# CJC-1295 / Dosage — Research-context only, never a recommendation

> What CJC-1295 doses were actually administered in published preclinical and Phase 1/2 research, framed strictly as research-context. CJC-1295 is not approved for human use; this page does not provide dosing for any non-research use.

Research-context only. CJC-1295 is not approved for human use, and the doses below are the doses that were administered in named studies — not a recommendation for any reader.

## 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.

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An editorial summary of peer-reviewed findings — not a clinical recommendation, not a vendor, not a node in any supply graph.
