# CJC-1295 dosing in the research literature — what doses were actually studied > Doses, routes, half-lives, and study durations reported in the published CJC-1295 literature. Research-context only — not a dosing recommendation. CJC-1295 is not FDA approved for any human indication. Every dose on this page is reported because a published study used it. None of it is a recommendation for any human. CJC-1295 is not FDA approved. Routine 503A compounding access was closed in 2024. ## A note before you read the numbers Every dose number on the dosage page comes from a published study. None of it is a recommendation for any human use. CJC-1295 is not FDA approved; it has no approved human dose. The clinical development program that would have established therapeutic dosing was terminated in 2006 [10]. The published human doses are from the Teichman 2006 Phase 1 study: 30, 60, 125, and 250 micrograms per kilogram, given subcutaneously to healthy adult volunteers as single injections or weekly and biweekly multi-dose regimens [2]. The mouse rescue study used 2 micrograms per injection [5]. The equine work used research doses confirmed by LC-MS/MS blood sampling [12]. The page also covers the DAC versus no-DAC half-life distinction in detail, because the factor-of-two-hundred difference in plasma half-life is the single most important pharmacokinetic fact for anyone trying to interpret dosing-interval discussion — and the popular literature gets it wrong most of the time. And it covers the CJC-1295 plus ipamorelin pairing: the two-receptor synergy rationale and what the existing evidence actually supports. ## How to read this page Dose numbers cited below are pulled directly from the published literature — Teichman 2006 for the Phase 1 human PK cohorts, Alba 2006 for the GHRH-knockout mouse rescue, Jetté 2005 for the rat PK/PD work, and the Timms 2019 equine studies. Every quantitative claim cites a study. None of this is framed as guidance for any human use. The page is organized by study population rather than by route or interval, because that is how the record is actually shaped — a small set of well-defined experiments rather than a continuous dose-finding tradition. There is no contemporary dose-titration framework for CJC-1295 because no Phase 3 program ever ran. ## Human Phase 1 PK doses — Teichman 2006 The Teichman 2006 Phase 1 study in *Journal of Clinical Endocrinology and Metabolism* used four single-dose cohorts of healthy adult volunteers at 30, 60, 125, and 250 μg/kg administered subcutaneously [2]. Across those cohorts, mean plasma GH increased two- to ten-fold above baseline and stayed elevated for at least six days [2]. IGF-1 increased 1.5- to three-fold and remained elevated for nine to eleven days [2]. Multi-dose cohorts dosed weekly or biweekly for 28 to 49 days maintained IGF-1 elevation for up to twenty-eight days [2]. The estimated mean plasma half-life across those dose cohorts was 5.8 to 8.1 days — the headline pharmacokinetic finding [3]. This is the entire published human dose-finding record. Healthy adults, single subcutaneous injection or weekly/biweekly multi-dose, four dose levels, small cohorts. Nothing in the literature establishes a dose-response curve for any clinical endpoint in any patient population, because the Phase 2 trial that would have done that work was terminated [10]. The later Phase 2 HIV-lipodystrophy program (NCT00267527) used weekly subcutaneous injections at doses not fully disclosed in the public ClinicalTrials.gov record prior to its 2006 termination [10]. No primary efficacy data ever appeared in peer-reviewed publication. ## Half-life as a dosing-interval determinant The 5.8 to 8.1 day plasma half-life of CJC-1295 DAC [3] is the single most important pharmacokinetic fact for understanding the dosing intervals used in the literature. Five elimination half-lives correspond to roughly 97% washout; for a half-life of 7 days that is approximately five weeks. A weekly dosing interval, as used in the Teichman multi-dose cohort and the terminated Phase 2 trial, therefore produces meaningful accumulation across the first several doses [2][10]. The non-DAC modified GRF(1-29) variant — also marketed as *CJC-1295 without DAC* or *Mod GRF 1-29* — has a plasma half-life of approximately 30 minutes [6]. The implications for dosing interval are completely different. A 30-minute half-life and a 7-day half-life do not belong in the same dosing framework, and the persistent confusion between the two forms in marketing copy is the most consequential