CJC-1295
Also known as: CJC-1295 with DAC, DAC:GRF, Modified GRF (1-29), Mod GRF 1-29
CJC-1295 with DAC produces 2- to 10-fold elevations in plasma GH for six days and 1.5- to 3-fold elevations in IGF-1 for nine to eleven days from a single subcutaneous injection — the longest sustained GH-axis stimulus of any peptide on this site.
- Primary sources
- 5
- Mechanism dossiers
- 32
- Documented cycles
- 3
- Last reviewed
- 2026-04-28
2 tier 1
26 decision
Across all tiers
CJC-1295 is a tetrasubstituted analog of growth-hormone-releasing hormone (GHRH 1-29) — the active fragment of native GHRH — engineered first for resistance to enzymatic degradation and, in the DAC ("Drug Affinity Complex") variant, for covalent in-vivo bioconjugation to circulating plasma albumin. The four amino-acid substitutions (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) protect against dipeptidyl-peptidase IV cleavage and proline isomerization; the DAC linker — a maleimidopropionic acid (MPA) group appended at Lys³⁰ — reacts covalently with the free thiol on Cys³⁴ of serum albumin once injected, anchoring the GHRH analog to a 19-day plasma-residence carrier (Jetté et al. 2005). The DAC strategy was developed by ConjuChem, who screened three candidate hGRF(1-29)-MPA bioconjugates in rats and selected CJC-1295 on the basis of a four-fold GH-AUC increase over unmodified hGRF(1-29) and immunoreactive plasma persistence beyond 72 hours.
Two distinct molecules circulate in practitioner use under closely related names. CJC-1295 with DAC is the original Jetté/ConjuChem molecule — albumin-anchored, plasma half-life of roughly 6 to 8 days in humans, and the compound tested in the published Phase 1 program. CJC-1295 without DAC — frequently labeled "Modified GRF (1-29)" or "Mod GRF 1-29" and sometimes loosely conflated with sermorelin — carries the same four substitutions but lacks the MPA linker and clears within roughly half an hour. Both molecules act at the same receptor target: GHRH-receptor agonism on pituitary somatotrophs, driving endogenous pulsatile GH release and downstream hepatic IGF-1 production. The mechanistically loaded question for the DAC variant is whether continuous receptor occupancy from a multi-day albumin-anchored agonist flattens the somatostatin-gated pulse architecture into a tonic signal. Ionescu and Frohman 2006 addressed that question directly: at one week post-injection of 60 or 90 μg/kg CJC-1295 with DAC in healthy men, overnight 20-minute sampling showed trough GH elevated 7.5-fold and IGF-1 elevated 45% versus baseline, while the frequency and amplitude of discrete GH secretory pulses were unaltered. CJC-1295 raises the floor without erasing the ultradian rhythm — a different pharmacological profile from the persistent ghrelin-receptor occupancy of MK-677, where the secretagogue signal is continuous rather than pulse-preserving.
The CJC-1295 evidence base is built on three foundational papers from the original ConjuChem development program. Jetté et al. 2005 is the discovery paper — the in-vitro pharmacology, the DAC chemistry, the rat selection of CJC-1295 from a panel of three candidate bioconjugates. Teichman et al. 2006 is the Phase 1 human pharmacokinetic and pharmacodynamic study — two ascending-dose randomized placebo-controlled trials (28 and 49 days) in healthy adults aged 21 to 61, establishing the 5.8- to 8.1-day plasma half-life, the 2- to 10-fold single-dose GH elevation sustained for six days, the 1.5- to 3-fold IGF-1 elevation lasting nine to eleven days, and the maintenance of IGF-1 above baseline for up to 28 days with repeated dosing. Ionescu and Frohman 2006 is the mechanism paper — the demonstration that the multi-day albumin-anchored agonist preserves pulse architecture rather than collapsing it. Together those three papers, all from 2005-2006 and all funded by ConjuChem, are the core regulatory-grade evidence record on CJC-1295.
The development arc did not finish there. ConjuChem's CJC-1295 program never reached an FDA approval. Like other GH-secretagogue programs of the same era — Helsinn's ipamorelin development for postoperative ileus is the closest parallel — the molecule stalled at the pharmaceutical-development stage and migrated into the research-only and off-label space where it now lives. The original sponsor program encountered a serious safety event during a hypertension subindication trial that contributed to the development pause, though the event was not directly attributed to CJC-1295. No subsequent sponsor has carried the molecule into Phase 2 efficacy trials for the body-composition or GH-deficiency indications its pharmacology most plausibly suggests.
