What was administered in the published trials.

The context before the numbers

CJC-1295 is not approved for human use by any regulator. The doses on this page are the doses that were administered to research subjects in specific, named published studies — not protocols for any reader.

The key pharmacokinetic fact is that the long-acting DAC form stays active for days rather than minutes. The Phase 1 trials in healthy adults used single subcutaneous doses between 30 and 250 micrograms per kilogram ^[2]; multiple doses were given weekly at 60 micrograms per kilogram for up to seven weeks ^[2]. A pulsatility substudy used single doses of 60 or 90 micrograms per kilogram ^[3]. Each of these numbers belongs to a named study and a named population — healthy adult volunteers in controlled conditions. They are not translated here into any individual recommendation.

The 'no-DAC' form (Modified GRF 1-29) clears in roughly thirty minutes and is pharmacologically very different, even though it shares the same four amino-acid substitutions ^[1]. Marketing materials often conflate the two; the published literature does not.

How to read this page

This page reports the doses, routes, and intervals that were administered to research subjects in published preclinical and clinical studies on CJC-1295. The compound is not approved for human use by any regulator. Nothing on this page constitutes a recommendation, a protocol, or a dosing instruction for any reader.

Doses are reported in the units used by the original investigators (microgram per kilogram for human pharmacokinetic work, microgram per animal for the mouse-rescue study, nanomole per kilogram for the rat discovery study). Routes are reported as administered. Intervals reflect the protocol of each study. Where a study halted early, that is noted in the entry.

Preclinical research administration

Rat (Jetté et al., 2005). The original characterization paper administered single subcutaneous doses to male Sprague-Dawley rats, including 100 nanomole per kilogram. The hGRF(1-29)-albumin bioconjugate produced a four-fold increase in growth-hormone area-under-the-curve over two hours versus unmodified hGRF(1-29), with detectable plasma drug beyond 72 hours ^[1]. This was the experiment that established CJC-1295 as a long-acting GRF analog rather than a brief pulse.

Mouse (Alba et al., 2006). GHRH-knockout mice received subcutaneous CJC-1295 at two microgram per animal at three different intervals — every 24 hours, every 48 hours, and every 72 hours — for five weeks ^[4]. The once-daily arm produced full normalization of body weight, body length, femur length, tibia length, and pituitary GH messenger RNA. The 48-hour and 72-hour arms produced partial normalization. Somatotroph hyperplasia (increased pituitary GH mRNA content) was observed across all dosed arms ^[4].

Cross-species mechanistic comparison (Cunha and Mayo, 2002). In vitro work in HEK293 cells transfected with both GHRH-R and GHS-R1a, and in vivo rat and human work referenced in the same paper, demonstrated that matched-dose co-administration of a GHRH analog with a growth-hormone-releasing peptide (GHRP, GHS-R1a agonist) produces six- to tenfold greater GH release than either single agent — the mechanistic basis for the widely studied CJC-1295 plus ipamorelin research pairing ^[13].

Human research administration

Phase 1 single ascending dose (Teichman et al., 2006). Healthy adult volunteers received single subcutaneous CJC-1295 doses of 30, 60, 125, or 250 microgram per kilogram ^[2]. Mean plasma GH rose two- to tenfold and remained elevated for six or more days. IGF-1 rose 1.5- to threefold and remained elevated for nine to eleven days. Estimated plasma half-life: 5.8 to 8.1 days ^[2].

Phase 1 multiple dose (Teichman et al., 2006). Healthy adults received subcutaneous CJC-1295 at 60 microgram per kilogram weekly for 28 to 49 days ^[2]. Cumulative IGF-1 elevation lasted approximately 28 days. Injection-site reactions were the most frequently reported adverse event. No serious drug-related adverse events were reported at doses up to and including 60 microgram per kilogram ^{[2] [14]}.

Pulsatility substudy (Ionescu and Frohman, 2006). Healthy men aged 20 to 40 received a single subcutaneous CJC-1295 dose of 60 or 90 microgram per kilogram, followed by twelve-hour overnight GH sampling one week later ^[3]. GH pulse frequency and amplitude were preserved; trough GH rose 7.5-fold, total GH secretion rose 46 percent, and IGF-1 measured the following morning was 45 percent higher than baseline ^[3].

Phase 2 in HIV-lipodystrophy (NCT00267527). 192 HIV-positive adults with visceral lipodystrophy were randomized to once-weekly subcutaneous CJC-1295 in escalating low-dose (60 / 90 / 120 microgram per kilogram) or high-dose (60 / 120 / 240 microgram per kilogram) cohorts, or placebo, for twelve weeks ^[11]. The trial was halted after a participant cardiac death two hours after the eleventh weekly dose; the event was adjudicated as drug-unrelated. Body-composition endpoints were never published in peer-reviewed literature ^[11].

Half-life — the dose-frequency context

The pharmacokinetic feature that governs CJC-1295's dose intervals is its plasma half-life. In healthy humans, CJC-1295 with DAC has an estimated plasma half-life of 5.8 to 8.1 days ^[2]. Sermorelin — the unmodified parent peptide hGRF(1-29) — has a plasma half-life of approximately 11 to 12 minutes. Modified GRF(1-29) (the same tetra-substituted backbone as CJC-1295 but without the DAC maleimide group, sometimes sold under the gray-market name 'CJC-1295 no DAC') has a plasma half-life of approximately 30 minutes. Tesamorelin — a different acetyl-protected GHRH analog — clears in approximately 26 to 38 minutes ^[16].

The practical implication of a multi-day half-life is that a single dose commits the subject to days of GH/IGF-1 elevation. There is no rapid clearance and no easy way to stop the exposure once initiated. The Alba mouse data suggest a daily-equivalent biological window of activity in spite of the multi-day plasma half-life — the once-daily arm outperformed the every-48-hour and every-72-hour arms — but the human trials administered weekly intervals and reported sustained pharmacodynamic effect across the week ^{[2] [4]}.

Stability and compound integrity in research

The four amino-acid substitutions in the CJC-1295 backbone (D-Ala-2, Gln-8, Ala-15, Leu-27) confer resistance to dipeptidyl peptidase-4 cleavage, asparagine rearrangement, and methionine oxidation, respectively — they protect the peptide against its three most common in-solution failure modes ^[1]. The maleimide group on Lys30 is reactive toward thiols and progressively quenched in solution; once conjugated to albumin Cys34 in vivo, the resulting drug-albumin conjugate is highly stable in circulation ^[1].

A practical research-laboratory note from the seized-product literature: Henninge 2010 identified the contents of an unknown pharmaceutical preparation, seized by Norwegian authorities in 2009, as CJC-1295 ^[10]. The forensic identification confirmed both that CJC-1295 was present in gray-market distribution channels by that date and that the analytical methods to identify CJC-1295 by mass spectrometry were operational at the time. Many products sold under the name 'CJC-1295' are actually modified GRF(1-29) without DAC — the maleimide group is reactive and gray-market manufacturing may not preserve it. This is the kind of distinction the published analytical literature can confirm but the marketing language frequently elides ^[10].

Routes studied

Subcutaneous administration is the route used in every published Phase 1 and Phase 2 human trial and in every published rodent study on CJC-1295 ^{[1] [2] [3] [4] [11]}. Single-dose pharmacokinetic work in rats also includes intravenous administration as a comparator. No oral, intranasal, transdermal, or other route has been characterized in the published literature for this compound.