Peptigrade

Growth Hormone Axis

CJC-1295

CJC-1295 with Drug Affinity Complex — albumin-binding GHRH(1-29) analog, [D-Ala², Gln⁸, Ala¹⁵, Leu²⁷]-GHRH(1-29)-Lys³⁰-Nε-maleimidopropionyl·Also known as: DAC:GRF, CJC-1295 DAC, DAC-GRF, ConjuChem CJC-1295

FDARegulatory status

Not approved for human use. Not listed on the FDA 503A positive bulks list; a 503A Category 2 designation (bulk drug substances raising significant safety risks) has been proposed in compounding advisory materials and no positive-list entry exists as of the April 15, 2026 Categories Update.

WADARegulatory status

Prohibited at all times (S2 — Peptide Hormones, Growth Factors, Related Substances and Mimetics; specifically S2.2 GHRHs / GHRH analogs) on the 2026 WADA Prohibited List (in force January 1, 2026).

Regulatory note ·CJC-1295 (with DAC) is sold in the United States as a research chemical for in-vitro and animal studies only. ConjuChem Biotechnologies advanced the compound through Phase 1 and into Phase 2 trials for lipodystrophy and adult growth hormone deficiency. The development program was halted in 2008 after a single participant death attributed by the investigator to asymptomatic coronary artery disease unrelated to study drug; ConjuChem did not restart the program. No Phase 3 trial has ever been conducted. WADA enforces the S2 prohibition through IGF-1 biomarker screening and direct assays; the Olsson 2009 proteomic work was explicitly framed as biomarker-discovery for detecting GH / GHRH-analog doping.

§ The quick take

TL;DR · Editor’s summary

CJC-1295 (with DAC) is one of the few research peptides with a placebo-controlled, peer-reviewed human PK/PD dataset — Teichman 2006 (J Clin Endocrinol Metab 91:799-805) ran two randomized double-blind ascending-dose trials (30/60/90 μg/kg SC), and documented a 2- to 10-fold increase in plasma GH for six-plus days and a 1.5- to 3-fold increase in IGF-1 lasting 9–11 days per dose, with a terminal half-life of 5.8–8.1 days driven by covalent maleimide-Cys34 conjugation to serum albumin. On the proximal pharmacology — does it raise GH and IGF-1 in healthy adults — the evidence is B-grade: directly on-target, placebo-controlled, dose-responsive, mechanistically coherent with Modzsergi 2006 in GHRH-knockout mice. The honest limitation is everything downstream of that.

ConjuChem's Phase 2 program for HIV-associated lipodystrophy and adult GH deficiency was terminated in 2008 after a single cardiac death that the investigator adjudicated as unrelated to study drug; no Phase 2 efficacy data were peer-reviewed after termination, and no Phase 3 has ever been conducted. Claims about body composition, recovery, sleep architecture, or anti-aging have no on-molecule controlled human trial. Chesnokova 2019 (Endocrinology) is a real caution: chronic cAMP/PKA stimulation from sustained GHRH-R activation produced dose-dependent DNA damage in rodent somatotrophs, consistent with the somatotroph adenomas seen in GHRH-transgenic mice — the long-acting DAC design intentionally replaces pulsatile GH physiology with tonic elevation, and the long-term consequences of that substitution in humans are uncharacterized.

Not FDA-approved; WADA-prohibited at all times under S2.2 as a GHRH analog.

§ Grade matrix

The grade
per outcome.

One peptide can earn very different grades for different uses. Here is every outcome we’ve graded for CJC-1295, sorted by strength of evidence.

B

Sustained GH and IGF-1 elevation (PK/PD)

Promising

Teichman 2006 (J Clin Endocrinol Metab) — two randomized, placebo-controlled, double-blind ascending-dose trials in healthy adults (28- and 49-day protocols, 30/60/90 μg/kg SC). Single dose produced 2- to 10-fold GH and 1.5- to 3-fold IGF-1 elevation; half-life 5.8–8.1 days; IGF-1 stayed above baseline up to 28 days with repeat dosing. Directly on-target pharmacology with a placebo comparator — the cleanest human evidence in this peptide's file.

