# CJC-1295 FAQ — The questions a careful reader brings

> Direct answers to the questions a careful reader brings to CJC-1295: DAC vs without DAC, half-life, what happened to the Phase 2 trial, FDA and WADA status, why ipamorelin is the common pairing.

Direct, sourced answers. If a claim is not in the published research, it is not asserted here.

## What is CJC-1295?

CJC-1295 is a synthetic 30-amino-acid analog of growth hormone-releasing hormone. It consists of the first 29 residues of human GHRH with four protective amino-acid substitutions (D-alanine at position 2, glutamine at 8, alanine at 15, leucine at 27) plus a C-terminal maleimidopropionic acid group that covalently binds the free thiol on cysteine 34 of circulating serum albumin after subcutaneous injection [1]. The albumin tether dramatically extends plasma half-life relative to native GHRH or the un-tethered modified backbone.

## What is the difference between CJC-1295 with DAC and CJC-1295 without DAC?

The 'with DAC' (Drug Affinity Complex) variant carries the C-terminal maleimide and binds albumin, producing a measured plasma half-life of 5.8 to 8.1 days [2]. The 'without DAC' variant is the same 29-residue substituted backbone without the maleimide; it is more accurately called modified GRF(1-29) or mod GRF 1-29 and has a plasma half-life of approximately 30 minutes [1]. The two are pharmacokinetically distinct, despite the shared 'CJC-1295' marketing name in research-chemical channels. Most published clinical data — including the Teichman 2006 Phase 1 paper and the terminated Phase 2 program — pertain to the DAC variant.

## How does CJC-1295 work?

CJC-1295 binds the GHRH receptor on anterior pituitary somatotroph cells. Receptor activation triggers a Gs-protein/adenylyl-cyclase/cAMP/protein-kinase-A signaling cascade that drives growth hormone gene transcription and pulsatile GH release [1][5]. The downstream effect is elevated hepatic IGF-1 production. The four amino-acid substitutions confer resistance to dipeptidyl peptidase-4 cleavage and deamidation; the albumin tether produces the multi-day half-life that distinguishes CJC-1295 from earlier GHRH analogs like sermorelin.

## What is the half-life of CJC-1295?

The DAC variant has a measured plasma half-life of 5.8 to 8.1 days in healthy adults [2]. The non-DAC variant (modified GRF(1-29)) has an estimated half-life of approximately 30 minutes — versus roughly 7 minutes for native human GHRH [1]. The half-life figures for the DAC variant are the basis for the once-weekly dosing schedule used in the now-terminated Phase 2 program.

## What does the human research literature actually show?

The single published human study is Teichman and colleagues, 2006, in the *Journal of Clinical Endocrinology and Metabolism* [2]. Two ascending-dose Phase 1 trials in healthy adults aged 21-61 demonstrated dose-dependent rises in growth hormone (two- to ten-fold for ≥6 days) and IGF-1 (1.5- to three-fold for 9-11 days) after single subcutaneous injections at 30 to 250 micrograms per kilogram. Multiple-dose cohorts sustained elevated IGF-1 above baseline for up to 28 days. No serious adverse reactions were reported. Beyond Teichman 2006 and a small pharmacodynamic substudy (Ionescu and Frohman, 2006 [5]), there is no published prospective human efficacy data on CJC-1295.

## What happened to the CJC-1295 clinical trials?

A Phase 2 randomized double-blind placebo-controlled trial in HIV-associated visceral obesity (ClinicalTrials.gov NCT00267527) enrolled 192 participants beginning December 2005 [3]. In October 2006 the trial was terminated after a participant died of an acute coronary event approximately two hours after their eleventh weekly dose. An independent clinical review attributed the death to pre-existing undiagnosed coronary artery disease and judged the event unrelated to study drug. The sponsor (ConjuChem Biotechnologies) did not restart the program. Primary outcome data on body composition were never published. There has been no further sponsor-funded clinical development of CJC-1295 since.

## Is CJC-1295 FDA approved?

No. CJC-1295 is not approved by the FDA, the EMA, or any major regulator for any human indication. In 2023 the FDA placed CJC-1295 in Section 503A bulk drug substances list Category 2, effectively prohibiting routine compounding pharmacy use. The Pharmacy Compounding Advisory Committee reviewed CJC-1295 alongside several other peptides at meetings in October and December 2024 and did not recommend inclusion on the 503A bulks list [7][8].