factual error in the popular CJC-1295 literature. ## Animal study doses Alba 2006 administered CJC-1295 to GHRH-knockout mice at 2 μg per injection at 24, 48, or 72 hour intervals for five weeks [5]. In a 25 g mouse that is approximately 80 μg/kg per injection. Once-daily dosing fully normalized linear growth and body weight; 48- and 72-hour intervals produced partial restoration [5]. The study also documented increased pituitary somatotroph proliferation and GH mRNA at the once-daily interval [5]. Jetté 2005 used single subcutaneous bolus doses at low μg/kg levels in dose-ranging rat experiments, demonstrating roughly four-fold increases in GH area-under-the-curve over two hours and bioactivity sustained beyond 72 hours after a single dose [1]. The Timms 2019 equine studies used single subcutaneous administrations to thoroughbreds at undisclosed research doses, confirmed by post-administration plasma sampling with the LC-MS/MS method detecting CJC-1295 down to 180 pg/mL [12]. None of these animal studies translate directly to any human dose. Allometric scaling between rodents and humans is approximate at best for peptides with carrier-protein binding behavior, and the GHRH-knockout mouse is a phenotypic rescue model rather than an efficacy model in normally functioning physiology. ## Routes that have been studied Subcutaneous injection is the predominant route in every published human and animal study of CJC-1295 [1][2][5]. Intraperitoneal administration appears in some rodent mechanistic work. Intravenous administration shows up in a limited set of early comparator GHRH studies and in equine pharmacokinetic work [12]. The DAC variant's bioactivity depends on its reactive maleimide group encountering the free thiol on serum albumin Cys34. Subcutaneous injection delivers the peptide into a tissue compartment with access to systemic albumin without first-pass exposure issues; that is the route the Teichman PK numbers describe [2][3]. No oral, sublingual, intranasal, or transdermal formulation of CJC-1295 has been characterized in peer-reviewed publication. ## The CJC-1295 + ipamorelin pairing The single most frequently co-supplied combination in research-chemical and compounded peptide channels is *CJC-1295 + ipamorelin* — typically a 1:1 mg/mg blend in a single vial. The pharmacological rationale traces back to Bowers and colleagues 1990, who demonstrated that combined administration of a GHRH agonist (1 μg/kg intravenous) with a ghrelin-receptor agonist (GHRP-6 at 1 μg/kg intravenous) produced a GH secretory response several-fold larger than either agent alone [11]. The mechanism is dual-receptor activation: GHRH binds GHRHR while the GHRP/ghrelin-receptor agonist binds GHS-R1a, and the two pathways converge on enhanced GH release with greater-than-additive synergy [11]. Ipamorelin is the modern selective GHS-R1a agonist most commonly paired with CJC-1295 in research-chemical channels because it has a more favorable off-target profile than older GHRPs — specifically, less stimulation of cortisol and prolactin than GHRP-2 or GHRP-6 at typical study doses. No peer-reviewed RCT has evaluated the CJC-1295 + ipamorelin combination specifically; the rationale is mechanistic extrapolation from the 1990 Bowers work [11]. ## Stability, storage, and lyophilized vial mass Lyophilized CJC-1295 — both DAC and non-DAC — is supplied as a white freeze-dried powder, typically as a trifluoroacetate (TFA) salt with HPLC purity reported at 95-99% [20]. The lyophilized form is stable at refrigerated or frozen temperatures for extended storage; reconstituted peptide is sensitive to freeze-thaw cycles and elevated temperatures. The DAC variant's bioactivity depends on intact reactive maleimide chemistry, which can be compromised by improper handling. The key sourcing point: a research-grade lyophilized vial's gross mass exceeds the net peptide mass, because the powder includes residual TFA counterion plus any other excipients. A vial labeled *5 mg CJC-1295* typically contains less than 5 mg of net peptide. The Certificate of Analysis reports net peptide weight per gross vial weight; without the CoA there is no practical way to verify the labeled-vs-actual content of any research-chemical preparation [20]. Vendor-to-vendor variance in purity, residual TFA, and net peptide mass is real and is one of the standing reproducibility problems in non-pharmaceutical peptide supply [8]. --- A photocopied reading-room digest of the peer-reviewed record — not a clinic, not a vendor, not a prescription.