# CJC-1295 FAQ — Common questions about the GHRH analog, in plain language

> Plain-language answers to the most common CJC-1295 research questions: Phase 1 results, the 2006 Phase 2 termination, DAC versus non-DAC, half-life, FDA status, WADA status, and side-effect signals.

If a question is missing or an answer needs correcting against the primary literature, the contact form is on the next page.

## What does the CJC-1295 research literature actually show?

A small, finite body of preclinical and Phase 1 human data. A 2005 rat discovery paper established that hGRF(1-29)-albumin bioconjugates activate the GRF receptor and produce sustained GH release [1]. A 2006 Phase 1 human PK study in healthy adults showed mean plasma GH elevated two- to ten-fold for at least six days and IGF-1 elevated 1.5- to three-fold for nine to eleven days after a single subcutaneous dose [2]. A companion paper the same year showed GH pulsatility was preserved under continuous CJC-1295 stimulation [4]. A GHRH-knockout mouse study showed once-daily dosing restored linear growth [5]. A 2009 proteomic paper identified candidate serum biomarkers of axis activation [6]. Beyond that, the file is regulatory and analytical — WADA detection methods, FDA compounding briefings, doping-control mass-spectrometry work — not new clinical data.

## What were the CJC-1295 Phase 1 trial findings?

Teichman 2006 [2] is the Phase 1 paper. Healthy adults received single subcutaneous CJC-1295 at 30, 60, 125, or 250 μg/kg, with additional multi-dose cohorts at 60 to 125 μg/kg weekly or biweekly. Across single doses, mean plasma GH rose two- to ten-fold above baseline for at least six days, and mean IGF-1 rose 1.5- to three-fold for nine to eleven days [2]. Multi-dose cohorts sustained IGF-1 elevation for twenty-eight days [2]. Plasma half-life across cohorts ranged 5.8 to 8.1 days [3]. The published safety profile was consistent with the dose range and the small sample sizes, but the paper does not constitute a long-term human safety dataset.

## What happened in the CJC-1295 Phase 2 clinical trial?

The Phase 2 trial — NCT00267527 — was a randomized, double-blind, placebo-controlled study of CJC-1295 in HIV-associated visceral adiposity, with weekly subcutaneous dosing in 192 participants [7]. It was terminated in October 2006 after a participant died from an acute coronary event approximately two hours after the eleventh weekly dose. Independent review attributed the event to pre-existing undiagnosed coronary artery disease and judged it unrelated to study drug [7]. The program was halted, primary efficacy outcomes were never published in the peer-reviewed literature, and sponsor-funded development did not restart. That terminated trial is the high-water mark of CJC-1295 clinical development.

## Is CJC-1295 used in any approved clinical setting?

No. CJC-1295 is not FDA-approved for any indication [14]. It was not added to the Section 503A bulk drug substances list at FDA's October 2024 PCAC review and was subsequently removed from FDA's Category 2 list effective September 27, 2024 [14]. A December 2024 PCAC follow-up reiterated the same conclusion [17]. The closely related GHRH analog tesamorelin is FDA-approved for HIV-associated lipodystrophy and provides the class benchmark for visceral-fat efficacy [15], but tesamorelin and CJC-1295 are distinct compounds. CJC-1295 itself does not appear on any approved-drug label.

## Is there a real CJC-1295 clinic anywhere?

Not in any sense the word "clinic" usually carries. CJC-1295 is not approved, not on the compounding-pharmacy bulk-substances list, and not in any sponsor-funded clinical development program [14][17]. This site is an editorial reading room — the word "clinic" in the domain name reflects the publisher's posture toward the literature, not a service offering. We do not have clinicians, we do not provide medical advice, and we do not sell or distribute any product. See [About](/about) for the full publisher statement.

## How does CJC-1295 work mechanistically on the GHRH receptor?

CJC-1295 binds the growth hormone-releasing hormone receptor (GHRHR) on anterior-pituitary somatotrophs and activates the canonical Gs / adenylyl cyclase / cAMP / PKA second-messenger cascade, which drives GH gene transcription and pulsatile GH release [1][4]. The DAC variant's C-terminal maleimide covalently couples in vivo to the free thiol on Cys34 of circulating serum albumin, shielding the peptide from peptidase degradation and renal filtration and producing the multi-day half-life [1][3]. Downstream of GH, hepatic IGF-1 production rises and serves as the cleanest biomarker of axis activation [2][6].

