What Is CJC-1295? GHRH Analogue Mechanism & Research Applications

TL;DR: CJC-1295 (also known as DAC:GRF) is a 30-amino acid synthetic analogue of growth hormone–releasing hormone (GHRH) that incorporates Drug Affinity Complex (DAC) technology — a maleimide moiety that forms a stable covalent thioether bond with cysteine-34 on circulating albumin. This covalent albumin linkage extends the plasma half-life from minutes (native GHRH) to approximately 6–8 days, making CJC-1295 the dominant long-acting GHRH tool compound in growth hormone axis research.

What Is CJC-1295?

CJC-1295 is a modified analogue of human GHRH(1-29)-NH2, the physiologically active N-terminal fragment of growth hormone–releasing hormone. Native GHRH(1-29) has a plasma half-life of less than 10 minutes due to DPP-4 cleavage at the Ala2-Val3 bond and rapid renal clearance of the resulting fragments.

CJC-1295 addresses this limitation through two types of structural modification. First, substitutions at positions 2, 8, 15, and 27 (Ala2→Aib, Cys8→Abu, Asn15→Gln, and Lys27→Arg+maleimide) provide DPP-4 resistance and introduce the reactive DAC maleimide group. Second, the maleimide reacts spontaneously with the thiol of Cys-34 on serum albumin in a Michael addition, forming a stable covalent thioether linkage. This permanent albumin conjugation dramatically extends half-life to approximately 6–8 days in humans and rodents.

The molecular weight of CJC-1295 free acid is 3647.15 Da, and its CAS number is 863288-34-0 (with DAC). The compound is supplied as a lyophilized white powder and is reconstituted in sterile water or bacteriostatic water for in vitro and in vivo studies.

Mechanism of Action

CJC-1295 acts as a full agonist at the GHRH receptor (GHRHR), a class B GPCR expressed primarily on somatotroph cells in the anterior pituitary gland. GHRHR activation couples to Gαs, increasing intracellular cAMP via adenylate cyclase and activating PKA, which promotes GH gene transcription and exocytosis.

Pituitary Somatotroph Stimulation

In anterior pituitary somatotroph cells, GHRHR activation by CJC-1295 drives cAMP-PKA signaling that phosphorylates CREB, upregulates GH1 gene transcription, and triggers GH release from storage granules. CJC-1295’s extended half-life sustains this stimulation, producing prolonged elevated GH plasma levels versus the pulsatile profile of native GHRH — a pharmacodynamic distinction important for experimental design in GH axis studies.

IGF-1 Axis Downstream Effects

Sustained GH release from CJC-1295 stimulates hepatic IGF-1 (insulin-like growth factor 1) synthesis via JAK2-STAT5b signaling. IGF-1 in turn drives anabolic effects in bone, muscle, and adipose tissue. In growth hormone research, measuring GH and IGF-1 plasma levels alongside body composition endpoints is standard practice when using CJC-1295 to characterize the GH/IGF-1 axis response to extended GHRHR stimulation.

Somatostatin Feedback Interaction

GH secretion is normally inhibited by somatostatin (SRIF) from hypothalamic neurons and paracrine sources. CJC-1295’s sustained GHRHR activation creates a continuous pro-GH signal that competes with somatostatin tone. Researchers studying CJC-1295 in the context of normal GH pulsatility should be aware that the compound shifts the GH secretory pattern from pulsatile to tonic — a meaningful distinction for endpoints like GH receptor desensitization and tissue-specific GH signaling.

CJC-1295 Research Applications

CJC-1295 is used as a long-acting GHRH tool compound in studies of the hypothalamic-pituitary-somatotropic (HPS) axis — particularly when chronic, sustained GH stimulation is experimentally desirable rather than the pulsatile pattern produced by short-acting GHRH peptides.

For procurement details, see the CJC-1295 + Ipamorelin Stack product page.

CJC-1295 With DAC vs. Without DAC

A common source of confusion in growth hormone research is the distinction between CJC-1295 with DAC (the compound described in this guide) and CJC-1295 without DAC (also called Modified GRF 1-29 or Mod GRF 1-29). Both are modified GHRH(1-29) analogues with DPP-4-resistant substitutions. The key difference is the maleimide DAC group.

CJC-1295 with DAC: covalent albumin binding via maleimide → ~6–8 day half-life → tonic, sustained GH elevation. Appropriate for chronic stimulation studies where stable steady-state GH elevation is required.

CJC-1295 without DAC (Mod GRF): no albumin binding → ~30-minute half-life → pulsatile GH stimulation mimicking native GHRH pulses. Appropriate for studies of normal GH pulsatility. Researchers should confirm which variant they are using and select the appropriate form based on whether their study requires tonic or pulsatile GH stimulation.

Key Takeaways

  1. CJC-1295 is a GHRH(1-29) analogue with DAC (Drug Affinity Complex) technology — a maleimide group that covalently bonds to albumin Cys-34 in vivo, extending half-life to ~6–8 days.
  2. Mechanism: full agonism at pituitary GHRHR (Gαs/cAMP/PKA), driving somatotroph GH synthesis and release, followed by hepatic IGF-1 production via JAK2/STAT5b.
  3. CJC-1295 produces tonic GH elevation rather than the pulsatile profile of native GHRH — an important experimental consideration for receptor desensitization and tissue-specific GH signaling studies.
  4. Often co-used with Ipamorelin in dual GHRH+GHRP protocols targeting both GHRHR and the ghrelin receptor simultaneously for synergistic GH secretion.
  5. Distinct from Mod GRF 1-29 (CJC-1295 without DAC), which lacks albumin binding and produces a short-acting pulsatile GH response appropriate for pulsatility studies.

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Published by Bulk Peptides, a US-based wholesale supplier of research-grade peptides. All products are for in vitro laboratory research use only (RUO) — not for human or veterinary use. Last reviewed August 2026.