CJC-1295 with DAC

Your 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 that stays active far longer. Four amino acid swaps make it resistant to the enzymes that normally chew it up, 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. The result keeps nudging the pituitary to release growth hormone for roughly six to eight days after a single injection, which is why protocols usually dose it once or twice a week rather than daily. It was developed in the early 2000s by a Canadian biotech, ConjuChem, as an investigational drug for HIV-related wasting and growth hormone deficiency, and reached Phase II trials before development was halted in 2006 and never resumed. Today it exists primarily in the gray market of "research peptides," with no approval from any major regulator for any indication.

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. Within approximately 5–15 minutes of subcutaneous injection, the electrophilic maleimide undergoes a Michael addition reaction with the free thiol of Cys-34 on endogenous human 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 documented in one mechanistic human study; downstream hepatic IGF-1 synthesis follows. Molecular formula C₁₆₅H₂₆₉N₄₇O₄₆; MW 3,647.28 g/mol (free base). Critically, all published human PK/PD data for this compound trace to ConjuChem-sponsored trials or the Frohman group — no independent academic replication exists.

• Injection-site reactions (induration, erythema, pruritus; resolved within 48–72 hours in Teichman 2006)
• Transient flushing shortly post-injection
• Headache (mild, early dosing period)
• Fatigue post-injection (mild, early dosing period)
• Water retention / peripheral edema at longer durations — mechanistically consistent with GH-induced sodium and water retention
• Myocardial infarction — one death in the terminated NCT00267527 Phase II trial (n=192; event at ~3 hours post-dose #11; attributed by investigator to pre-existing CAD; causality formally unresolved)
• IMPORTANT: All reported human safety data comes from short-term (≤49 day) published studies or from the unpublished 12-week Phase II trial. Chronic use beyond two months has no published safety characterization.

• Active malignancy or history of hormone-sensitive cancers (IGF-1 proliferation concern; theoretical, mechanism-based)
• Proliferative retinopathy or uncontrolled diabetes (GH counter-regulatory effects; theoretical)
• Acromegaly, gigantism, or active pituitary tumors
• Severe edema or decompensated heart failure
• Pregnancy and breastfeeding (no safety data in any species)
• Pediatric patients with open growth plates (unpredictable GH-axis effects)
• Known hypersensitivity to GHRH analogs or any component of a given compounded preparation

• No formal drug-interaction studies in humans have been conducted.
• Insulin and oral antidiabetics — GH has counter-insulin effects; chronic GH elevation may antagonize glucose-lowering action
• Exogenous GH — additive effects; co-administration not studied
• Glucocorticoids — can attenuate GH response at the pituitary level
• Thyroid hormones — GH/IGF-1 metabolism intersects with thyroid function
• Somatostatin analogs (octreotide, lanreotide) — pharmacological antagonists; combination expected to blunt or abolish GH response

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; its half-life is approximately 30 minutes. They require completely different injection schedules. 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. If you cannot confirm by COA + mass spectrometry which form you have, you cannot know what you're actually injecting.

The attending physician concluded the most likely cause was pre-existing, asymptomatic coronary artery disease — not the drug. However, no independent regulatory adjudication of causality was ever published, because ConjuChem halted the trial voluntarily and the compound was never approved. The honest answer is that the death was most likely coincidental, but the data needed to formally confirm this (autopsy findings, full trial 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 ~191 participants was never reported either.

As of April 22, 2026: almost certainly not under standard 503A. The FDA Pharmacy Compounding Advisory Committee voted against CJC-1295 and CJC-1295 DAC inclusion on the 503A Bulks List on December 4, 2024. HHS Secretary Kennedy announced in February 2026 an intent to restore many peptides to Category 1, and the April 15, 2026 FDA update removed 12 peptides from Category 2, but CJC-1295 DAC's inclusion in that April action is NOT confirmed from primary sources accessible to this research. Until a formal Federal Register notice explicitly adds CJC-1295 DAC to the 503A Bulks List, compounding is not authorized. Anyone claiming otherwise should be asked to produce the specific FDA document.