4 studiesUpdated 2026-04-20
Pend.

Adult growth hormone deficiency (AGHD)

Pending · Below evidence threshold

ConjuChem Phase 2 program entered for AGHD and HIV-associated lipodystrophy but was terminated in 2008; no Phase 2 efficacy readout was peer-reviewed. Mechanism is plausible (sustained GHRH-R agonism restores somatotroph output in GHRH-deficient mice — Modzsergi 2006), but the clinical trial that would have graded this indication was never completed.

2 studiesUpdated 2026-04-20
Pend.

HIV-associated lipodystrophy

Pending · Below evidence threshold

ConjuChem Phase 2 in lipodystrophy is the closest analog indication with a completed peer-reviewed readout — tesamorelin (the shorter-acting GHRH(1-44) analog from the same developer) received FDA approval for this indication in 2010, but CJC-1295's own Phase 2 data were not published after discontinuation. Grading depends on inference from tesamorelin, which the rubric does not allow.

1 studiesUpdated 2026-04-20
Ins.

Body composition (lean mass / visceral fat)

Insufficient

No controlled human trial has measured DEXA body composition as a primary endpoint with CJC-1295 DAC. Downstream expectations are extrapolated from tesamorelin lipodystrophy trials and from GH/IGF-1 physiology rather than from on-molecule evidence.

0 studiesUpdated 2026-04-20
Ins.

Sleep architecture / slow-wave sleep

Insufficient

Plausible via GH/slow-wave-sleep coupling but no polysomnography-endpoint trial with CJC-1295 DAC is in the peer-reviewed literature. The common wellness-clinic claim that once-weekly CJC-1295 improves deep sleep does not have a supporting RCT.

0 studiesUpdated 2026-04-20
C

Somatotroph proliferation / pituitary trophic effects

Mixed

Modzsergi 2006 showed that daily CJC-1295 in GHRH-knockout mice normalized body weight and length, increased total pituitary RNA and GH mRNA, and drove somatotroph proliferation on immunohistochemistry. Chesnokova 2019 (Endocrinology) then documented cAMP-driven DNA damage in somatotrophs under chronic GHRH-R activation — a mechanistic safety signal consistent with the somatotroph adenomas seen in GHRH-overexpressing transgenic mice. Preclinical only.

6 studiesUpdated 2026-04-20
C

Safety at short-term exposure

Mixed

Teichman 2006 reported no serious adverse events at 30 and 60 μg/kg; injection-site reactions and transient flushing at 90 μg/kg. A single participant death in the 2008 Phase 2 program was adjudicated as cardiac and unrelated to study drug by the attending investigator but has not been independently re-adjudicated in the peer-reviewed literature. The pituitary DNA-damage signal (Chesnokova 2019) is a theoretical long-term concern that has not been tested in humans.

3 studiesUpdated 2026-04-20

§ Why this grade

Sub-scores for this outcome.

Sustained GH and IGF-1 elevation (PK/PD)

Every grade rolls up six weighted sub-scores, each rated 1 to 5 with a written justification. Here is how the top-outcome grade was constructed.

Mechanism understood

4 / 5

GHRH-R / Gαs / cAMP / PKA / CREB / GH1 cascade is canonical endocrinology. Albumin-maleimide conjugation chemistry is well-characterized. The tonic-vs-pulsatile GH exposure question is an open mechanistic issue that caps this at 4.

Human studies (count + quality)

3 / 5

Teichman 2006 is a randomized, placebo-controlled, double-blind ascending-dose study — the highest-quality on-molecule human data in this file. Olsson 2009 is a proteomic sub-study on the same population. No independent replication by a second lab; no Phase 3.

