# CJC-1295 — Research dosing context, half-life, and routes studied > Research-context only summary of the doses, routes, and half-lives studied in the CJC-1295 literature: Teichman 2006 Phase 1 PK, Jetté 2005 rat studies, Alba 2006 GHRH-knockout mouse work, and the long-acting DAC half-life of 5.8 to 8.1 days. A research-context-only summary of doses, routes, and half-lives from the small CJC-1295 literature. This page describes what investigators administered to animals and to Phase 1 healthy-volunteer cohorts. It is not a guide to human use, and it is not a recommendation. ## What the studies actually administered This page summarizes the doses, routes, and half-lives from the four sources that make up the entire published CJC-1295 dosing record. None of those numbers should be read as a recommended human amount. CJC-1295 has never been approved for human use — there is no FDA-labeled dose range, no completed Phase 3 safety program, no established safe level. The literature contains: Teichman 2006, which administered 30 to 250 micrograms per kilogram subcutaneously in healthy adults; Alba 2006, which used 2 micrograms per injection in mice; the terminated Phase 2 trial, which did not publish its dosing protocol. The 5.8-to-8.1-day half-life of the long-acting DAC form means a single dose keeps growth hormone elevated for days — a pharmacological fact that makes the DAC versus no-DAC distinction practically important, not merely technical. ## Doses described in the published record The published CJC-1295 dosing record comes from four sources. None of them supports a *recommended human dose*; what they support is a description of what investigators administered in specific research contexts, for specific purposes, under specific oversight regimes. **Phase 1 healthy-adult PK/PD trial (Teichman 2006).** Subcutaneous CJC-1295 at single-dose cohorts of 30, 60, 125, and 250 μg/kg in 21- to 61-year-old healthy adults; multi-dose cohorts dosed weekly or biweekly for 28 to 49 days [2]. Endpoints were plasma GH, IGF-1, and safety. The 30 μg/kg cohort produced 2-fold mean plasma GH elevation; the 250 μg/kg cohort produced 10-fold; IGF-1 elevation persisted 9 to 11 days after a single injection [2]. This is the only Phase 1 dataset in healthy adults and the source of essentially all human PK that exists for the compound. **Rat PK characterization (Jetté 2005).** Subcutaneous bolus dose-ranging at low-μg/kg levels in adult rats, demonstrating identification of CJC-1295 as a long-lasting GRF analog; the 4-fold increase in GH AUC and >72-hour circulation persistence anchor the long-acting characterization [1]. **GHRH-knockout mouse studies (Alba 2006).** 2 μg per injection at 24-, 48-, or 72-hour intervals for five weeks — approximately 80 μg/kg in a 25 g mouse. Once-daily dosing normalized linear growth and body weight; longer intervals yielded partial restoration [4]. **Phase 2 HIV-associated visceral obesity (NCT00267527).** Weekly subcutaneous regimen; specific μg/kg not fully disclosed in the literature before the trial was terminated [7]. The trial enrolled 192 participants but did not publish primary endpoints. What the record does not contain: any FDA-approved label, any USP/NF monograph, any peer-reviewed dose-finding study above the Phase 1 healthy-volunteer scale, and any long-term safety dataset. ## Half-life and the engineering choice that produced it The phrase *long-acting* attaches to CJC-1295 because of one engineering decision: the maleimidopropionic acid tether at the C-terminus that covalently binds the free thiol on Cys34 of circulating serum albumin. That tether converts a peptide that would otherwise clear from plasma in minutes into one that circulates in the day-scale range [1][3]. The Teichman 2006 trial estimated a mean plasma half-life of 5.8 to 8.1 days in healthy adult humans across the four dose cohorts [3]. The non-DAC variant — *modified GRF(1-29)*, the same backbone without the albumin tether — has a half-life of approximately 30 minutes in plasma, compared to roughly 7 minutes for native GHRH. The four amino acid substitutions (D-Ala²/Gln⁸/Ala¹⁵/Leu²⁷) are what produces the four-fold extension over native GHRH; the maleimide tether is what produces the additional several-hundred-fold extension over the modified GRF(1-29) backbone alone [9]. The pharmacological consequence — beyond the obvious dosing-frequency reduction — is that CJC-1295 produces sustained, multi-day elevation of mean GH and IGF-1 while preserving pulsatile GH architecture. Ionescu and Frohman showed in 2006 that during continuous stimulation by CJC-1295, single doses raised basal (trough) GH levels approximately 7.5-fold while preserving normal pulse architecture, with mean GH approximately 46% above baseline [5]. This is a different pharmacological profile from exogenous recombinant GH, which overwrites the endogenous pulse pattern. ## Routes and stability notes from the research record All human and most animal studies in the CJC-1295 record used subcutaneous administration. Some rodent mechanistic work used intraperitoneal dosing; early comparator GHRH studies used intravenous routes, but no human study uses IV. The DAC variant's bioactivity depends on covalent attachment to the free thiol of albumin Cys34 after injection. Reconstituted peptide is typically stored refrigerated for short-term research use and frozen for longer-term storage; freeze-thaw cycles and elevated temperatures degrade activity. The non-DAC variant degrades faster because it lacks albumin tethering. For research-chemical preparations specifically, identity and purity are not assured by the *research use only* label. A 2010 paper from the Oslo anti-doping laboratory identified an unknown peptide pharmaceutical preparation as CJC-1295 via LC-HRMS/MS sequence determination — a study undertaken precisely because such preparations circulate outside any approved regulatory channel and require independent forensic confirmation of identity [8]. The same FDA briefing that catalogued the toxicology concerns also flagged immunogenicity risk of compounded preparations as an unaddressed concern [13]. ## A note on register Every quantitative claim on this page is attributed to a published study by the cohort, species, route, and dose the investigators actually used. None of those numbers should be read as a recommended human dose. CJC-1295 has never been approved for any human indication; there is no FDA-labeled dose range, no titration schedule, and no human safety profile characterized at the scale required for marketing approval [13]. The Phase 2 program in HIV-associated visceral adiposity was terminated in 2006 and never restarted [7]. The regulatory record describes the doses used in the studies that exist. It does not describe an appropriate dose for human use, because the regulatory question of an appropriate human dose has never been adjudicated for this compound. That is the gap the 2024 PCAC vote was reading [13]. --- An independent editorial reading of the regulatory record — not legal advice, not medical guidance, not a vendor.