET PEPTIDE CONTENT distinct from HPLC chromatographic purity; TFA and acetate counterions plus residual water contribute to stated vial mass. COAs should report peptide content as a percentage of gross weight and identify the salt form (free base vs acetate vs TFA). (4) ENDOTOXIN (LAL) testing per USP <85>. (5) CHIRAL confirmation of D-Ala at position 2; reverse-phase HPLC does NOT detect D to L racemization, which would restore DPP-IV susceptibility. A COA showing only "at least 98% purity by HPLC" without these five items has not characterized what is actually in the vial.
Last researched: Apr 22, 2026
Get the ClearBatch Report
Bi-weekly: new peptide reference profiles, third-party-tested batches, and sourcing updates.
Two emails a month. Unsubscribe anytime.