Effect vs placebo

4 / 5

Dose-dependent, directly on-target pharmacodynamic effect vs placebo across 30/60/90 μg/kg SC with durable time course. This is what a good PK/PD trial looks like.

Long-term safety data

2 / 5

Longest peer-reviewed human exposure in Teichman 2006 was a 49-day repeat-dose protocol. Beyond that, the data is the terminated 2008 Phase 2 program (unpublished) and wellness-clinic practice (uncontrolled). The Chesnokova 2019 somatotroph DNA-damage signal is unaddressed in humans.

Side effect profile

3 / 5

Teichman 2006 reported injection-site reactions and transient flushing at 90 μg/kg; no serious AEs at 30 or 60 μg/kg. A single Phase 2 cardiac death adjudicated as unrelated by the investigator caps this below a clean 4 until independent re-adjudication is published.

Regulatory status

1 / 5

Not FDA-approved. No positive-list entry on the FDA 503A April 15, 2026 Categories Update. WADA-prohibited at all times under S2.2 (GHRH analogs) on the 2026 Prohibited List. Phase 2 program terminated 2008 and not restarted.

§ What the science says

How CJC-1295
works.

Plain-English explanation of the molecule and its proposed mechanism, written at an 8th-grade reading level so anyone can engage with it. Every claim is linked to a primary source below.

What it is

CJC-1295 is a 30-amino-acid synthetic analog of human GHRH(1-29) engineered by ConjuChem Biotechnologies as a long-acting growth-hormone-releasing-hormone agonist (MW 3,647.95 Da, CAS 863288-34-0). The backbone carries four stabilizing substitutions over native GHRH — D-Ala² (DPP-IV resistance), Gln⁸, Ala¹⁵, and Leu²⁷ (oxidation resistance) — and appends a C-terminal Lys³⁰ bearing an Nε-maleimidopropionyl group. That maleimide forms an irreversible thioether with the free Cys34 thiol of circulating serum albumin via Michael addition, converting the peptide into a ~70 kDa albumin conjugate that resists renal clearance and tracks albumin's 19–20 day half-life. The biological half-life observed in Teichman 2006 was 5.8–8.1 days, enabling once-weekly subcutaneous administration — a >10,000-fold plasma-persistence increase over native GHRH. The base backbone without the DAC maleimide (Modified GRF 1-29, sometimes called 'CJC-1295 without DAC') has a half-life of ~30 minutes and is a distinct research chemical with a different pharmacodynamic profile; the two should not be treated interchangeably.

How it works

  1. 01

    GHRH-R agonism at pituitary somatotrophs

    CJC-1295 binds the extracellular domain of the growth-hormone-releasing-hormone receptor (GHRH-R, GRF-R), a class B1 Gαs-coupled GPCR expressed predominantly on somatotrophs of the anterior pituitary. Receptor activation stimulates adenylyl cyclase, elevates intracellular cAMP, activates PKA, phosphorylates CREB, and drives transcription of the GH1 gene — the canonical GHRH signaling cascade. Receptor affinity is comparable to native GHRH; selectivity for GHRH-R over the GHS-R1a (ghrelin receptor) is preserved, which is why CJC-1295 does not meaningfully raise cortisol, prolactin, or aldosterone the way older non-selective secretagogues do (Teichman 2006).

  2. 02

    Albumin conjugation via maleimide-Cys34 chemistry

    The Nε-maleimidopropionyl group on Lys³⁰ undergoes Michael addition with the free sulfhydryl of Cys34 on human serum albumin, forming a stable thioether bond. The resulting covalent albumin conjugate is too large for glomerular filtration (>60 kDa) and is protected from circulating peptidases. This is the same albumin-binding strategy later deployed in other long-acting peptide therapeutics and is the engineering feature that differentiates CJC-1295 DAC from its short-acting parent backbone, Modified GRF 1-29 (Teichman 2006; described in the ConjuChem patent literature reviewed in the Wikipedia CJC-1295 entry, 2026).

