CJC-1295

DAC vs. Without DAC — A Key Distinction

CJC-1295 exists in two meaningful forms, and confusing them is common:

• CJC-1295 DAC: Contains a Drug Affinity Complex that binds to serum albumin, dramatically extending the half-life to 6–8 days. Results in a sustained elevation of GH rather than a discrete pulse.
• CJC-1295 without DAC (Mod GRF 1-29): Half-life of ~30 minutes. Used just before sleep or training to create a discrete, pulsatile GH release — more closely mimicking natural physiology.

Most performance-focused community protocols prefer Mod GRF 1-29 for this reason.

The Standard Stack: CJC-1295 + Ipamorelin

CJC-1295 is a GHRH analog — it tells the pituitary to release GH. Ipamorelin is a GHRP (growth hormone releasing peptide) — it amplifies that signal. Using both together creates a synergistic effect on GH output that is greater than either alone.

Typical community protocol:

• 100–200 mcg CJC-1295 (Mod GRF) + 100–200 mcg Ipamorelin
• Injected subcutaneously 30 minutes before sleep
• 5 days on / 2 days off, or continuous for 8–16 weeks

What the Human Data Actually Shows

The human evidence for CJC-1295 is thin and rests largely on a single early study. In Teichman et al. (JCEM, 2006) — two randomized, placebo-controlled single-dose trials in healthy adults using the DAC form — a single subcutaneous injection produced a dose-dependent 2–10× rise in GH sustained for 6+ days and a 1.5–3× rise in IGF-1 lasting 9–11 days, with an estimated half-life of 5.8–8.1 days. Importantly, the natural pulsatile pattern of GH release was preserved, and there was no rise in prolactin, ACTH, or cortisol.

Beyond this PK/PD study, there are no large, long-term efficacy or safety trials of CJC-1295. Claims about body composition, recovery, anti-aging, or performance are extrapolated from GH physiology — not demonstrated in controlled human outcome trials.

Safety Note: The ConjuChem Trial

In July 2006, ConjuChem halted a Phase II trial of CJC-1295 (DAC form, in HIV-associated lipodystrophy) after a participant died. It is important to be precise here: causality was never established. The trial physician's leading hypothesis was pre-existing asymptomatic coronary artery disease — i.e., likely unrelated to the drug — and the specific circumstances were reported only anecdotally in contemporaneous news coverage, never in a peer-reviewed publication. ConjuChem subsequently discontinued development. This is worth knowing, but it should not be overstated as a proven drug-caused death.

Regulatory Status

CJC-1295 is not FDA-approved for any indication, development was discontinued after 2006, and it is prohibited in sport (WADA category S2, peptide hormones / GH secretagogues). Any current material is research-use-only and not quality-controlled for human use.