The most-cited practitioner application sits downstream of that absent pharmaceutical program: the CJC-1295 + Ipamorelin stack. The rationale is parallel-pathway engagement — CJC-1295 supplying tonic GHRH-receptor stimulus on somatotrophs while Ipamorelin contributes a clean ghrelin-receptor (GHS-R1a) pulse on top, producing a stronger combined GH response than either alone in animal pharmacology. The GH axis dossier walks the receptor stacking and the GH-secretagogue discontinuation playbook covers the cycling logic. The combination is widely used and rarely studied at the RCT level; no large randomized trial has tested the specific stack for the recomposition outcomes biohackers most care about. The recent Mendias and Awan 2026 Sports Medicine review places CJC-1295 explicitly within the "unapproved gray-market" framing alongside ipamorelin, BPC-157, GHK-Cu, MOTS-C, and TB-500, and flags the social-media-amplified placebo channel as a credible-journal concern for the broader category. The choice between the DAC and non-DAC forms is consequential, not cosmetic: the DAC variant produces sustained tonic IGF-1 elevation over weeks, while non-DAC Modified GRF (1-29) is used for pulse-timed per-injection dosing more akin to the sermorelin pharmacological window.
The honest framing has three parts. Regulatory status is research-only with no FDA approval and no active sponsor-led development program. The human evidence base is the small Teichman Phase 1 cohort — pharmacokinetic and pharmacodynamic in scope, not powered for efficacy or for uncommon adverse events. Everything else — receptor pharmacology, pulse-preservation mechanism, body-composition extrapolation — rests on rodent work, single-dose human PK studies, and class-level inference from GHRH-axis biology. Treat the Jetté-Teichman-Ionescu chronology as the load-bearing primary literature; treat the stacking, dosing, and chronic-use claims as practitioner extrapolation that the development program itself was designed but never completed to test.
Each entry below is graded on the four-tier evidence scale (peer-primary → practitioner) and carries an independent strength label that captures how robustly the source supports the claim it backs on this page.
- Tier 1 · Peer primarymoderatePulsatile Secretion of Growth Hormone (GH) Persists during Continuous Stimulation by CJC-1295, a Long-Acting GH-Releasing Hormone Analog
Ionescu M, Frohman LA · 2006 · Journal of Clinical Endocrinology & Metabolism
- Tier 1 · Peer primarystrongProlonged 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, et al. · 2006 · Journal of Clinical Endocrinology & Metabolism
- Tier 2 · Peer secondarymoderateSafety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries and Athletic Performance
Mendias CL, Awan TM · 2026 · Sports Medicine
- Tier 2 · Peer secondarystrongSarcopenia: revised European consensus on definition and diagnosis
Cruz-Jentoft AJ, Bahat G, Bauer J, et al. · 2019 · Age and Ageing
- Tier 2 · Peer secondarystrongHuman Growth Hormone-Releasing Factor (hGRF)1-29-Albumin Bioconjugates Activate the GRF Receptor on the Anterior Pituitary in Rats: Identification of CJC-1295 as a Long-Lasting GRF Analog
Jetté L, Léger R, Thibaudeau K, et al. · 2005 · Endocrinology
Goal-oriented comparisons and mechanism deep-dives that cover CJC-1295. Decision guides compare the realistic options for a goal (peptide / drug / lifestyle); mechanism dossiers walk the pathway in depth.
