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What doses appear in the published record?
A literal reading of what investigators administered in animal and Phase 1 human studies. Not a prescribing guide.
The short version
There is no FDA-approved dose for CJC-1295. No regulatory agency has reviewed a label, and no Phase 2 or Phase 3 efficacy trial has established a dose-response relationship for any clinical benefit [14].
This page reports what was actually administered in published studies: four single-injection dose cohorts (30, 60, 125, and 250 micrograms per kilogram, subcutaneous) in the Teichman 2006 Phase 1 trial [2], and 2 micrograms per dose in GHRH-knockout mice [4]. These are bibliographic records of what investigators used under IRB protocols — not prescribing guidance and not a recommendation for any exposure.
The distinction between the long-acting DAC form (half-life 5.8–8.1 days) and the short-acting no-DAC backbone (half-life roughly 30 minutes) matters enormously here — they are pharmacokinetically very different molecules despite sharing a name [3][9].
A note on what this page is
There is no FDA-approved dosing regimen for CJC-1295. No agency has ever reviewed a label for the compound. No clinical-trial sponsor has submitted Phase 2 or Phase 3 efficacy data to support a dose-response statement [14].
This page reports what was administered in the published research — to rats, to GHRH-knockout mice, and to Phase 1 healthy adult volunteers under an Institutional Review Board protocol. The intent is bibliographic. Reading what doses were studied is not the same as recommending them, and this site does not recommend anything to anyone.
This is an independent editorial reading of the published research record.
Phase 1 human dose cohorts (Teichman 2006)
The only published Phase 1 trial used four single-injection dose cohorts: 30, 60, 125, and 250 μg/kg subcutaneous [2]. Each cohort received a single subcutaneous administration; pharmacokinetic and pharmacodynamic measurements were collected over the following several days.
A companion multi-dose substudy administered weekly or biweekly injections at the same dose levels for 28 to 49 days, with IGF-1 elevation sustained out to 28 days at higher cohorts [2]. The volunteers were healthy adults aged 21 to 61, and the trial was reported in JCEM in 2006. Sample sizes per cohort were small — eleven or more participants — consistent with a Phase 1 PK/PD design.
No subsequent Phase 1 paper has been published on a different dose range. The Teichman 2006 grid (30/60/125/250 μg/kg, single SC) is the entirety of the peer-reviewed human dose record.
Animal model dosing
The GHRH-knockout mouse study (Alba et al. 2006) used 2 μg per injection, administered subcutaneously at 24-, 48-, or 72-hour intervals for five weeks [4]. In a 25 g mouse, that works out to roughly 80 μg/kg per dose. Once-daily dosing normalized linear growth, body weight, and lean body composition; longer dosing intervals produced only partial restoration.
The Jetté 2005 rat work used subcutaneous bolus dose-ranging at low μg/kg levels, with the primary readouts being plasma GH area-under-curve over two hours and circulating bioactivity at 72 hours [1].
These animal doses are not directly translatable to humans by simple body-weight scaling — interspecies allometric differences in receptor density, albumin concentration, and clearance kinetics complicate the conversion — and they are not presented here as a guide for any human exposure.
Half-life and what it implies for hypothetical scheduling
In healthy adults, the mean plasma half-life of CJC-1295 (DAC variant) was 5.8 to 8.1 days across the Teichman 2006 dose cohorts [3]. That multi-day persistence is the entire reason the DAC modification exists — it shields the peptide from peptidase degradation and renal clearance long enough to span the circadian cycle.
The un-tethered backbone — modified GRF(1-29), often mis-marketed as "CJC-1295 without DAC" — has a plasma half-life of approximately 30 minutes, compared with about seven minutes for native GHRH [9]. The four amino-acid substitutions account for the four-fold extension over native peptide; the DAC modification accounts for the additional roughly 300-fold extension over the substituted backbone. Calling both molecules "CJC-1295" obscures a pharmacologically enormous difference.
The Phase 2 trial that was halted in 2006 used a weekly subcutaneous regimen [8]. Whether the multi-day half-life makes once-weekly dosing pharmacologically reasonable on paper is a separate question from whether any pathway exists to obtain a clinical-grade product.
Route, stability, and formulation considerations
All published human work used the subcutaneous route [2][3]. Rodent mechanistic studies have also used intraperitoneal and intravenous routes [1]. Subcutaneous administration is the only route relevant to any hypothetical human use scenario.
The DAC variant's bioactivity depends on covalent attachment to the free thiol of albumin Cys34 — a Michael-addition reaction between the peptide's terminal maleimide and albumin's single reactive cysteine. Reconstituted peptide is therefore sensitive to oxidation, to freeze-thaw cycling, and to anything that disrupts the albumin-binding chemistry. Research storage protocols typically call for refrigeration for short-term use and freezer storage for longer terms, with minimization of freeze-thaw cycles. Any hypothetical regulated prescription product would face the same constraints, likely requiring either a cold-chain distribution model or a lyophilized formulation reconstituted at point of care.
These constraints are part of why an approvable formulation has not materialized: the molecule is workable in a research setting but presents practical formulation challenges at commercial scale. The closest FDA-approved comparator — tesamorelin, a different GHRH analog — is supplied as a lyophilized powder for daily subcutaneous reconstitution at a 2 mg dose [19]. That comparator is informative about what a regulated GHRH-analog prescription product looks like, and what CJC-1295 is not.
Why "research dose" is not the same as "prescribing dose"
The doses summarized above come from two contexts. The animal doses are mechanistic — they answer a question about whether the molecule activates its target receptor and produces a downstream readout. The Phase 1 human doses are pharmacokinetic — they answer a question about how the molecule behaves in healthy adult plasma over a few days. Neither category is a prescribing dose in the sense a clinician would use the term.
A prescribing dose comes from Phase 2 and Phase 3 efficacy trials, where investigators identify the lowest dose that produces the labeled clinical benefit at an acceptable safety profile, and where a regulatory agency reviews that dose-response evidence before authorizing a label. No such trial exists for CJC-1295. The Phase 2 trial that would have started to generate that evidence (NCT00267527) was halted in October 2006 [8], and no subsequent sponsor has reopened the question.
What the published record supports, then, is a description of what the molecule does at the doses that were administered. It does not support a recommendation about what dose anyone should take, because the trial structure required to ground such a recommendation has not been completed.