What the studies dosed, in the species and at the intervals they reported.

What the studies dosed, plainly put

The only published human dose data for CJC-1295 come from the 2006 Teichman Phase 1 trial. Participants received single subcutaneous injections at four dose levels — 30, 60, 125, and 250 micrograms per kilogram of body weight — or repeated weekly and biweekly doses in the middle of that range. Those are research-context figures: they describe what was administered to healthy adults in a controlled trial, not a protocol for any purpose outside that study.

For the short-acting no-DAC form (Modified GRF 1-29), there are no published human dose-ranging studies at all — the figures circulating online are not derived from controlled trials.

This page summarizes what the animal and human studies actually dosed, explains why the DAC form and the no-DAC form behave so differently, and names, without filling in, the many questions the published record leaves open.

The published human cohorts

The only published human dosing dataset for CJC-1295 is Teichman 2006 ^[2]. Healthy adult participants received single subcutaneous injections at four dose levels: 30, 60, 125, and 250 μg/kg ^[2]. Multi-dose cohorts received either weekly or biweekly dosing at 60 to 125 μg/kg for 28 to 49 days ^[2].

In the single-dose cohorts, mean plasma GH rose two- to ten-fold above baseline and remained elevated for at least six days; mean IGF-1 rose 1.5- to three-fold for nine to eleven days ^[2]. The multi-dose cohorts sustained IGF-1 elevation through twenty-eight days ^[2]. The Phase 2 trial (NCT00267527) used weekly subcutaneous dosing in 192 participants with HIV-associated visceral adiposity; specific μg/kg figures were not fully disclosed in the peer-reviewed literature before the trial was terminated ^[7].

That is the human dose record. There is no Phase 3 schedule, no FDA-labelled regimen, and no long-term efficacy or safety dataset.

Animal-model dosing

Alba and colleagues dosed GHRH-knockout mice with 2 μg of CJC-1295 per injection — roughly 80 μg/kg in a 25-gram animal — at 24-, 48-, or 72-hour intervals for five weeks ^[5]. The 24-hour schedule normalized linear growth and body weight; the 48- and 72-hour schedules produced partial restoration ^[5].

Jetté and colleagues' rat work used single subcutaneous bolus dosing across a low-microgram-per-kilogram range, with the four-fold GH AUC increase and >72-hour bioactivity persistence already described in the Research section ^[1]. The rodent record is consistent with the human PK profile: the multi-day plasma half-life supports multi-day pharmacodynamic effect.

Across species, the subcutaneous route dominates the published work. Intraperitoneal administration appears in some rodent mechanistic studies; intravenous administration is used primarily in early comparator GHRH work ^[9][13].

Half-life — the central pharmacokinetic fact

The plasma half-life of CJC-1295 with DAC in healthy adults is 5.8 to 8.1 days across single-dose cohorts (30 to 250 μg/kg) ^[3]. The half-life is attributable to covalent bioconjugation with serum albumin via the C-terminal maleimide, which shields the peptide from peptidase degradation and renal filtration ^[1][3].

The non-DAC variant — modified GRF(1-29), sometimes labelled Mod GRF 1-29 — has a plasma half-life of approximately 30 minutes in vivo, compared to roughly 7 minutes for native GHRH ^[8]. The four amino-acid substitutions in the backbone (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) account for the four-fold extension over native GHRH; the maleimide-albumin tether adds the multi-day extension on top of that baseline ^[8].

The DAC variant's pharmacodynamic effects on GH and IGF-1 persist well beyond the parent peptide's measurable plasma concentration — IGF-1 elevation extends to nine to eleven days after a single dose, and to twenty-eight days with weekly or biweekly multi-dosing ^[2].

Stability and handling notes

DAC variant bioactivity depends on the Michael addition reaction between the peptide's maleimide and the free thiol of albumin Cys34, a reaction that proceeds in vivo after subcutaneous administration. The non-DAC variant degrades faster in solution and in vivo because it lacks the albumin tether.

Reconstituted research peptide is typically stored refrigerated for short-term use and frozen for longer storage in published handling protocols; freeze-thaw cycles and elevated temperatures degrade activity. None of these handling notes describe a human-use protocol — they describe research-grade peptide handling in bench settings.

The pairing rationale, in research context

Bowers and colleagues' foundational work showed combined GHRH + GHRP-6 administration produces a GH response several-fold larger than either alone in healthy adults ^[9]. This is the mechanistic basis for pairing GHRH analogs with ghrelin-receptor agonists in research contexts. The CJC-1295 + ipamorelin combination is the most-discussed pairing in research-chemical and compounding-literature sources ^[9], with GHRP-2 and GHRP-6 as earlier-generation alternatives carrying broader off-target effects (cortisol and prolactin elevation) than ipamorelin.

Tesamorelin, an FDA-approved GHRH analog, is not paired with CJC-1295 in the research literature — both compounds target the same GHRHR, so co-administration is mechanistically redundant ^[15].

What the published literature does not tell you

There is no published human dose for a non-research indication. There is no labelled regimen, no titration schedule, no maintenance dose, no published safety dataset beyond the Phase 1 cohorts and the terminated Phase 2 program ^[2][7]. Long-term effects of sustained supraphysiological GH and IGF-1 elevation — insulin resistance, edema, joint pain, and theoretical neoplasia risk — are recognized class concerns in the endocrinology literature but are not characterized for CJC-1295 specifically.

FDA-cited safety concerns at the October 2024 PCAC review included immunogenicity, impurity-testing challenges, and adverse-event signals of increased heart rate and systemic vasodilatory reactions ^[14]. The committee's decision not to recommend 503A inclusion turned in part on the absence of any sponsor-led clinical development since 2006 ^[17]. The December 2024 PCAC follow-up consolidated public comment and adverse-event review for the GH-secretagogue class and reached the same conclusion ^[17].

What does exist outside the peer-reviewed file is a body of self-reported use documented in the netnographic literature ^[11] and adverse-event signals captured through compounding-pharmacy reporting channels. Neither is a clinical-trial dataset. Both informed the 2024 FDA review without filling the evidentiary gap the committee identified.

How the dosing record compares to a fully developed GHRH analog

Tesamorelin, the FDA-approved GHRH analog in the same chemical class, provides a useful contrast. Tesamorelin is dosed at 2 mg subcutaneously daily and produces a 15-20% reduction in visceral adipose tissue over twenty-six weeks in HIV-associated lipodystrophy ^[15]. That dose, that frequency, that duration, and that effect size are all published, peer-reviewed, and replicated. The trial is registered, the label is public, the safety profile is characterized.

CJC-1295's Phase 2 program targeted the same indication and was halted after eleven weekly doses in one cohort ^[7]. The two compounds share a mechanism and a class but not a clinical-development arc. Reading the tesamorelin literature alongside the CJC-1295 file is the cleanest way to see what a fully developed GHRH analog looks like — and what shape CJC-1295's development might have taken had it continued past 2006.