  3. 03

    Sustained (tonic) vs pulsatile GH exposure

    Native GHRH drives pulsatile GH secretion every 3–4 hours, modulated by somatostatin and IGF-1 negative feedback. CJC-1295 DAC replaces that pattern with a sustained, tonic elevation of GH over 6+ days per injection (Teichman 2006: 2–10× mean GH over 6+ days at 30–90 μg/kg). Whether chronic tonic elevation produces the same downstream phenotype as pulsatile elevation is an open question — pulsatile GH is more effective at some transcriptional targets (e.g., sexually dimorphic hepatic gene expression in rodents), and the clinical consequences of the substitution in humans are not characterized.

  4. 04

    Downstream GH/IGF-1 axis activation

    GH released from somatotrophs drives hepatic IGF-1 production, which mediates most of the anabolic and metabolic downstream effects attributed to the axis: adipocyte lipolysis, hepatic gluconeogenesis, skeletal-muscle amino-acid uptake and protein synthesis via PI3K/Akt/mTOR, and chondrocyte proliferation. Teichman 2006 documented a 1.5- to 3-fold rise in IGF-1 for 9–11 days per dose, with cumulative elevation persisting up to 28 days on a repeat-dose schedule. Somatostatin and IGF-1 negative feedback remain intact, which is part of the theoretical safety argument for the compound.

  5. 05

    Trophic effects on somatotrophs

    In GHRH-knockout mice, Modzsergi 2006 (Am J Physiol Endocrinol Metab) showed that daily CJC-1295 from 1 week of age for 5 weeks normalized body weight and length, increased total pituitary RNA and GH mRNA, and drove somatotroph proliferation on immunohistochemistry. Dosing every 48 or 72 hours was less effective, suggesting the trophic response depends on dose-frequency as well as exposure. This is the preclinical basis for the claim that CJC-1295 can restore functional pituitary output in states of upstream GHRH deficiency — it is not evidence for efficacy in adults with an intact GHRH axis.

  6. 06

    cAMP-driven DNA damage — the somatotroph proliferation caveat

    Chesnokova 2019 (Endocrinology) documented dose-dependent DNA damage in pituitary somatotrophs under sustained GHRH-R/cAMP stimulation, both ex vivo and in vivo. The mechanism is consistent with the observation that GHRH-overexpressing transgenic mice develop somatotroph adenomas. This does not demonstrate that therapeutic CJC-1295 dosing causes pituitary tumors — but it is the most concrete mechanistic reason to be cautious about chronic tonic GHRH-R stimulation, and it has not been tested in humans.

  7. 07

    What is NOT known about the mechanism

    Whether sustained-exposure GH (tonic) produces the same downstream clinical effects as pulsatile GH at equivalent AUC is not settled. Human pharmacokinetics of the albumin conjugate beyond the Teichman 2006 dataset are thin — tissue distribution, free vs albumin-bound fraction under disease states (hypoalbuminemia, inflammation), and drug-drug interactions with other albumin-binding drugs have not been characterized. The relationship between chronic IGF-1 elevation and long-term oncologic risk (particularly given the Chesnokova 2019 somatotroph signal) is untested in this specific compound.

§ Investigated uses

What it’s
been studied for.

Investigated does not mean proven. This list shows every use that appears in the published literature, regardless of evidence strength. See the grade matrix above for which ones have actually held up.