## What is CJC-1295's status under WADA anti-doping rules?

The World Anti-Doping Agency lists CJC-1295 under Section S2 — Peptide Hormones, Growth Factors, Related Substances, and Mimetics — and prohibits it at all times, both in-competition and out-of-competition, for any athlete subject to the WADA Code [9]. Validated nano-LC orbitrap mass spectrometry detection methods exist for routine urine analysis [10]. Use of CJC-1295 by a WADA-tested athlete is an Anti-Doping Rule Violation regardless of intent.

## Why is CJC-1295 often discussed alongside ipamorelin?

Ipamorelin is a selective ghrelin receptor (GHS-R1a) agonist. The pharmacological rationale for pairing a GHRH analog with a ghrelin-receptor agonist comes from foundational human pharmacodynamic work by Bowers and colleagues in 1990, who showed that combined GHRH plus GHRP-class agonist administration produces a growth hormone response several-fold larger than either alone [12]. The CJC-1295/ipamorelin combination is the modern instantiation of that dual-receptor pharmacology — one peptide engages the GHRH receptor, the other engages the ghrelin receptor, and the GH response is additive or synergistic. This pairing is widely discussed in research-chemical and compounding-pharmacy literature; it has not been the subject of a registered Phase 2 or later RCT in either FDA or EMA development.

## Why does it matter that CJC-1295 preserves pulsatile GH secretion?

Native growth hormone is secreted in discrete pulses several times per day. Exogenous recombinant GH (the FDA-approved injectable somatropin products) raises GH continuously and suppresses endogenous pulsatility. The Ionescu and Frohman 2006 pharmacodynamic data showed that CJC-1295 raises trough GH approximately 7.5-fold while preserving the natural pulse pattern [5] — a profile that some endocrinologists argue is closer to physiology than tonic GH replacement. Whether that distinction matters clinically over long durations of use has not been resolved in the published literature, because the long-duration trials were never completed.

## Can CJC-1295 be obtained through a compounding pharmacy?

Under current FDA policy, no — at least not routinely. CJC-1295 has been classified in Section 503A bulk drug substances list Category 2 since 2023, which precludes ordinary compounding use [7]. The PCAC reviewed the substance in October and December 2024 and did not recommend its addition to the 503A bulks list [8]. Compounders that supplied CJC-1295 prior to the reclassification largely stopped doing so during 2023-2024 in response to FDA enforcement. The compound continues to be available through research-chemical channels that are not subject to pharmaceutical-grade quality control; Henninge and colleagues, 2010, documented an example of an illicit peptide preparation identified as CJC-1295 by mass spectrometry [11].

## What were the doses used in published CJC-1295 studies?

The Teichman 2006 Phase 1 trials used single subcutaneous injections at 30, 60, 125, and 250 micrograms per kilogram, with multiple-dose cohorts at weekly or biweekly intervals [2]. The Alba 2006 mouse study used 2 micrograms per injection at 24-, 48-, or 72-hour intervals for five weeks in juvenile GHRH-knockout mice (approximately 80 μg/kg per dose) [4]. The Phase 2 trial (NCT00267527) used weekly subcutaneous dosing, but the specific μg/kg regimen was not published before the trial was terminated. See the [dosage](/dosage) page for a fuller reading; that page describes research doses and does not recommend doses for humans.

## What are the documented side effects?

The Teichman 2006 Phase 1 trials reported no serious adverse reactions and described the compound as 'safe and relatively well tolerated, particularly at doses of 30 or 60 micrograms per kilogram' [2]. The Phase 2 trial (NCT00267527) was terminated after a participant died of an acute coronary event two hours after the eleventh weekly dose; an independent review judged the event unrelated to study drug [3]. Beyond these two clinical sources, there is no peer-reviewed long-term safety data on CJC-1295. Theoretical concerns common to sustained GH/IGF-1 elevation — insulin resistance, edema, joint pain, neoplastic risk — have not been characterized for CJC-1295 specifically in any published trial.

## How does CJC-1295 compare to sermorelin or tesamorelin?

All three are GHRH analogs. Sermorelin is a synthetic GRF(1-29) with no protective substitutions and no albumin tether; plasma half-life is on the order of minutes. Tesamorelin (an FDA-approved compound for HIV-associated lipodystrophy with a 15-20% reduction in visceral adipose tissue over 26 weeks of daily SC dosing in registered trials [13]) is a different GHRH(1-44) analog with a hexenoic-acid N-terminal modification — pharmacokinetically intermediate and clinically validated. CJC-1295 sits at the long-half-life end of the class because of the albumin bioconjugation. The three compounds share a receptor target but have substantially different pharmacokinetic profiles and substantially different evidence bases.

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An independent reading of publicly available CJC-1295 research — not a clinic, not a vendor, not a treatment recommendation.