No. Sermorelin is hGRF(1-29) — the native 29-amino-acid N-terminal fragment of GHRH — with a half-life of ~30 min. 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 ~7 days. Sermorelin has FDA approval history (approved as Geref Diagnostic for GH deficiency diagnosis, then withdrawn from the US market for commercial reasons). Tesamorelin (Egrifta) is a different long-acting GHRH analog — a modified hGRF(1-44) rather than hGRF(1-29/30) — that completed Phase III trials and IS FDA-approved (2010) for HIV-associated lipodystrophy, the same indication ConjuChem was targeting before halting CJC-1295 DAC development. The comparison is instructive: tesamorelin demonstrates that GHRH analogs can achieve regulatory approval with the right development program. CJC-1295 DAC did not complete that program.

It does raise IGF-1 — this is the most robustly demonstrated human finding, with 1.5–3× elevations for 9–11 days after a single injection (Teichman 2006). Whether sustained IGF-1 elevation at those levels over months or years is beneficial, neutral, or harmful in healthy adults is genuinely unknown. IGF-1 is anabolic and lipolytic, which is the claimed benefit, but it is also a mitogen — it promotes cell division — and epidemiological data associates elevated serum IGF-1 with increased incidence of colorectal, breast, and prostate cancers. The magnitude of risk and the direction of causation are debated in the primary literature. The wellness narrative frames elevated IGF-1 as straightforwardly beneficial; the honest answer is "possibly at physiological levels for short durations, but long-term safety at CJC-1295 DAC's elevations has not been studied."

Ipamorelin is a GHRP — it acts on the ghrelin receptor (GHS-R1a) rather than the GHRH receptor. The two receptors use different signaling pathways and are synergistic when co-activated: GHRH receptor activation increases GH pulse amplitude while ghrelin receptor activation increases the number of somatotrophs releasing GH per pulse. The rationale is mechanistically sensible. However, no published human RCT has tested the CJC-1295 DAC + ipamorelin combination for any clinical endpoint. The combination is further complicated by the half-life mismatch: once-weekly CJC-1295 DAC plus multiple-daily ipamorelin creates an asymmetric dosing pattern that has never been studied pharmacologically in humans.

Yes, if the test panel covers GHRH analogs. CJC-1295 is explicitly prohibited under WADA S2 and has LC-HRMS/MS detection methodology in both human and equine plasma. Because of the ~6–8-day half-life, the detection window for CJC-1295 DAC is substantially longer than for the no-DAC form — potentially multiple days post-injection. Athletes subject to WADA testing should treat CJC-1295 DAC as prohibited at all times.

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 ~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). The December 2024 FDA PCAC materials treated all six salt/form entries as distinct commercial entities for good reason. (4) ENDOTOXIN (LAL) testing per USP <85> because the product is injectable. (5) CHIRAL confirmation of D-Ala at position 2 — reverse-phase HPLC does NOT detect D→L racemization, which would restore DPP-IV susceptibility. A COA showing only "≥98% purity by HPLC" without these five items has not characterized what is actually in the vial.

Approximately 5.8–8.1 days in healthy adults, directly measured in Teichman 2006. This is derived from covalent conjugation to serum albumin, which takes ~5–15 minutes after SC injection and depends on the maleimide ring being intact at the moment of injection. If the maleimide has hydrolyzed in solution before injection (ring-opened form), or if the individual has a low-albumin state (liver disease, malnutrition, nephrotic syndrome), the effective half-life can be much shorter — potentially approaching no-DAC kinetics (~30 min). Standard UV-HPLC purity testing cannot detect ring-opened product; a product that looks ≥98% pure can still be pharmacokinetically broken.

No completed, published RCT has measured body composition as an outcome. Claims that CJC-1295 DAC "builds lean mass" or "burns fat" are extrapolated from: (a) the established pharmacodynamics of GH and IGF-1; and (b) the incomplete Phase II trial in HIV lipodystrophy patients (NCT00267527, n=192), whose efficacy endpoints were never published. The mechanism is biologically plausible, but the specific clinical question has not been answered by evidence for this compound. Tesamorelin — a different FDA-approved GHRH analog — did complete Phase III trials in the same HIV lipodystrophy indication and does demonstrate visceral fat reduction. That's not evidence for CJC-1295 DAC; it's evidence that the class mechanism can work in a specific population when the development program is completed.