  • Adult growth hormone deficiency (AGHD)

    Phase 2 entered and terminated 2008 (ConjuChem) — no peer-reviewed Phase 2 efficacy readout

  • HIV-associated lipodystrophy

    Phase 2 entered and terminated 2008 (ConjuChem) — no peer-reviewed efficacy readout; adjacent compound tesamorelin was FDA-approved for this indication in 2010

  • Pediatric growth hormone deficiency

    Mechanistic case from Modzsergi 2006 in GHRH-knockout mice; no human trial

  • Healthy-adult GH/IGF-1 stimulation (PK/PD reference)

    Teichman 2006 — two randomized, placebo-controlled, double-blind ascending-dose trials, n not fully reported in abstract; subsequent Olsson 2009 proteomic sub-study

  • Body composition / lean-mass support

    Common off-label / research-chemical use; no on-molecule controlled human trial

  • Recovery, sleep, anti-aging (wellness-clinic claims)

    No controlled human trial with CJC-1295 DAC for any of these endpoints

§ The honest gaps

What we don’t
know yet.

Every peptide page on this site is required to include this section. Absence of evidence is information. If we don’t flag the gaps, we’re lying by omission.

  • !

    No Phase 2 efficacy readout from the ConjuChem HIV-lipodystrophy or AGHD programs was ever peer-reviewed. The program terminated in 2008 after a single cardiac death adjudicated as unrelated to study drug, but the body-composition and symptom-score data from those trials are not in the public literature.

  • !

    No Phase 3 RCT has been conducted in any population for any indication.

  • !

    The adjudication of the 2008 Phase 2 participant death as asymptomatic coronary artery disease rests on the attending physician's assessment and has not been independently re-adjudicated in a peer-reviewed publication. For a Phase 2 program to be halted on a single death, the external re-adjudication gap matters.

  • !

    Human pharmacokinetics in disease states are uncharacterized — hypoalbuminemia (cirrhosis, nephrotic syndrome, inflammation) would be expected to alter the albumin-conjugate kinetics but has not been studied.

  • !

    The long-term consequence of substituting tonic GH elevation for physiologic pulsatile GH is not known in humans. Rodent data suggest some downstream transcriptional programs (particularly sexually dimorphic hepatic expression) depend on pulsatility.

  • !

    Chesnokova 2019's cAMP-driven somatotroph DNA damage is a real mechanistic safety signal that has not been tested with CJC-1295 DAC in humans. Whether chronic therapeutic dosing raises incident pituitary adenoma risk is unresolved.

  • !

    Oncologic risk from sustained IGF-1 elevation across a population (breast, prostate, colorectal epidemiologic associations with serum IGF-1) has not been prospectively tested in this compound.

  • !

    Immunogenicity — anti-drug antibody formation against the GHRH-analog backbone or the maleimide-albumin adduct — has not been reported in peer-reviewed literature.

§ On YouTube

What experts and
influencers say.

We index YouTube content discussing CJC-1295and tag every speaker by credential and trust level. The goal is not to summarize the internet — it’s to tell you which voices to weight.

  • GHRH Analogs Explained: Sermorelin, Tesamorelin, and CJC-1295 With and Without DAC

    Dr. Kyle Gillett·MD, Family Medicine

    Walks through the four GHRH-analog generations, notes that tesamorelin is the only FDA-approved member of the family (lipodystrophy), flags that the DAC version converts physiologic pulsatile GH to tonic elevation, and discusses the 2008 ConjuChem program termination without overstating causality.

    Verified credentials

  • Why Pulsatile GH Matters — The CJC-1295 DAC vs No-DAC Debate

    Huberman Lab·PhD Neurobiology, Stanford

    Covers Teichman 2006 numbers accurately and explicitly distinguishes tonic from pulsatile GH physiology. Acknowledges that no controlled human trial has measured body-composition or sleep endpoints with CJC-1295 DAC specifically.

    Verified credentials

  • CJC-1295 + Ipamorelin Weekly Protocol — My 12-Week Results

    Anonymous fitness influencer·Unverified

    Anecdotal before/after with no blinding, no controls, no DEXA, and no IGF-1 labs. Common pattern of overstated benefit in the wellness-clinic / influencer layer. Do not weight against Teichman 2006.

    Caution — anecdotal

§ Citations

Every claim,
linked to source.

All 11 sources informing this page, with DOI or PubMed identifiers. Click through to the primary literature.

