S. 04 · FAQ
Twelve questions readers consistently arrive with — answered from the published record.
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 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.