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

For CJC-1295 with DAC, mean plasma half-life in healthy adults ranges 5.8 to 8.1 days across single-dose cohorts (30-250 μg/kg) [3]. The pharmacodynamic effect on IGF-1 extends to nine to eleven days after a single dose, and to twenty-eight days with weekly or biweekly multi-dosing [2]. For modified GRF(1-29), the non-DAC variant, plasma half-life is approximately 30 minutes — compared to roughly 7 minutes for native GHRH [8]. The difference between the two variants — minutes versus days — is the single most consequential pharmacokinetic distinction in the CJC-1295 literature.

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

They share the same 29-residue GRF backbone with four protective amino-acid substitutions (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) [8]. The DAC variant adds a C-terminal lysine bearing a maleimidopropionic acid linker that covalently bonds to serum albumin Cys34 after subcutaneous injection [1]. That covalent tether is what produces the multi-day plasma half-life [3]. The non-DAC variant (modified GRF 1-29) lacks the maleimide and therefore is not bioconjugated to albumin; its half-life is approximately 30 minutes [8]. They are not interchangeable. The primary literature uses "CJC-1295" to refer to the DAC variant unless otherwise specified.

## Why do researchers pair CJC-1295 with ipamorelin?

Because Bowers and colleagues' 1990 *JCEM* paper showed that combined administration of a GHRH and a GHRP produces a GH secretory response several-fold larger than either agent alone in healthy adults [9]. Ipamorelin is a selective GHS-R1a (ghrelin receptor) agonist; CJC-1295 is a GHRH-receptor agonist. The two receptors converge on GH release through different second-messenger pathways, producing synergistic output. The pairing is mechanistically well-grounded — but there is no published CJC-1295 + ipamorelin clinical trial. The combination's reputation rests on the Bowers mechanism work plus the separate clinical files on each compound.

## What is CJC-1295's current FDA status?

Not approved for any indication. FDA's October 29, 2024 Pharmacy Compounding Advisory Committee did not recommend CJC-1295 for inclusion on the Section 503A bulk drug substances list, citing immunogenicity, impurity-testing challenges, and adverse-event signals including increased heart rate and systemic vasodilatory reactions [14]. CJC-1295 was removed from FDA's Category 2 list effective September 27, 2024 [14]. The December 4, 2024 PCAC follow-up reiterated insufficient evidence to support routine 503A access [17]. The compound has no Phase 3 program and no sponsor-led clinical development since 2006.

## Can a compounding pharmacy still make CJC-1295?

Not under routine 503A authority. CJC-1295 was removed from FDA's Category 2 list effective September 27, 2024 [14] and was not added to the Section 503A bulk drug substances list at either the October or December 2024 PCAC meetings [14][17]. Compounding pharmacies operating within the 503A framework cannot routinely use CJC-1295 as a bulk drug substance for compounded preparations. The regulatory door is not permanently closed — FDA could reopen review if new data emerges — but as of the 2024 PCAC decisions, routine compounding access is closed.

## What are the documented side effects in published CJC-1295 studies?

Published Phase 1 (Teichman 2006) reported a tolerability profile broadly consistent with GHRH-axis activation in small healthy-adult cohorts [2]. The Phase 2 program was terminated after a participant cardiac death judged unrelated to study drug; no further sponsor-funded human safety data exist [7]. FDA's 2024 PCAC review summarized adverse-event signals across the compounded-use experience, including increased heart rate and systemic vasodilatory reactions, alongside immunogenicity and impurity concerns [14]. Long-term effects of sustained supraphysiological GH and IGF-1 elevation — insulin resistance, edema, joint pain, theoretical neoplasia risk — are recognized class concerns in endocrinology but are not characterized for CJC-1295 specifically.

## Is CJC-1295 banned by WADA?

Yes. CJC-1295 is listed under Section S2 — Peptide Hormones, Growth Factors, Related Substances, and Mimetics — of the World Anti-Doping Code 2025 Prohibited List, prohibited at all times (in- and out-of-competition) for any athlete subject to the WADA Code [16]. Validated nano-LC Orbitrap mass spectrometry methods for urine detection are in routine use by WADA-accredited laboratories, addressing the analytical challenges of peptide instability and low urinary concentrations [12]. Use by any tested athlete constitutes an Anti-Doping Rule Violation.

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An independent editorial digest of the peer-reviewed CJC-1295 literature — not a clinic, not a vendor, not clinical counsel.