Decision guides all guides →
Starting point
Biomarker monitoring guide for peptide users
Read
Discontinuation playbook
Coming off GH-secretagogue stacks (Ipamorelin / CJC-1295 / MK-677) — what to expect and how to taper
Read
Starting point
Compounding pharmacy regulatory landscape
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Starting point
DEA scheduling and criminal-law peptide landscape
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Decision guide
Fat loss — peptide, drug, and lifestyle options compared
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Starting point
IGF-1 lab platform reference range divergence
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Decision guide
Muscle preservation — peptide, drug, and lifestyle options compared
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Starting point
Pediatric peptide use review: approved, off-label, and the gray-market adolescent question
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Starting point
Peptide allergens and excipients reference
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Starting point
Peptide bioavailability comparison reference
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Peptide cold-chain logistics and travel reference
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Starting point
Peptide dose conversion math reference
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Starting point
Peptide dosing in hepatic impairment: a reference
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Starting point
Peptide drug-drug interactions reference
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Starting point
Peptide injection technique: a technical reference
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Starting point
Peptide manufacturing technical reference
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Starting point
Peptide nomenclature and sequence notation reference
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Starting point
Peptide pharmacokinetics matrix
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Starting point
Peptide receptor pharmacology atlas
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Starting point
Peptide storage and stability technical reference
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Starting point
Peptide time-to-effect reference
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Starting point
Pregnancy and lactation peptide safety registry
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Decision guide
Recovery and training adaptation — peptide, supplement, and lifestyle options compared
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Decision guide
Sleep quality — peptide, drug, and lifestyle options compared
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Starting point
Veterinary peptide literature: what animal clinical evidence does and doesn't tell us
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Starting point
WADA prohibited-status registry: peptides and competitive sport
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Mechanism dossiers
acromegaly
Acromegaly and peptides — when the GH-axis pharmacology this site covers extensively becomes the disease, not the desired effect
Read
HPG-axis-modulation
Andropause — late-onset hypogonadism, traditional TRT, and the HPG-axis-preserving peptide alternatives
Read
bone-formation
Osteoporosis and peptides — what the literature actually supports for low bone density and fragility fracture
Read
aging-musculoskeletal
Sarcopenia and peptides — what the evidence actually supports for age-related muscle loss
Read
GH-secretion
The growth-hormone axis
Read
visceral-adiposity-reduction
Visceral adiposity and peptides — what the literature actually supports for the deep-fat depot
Read
Editorially synthesized protocols below — derived from published RCTs and practitioner case-series, each citing its source. The full registry view (all editorial patterns, all community-reported cycles, and member-logged cycles with paired biomarker deltas and adverse-event incidence aggregated at k≥5) is published to members.
- Editorial protocols
- 2
- Community-reported cycles
- 1
- Member-logged cycles
- 0
- Editorial
01·Editorial protocol
Sustained GH pulse and IGF-1 elevation (DAC variant)
Protocol
2.0000 mg·weekly·subq
Outcome
4 / 5 synthesized rating
Provenance: Editorial pattern from the Teichman 2006 JCEM Phase 1 trial of CJC-1295 with DAC. The protocol approximates the practitioner weekly-DAC dosing convention; the trial measured GH and IGF-1 trajectories directly. Outcome rating reflects the PK/PD primary endpoints — downstream body-composition or recovery claims are practitioner extrapolation, not Teichman-trial findings. · Source - Editorial
02·Editorial protocol
Pulse-preserved GH trough and IGF-1 raise (single-dose mechanism protocol)
Protocol
75.0000 mcg·single dose (60–90 μg/kg)·subq
Outcome
3 / 5 synthesized rating
Provenance: Editorial pattern from the Ionescu-Frohman 2006 JCEM single-dose mechanism trial. The protocol is the weight-based single-dose escalation the paper tested directly; dose amount is the midpoint of the two tested arms. Outcome rating reflects the trial primary measurements with the small-N and single-window caveats; this is a mechanism-paper pattern, distinct from the weekly maintenance protocol drawn from Teichman 2006. · Source
→·See the full registry
Members see 2 editorial protocols, 1 community-reported cycle, 0 consented member cycles, paired biomarker delta aggregations, and adverse-event incidence by class — all for CJC-1295.
Reported adverse events in the published Phase I program were mild — injection-site reactions, transient flushing, occasional headache. The class-level cancer caution that applies to any IGF-1-elevating intervention applies here with extra weight given the duration and amplitude of the IGF-1 elevation produced by the DAC variant. Fluid retention, mild glycemic shift, and carpal-tunnel-type symptoms are documented for sustained GH-axis activation in the broader GH-replacement literature and are theoretical concerns at higher CJC-1295 doses. The original sponsor encountered a fatal cardiovascular event during a hypertension subindication trial that contributed to development being paused; the event was not directly attributed to CJC-1295 but is part of the safety record any honest reading of the file should acknowledge.
Contraindications
- Active or past cancer (sustained IGF-1 elevation; mitogenic interaction with many tumor types)
- Pregnancy or breastfeeding (no human data)
- Active proliferative retinopathy or other GH/IGF-1-sensitive ophthalmic disease
- Significant cardiovascular disease without specialist oversight (given the historical safety event in the development program)
- Hypopituitarism or other GH-axis disease without endocrinologist oversight
- Patients under 21 (developing GH/IGF-1 axis; safety not established)
- Athletes in WADA-tested competition (prohibited substance)
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