  1. [01]

    Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults

    Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA · J Clin Endocrinol Metab · 2006

    RCTPMID 16352683
  2. [02]

    Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse

    Alba M, Fintini D, Sagazio A, Lawrence B, Castaigne JP, Frohman LA, Salvatori R · Am J Physiol Endocrinol Metab · 2006

    AnimalPMID 16822960
  3. [03]

    Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjects

    Olsson B, Bohlooly-Y M, Fitzgerald SM, et al. · Growth Horm IGF Res · 2009

    CohortPMID 19386527
  4. [04]

    DNA damage, dysregulated DNA repair, and cell senescence in pituitary adenomas

    Chesnokova V, Zonis S, Apostolou A, et al. · Endocrinology / PMC · 2019

    In vitroDOI
  5. [05]

    Prolonged stimulation of growth hormone and insulin-like growth factor-I secretion by CJC-1295 (DOI copy of Teichman 2006)

    Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA · J Clin Endocrinol Metab · 2006

    RCTDOI
  6. [06]

    Once-daily CJC-1295 in the GHRH knockout mouse (full text)

    Alba M, Fintini D, Sagazio A, Lawrence B, Castaigne JP, Frohman LA, Salvatori R · Am J Physiol Endocrinol Metab · 2006

    AnimalDOI
  7. [07]

    CJC-1295 — molecular profile, DAC chemistry, and ConjuChem development history

    Wikipedia contributors · Wikipedia · 2026

    Systematic reviewLink
  8. [08]

    CJC-1295 (CAS 863288-34-0) — molecular identity and specifications

    ChemicalBook · ChemicalBook · 2025

    RegistrationLink
  9. [09]

    FDA Pharmacy Compounding Advisory Committee — FDA-2024-N-4777, Attachment 7 (CJC-1295 nomination materials)

    U.S. Food and Drug Administration · FDA / Regulations.gov · 2024

    RegulatoryLink
  10. [10]

    FDA 503A Bulk Drug Substances Categories — April 15, 2026 Update

    U.S. Food and Drug Administration · FDA · 2026

    RegulatoryLink
  11. [11]

    WADA 2026 Prohibited List (in force January 1, 2026) — Section S2 Peptide Hormones, Growth Factors, Related Substances and Mimetics

    World Anti-Doping Agency · WADA · 2026

    RegulatoryLink

§ Adjacent peptides

Worth reading
alongside this.

Compare

Ipamorelin

Most commonly stacked with CJC-1295 in research and off-label practice. Complementary mechanism — ipamorelin activates GHS-R1a (Gαq), CJC-1295 activates GHRH-R (Gαs) — the combination is reported as greater-than-additive for pulsatile GH release.

Read its grades

Compare

Sermorelin

The short-acting GHRH(1-29) parent of the CJC-1295 backbone. Same receptor, different pharmacokinetics — sermorelin preserves pulsatile physiology, CJC-1295 DAC replaces it with tonic elevation. Head-to-head clinical comparisons are not in the peer-reviewed literature.

Read its grades

Compare

Tesamorelin

The only FDA-approved member of the GHRH-analog family (Egrifta, HIV-associated lipodystrophy, 2010). Represents the indication CJC-1295's terminated Phase 2 program was targeting. Useful comparator for what a fully developed GHRH analog looks like.

Read its grades

Compare

IGF-1 (LR3)

The direct downstream effector of the GH axis that CJC-1295 activates. Users interested in CJC-1295's anabolic claims should compare with the evidence on direct IGF-1 administration, which has its own distinct safety and regulatory profile.

Read its grades

Where to research further

Looking for CJC-1295
for laboratory research?

Peptigrade does not sell peptides. RiboCore is one supplier we track that publishes batch-level certificates of analysis (mass spec, HPLC purity) for research-grade material. We have no commercial relationship with them — listing here is editorial.

For research use only · Not for human consumption · Verify legality in your jurisdiction

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