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CJC-1295 and Ipamorelin: The GHRH/GHRP Research Stack
May
- CJC-1295 (MOD-GRF 1-29, MW 3367.9 Da) is a 29-residue GHRH analogue with DAC modification enabling extended half-life via albumin binding.
- Ipamorelin (MW 711.9 Da) is a selective pentapeptide GHRP with low side-effect profile relative to earlier GHRP compounds.
- The stack co-activates GHRH receptor (baseline GH stimulation) and GHS-R1a (pulse amplification) at pituitary somatotrophs.
The GHRH/GHRP Co-Activation Research Framework
The pituitary growth hormone axis is regulated by two parallel receptor systems on somatotroph cells: the GHRH receptor (GHRHR, Gs-coupled, drives baseline GH secretion) and the GHS-R1a (ghrelin receptor, Gq-coupled, drives GH pulse amplification). Pharmacological co-activation of both receptor systems is a foundational research approach for investigating combined GH-axis pharmacology — and the CJC-1295 + Ipamorelin Blend is the canonical research-tool formulation for this co-activation approach. Available at Advanced Peptide Science within the Growth Hormone & Performance category.
Research Background
CJC-1295 (also called MOD-GRF 1-29) is a 29-residue GHRH analogue developed as an extended-half-life modification of the GHRH 1-29 sequence. The DAC (drug-affinity complex) modification enables non-covalent albumin binding, extending preclinical half-life substantially relative to unmodified GHRH analogues such as Sermorelin. Ipamorelin is a selective pentapeptide GHRP designed to provide GHS-R1a agonism with substantially reduced cortisol and prolactin stimulation relative to earlier GHRPs including GHRP-6 and GHRP-2. The combined CJC + Ipamorelin formulation thus pairs an optimised GHRH analogue with an optimised GHRP analogue.
Mechanism of Action
Mechanism research investigates simultaneous activation of two distinct pituitary somatotroph receptor systems. The CJC-1295 component activates GHRH receptor (GHRHR), a class B GPCR coupled to Gs/cAMP signalling driving GH gene transcription and baseline GH secretion. The Ipamorelin component activates GHS-R1a, a Gq-coupled GPCR driving PLC/IP3 signalling and amplifying GH pulse magnitude. The co-activation hypothesis is that combined receptor engagement yields synergistic GH-axis stimulation greater than either receptor system alone — a research question accessible through comparative experiments using mono- vs co-administration designs.
Key Research Findings
Baseline vs Pulse: Two Distinct Contributions
The GHRH-receptor and GHS-R1a contribute distinctly to GH-axis output. GHRH-receptor signalling drives baseline GH gene transcription and provides the foundation of GH secretory capacity. GHS-R1a signalling amplifies the magnitude of GH secretory pulses without independently driving baseline secretion. Combined co-activation engages both regulatory dimensions simultaneously.
Ipamorelin Receptor Selectivity
The defining research advantage of Ipamorelin within the GHRP class is its selective GHS-R1a agonism with substantially reduced engagement of receptor systems driving cortisol and prolactin release. This selectivity makes Ipamorelin a research-tool for isolated GHRP-pathway investigation without confounding stress-hormone responses present with earlier GHRP compounds.
DAC Modification: Extended Half-Life
The DAC modification on CJC-1295 provides non-covalent albumin binding, extending preclinical half-life from minutes (unmodified GHRH 1-29) to substantially longer time windows. This makes the compound suitable for research designs requiring sustained GHRH-receptor occupancy.
Research Applications and Triple Blend
Extended research applications include the GH Blend (CJC-1295 + Ipamorelin + GHRP-6) — a three-compound formulation adding the non-selective GHRP-6 to the selective Ipamorelin profile, enabling research into selective vs non-selective GHRP co-administration alongside GHRH activation. Comparative research is supported by the full Growth Hormone & Performance category stocking Sermorelin (short-acting GHRH 1-29), Tesamorelin (longer-chain GHRH 1-44 analogue), Hexarelin (GHRP with CD36 binding), and IGF-1 LR3 (downstream IGF-1 axis).
Research Specifications
| CJC-1295 (MOD-GRF 1-29) | 3367.9 Da, 29-residue GHRH analogue, DAC modification, GHRH receptor agonist |
| Ipamorelin | 711.9 Da, selective pentapeptide GHRP, GHS-R1a agonist (low side-effect profile) |
| Combined Mechanism | GHRH receptor (Gs/cAMP) + GHS-R1a (Gq/PLC) co-activation |
| Format | Lyophilized powder blend in sterile vial |
| Purity | ≥ 99% (HPLC verified) per compound |
| Storage | -20 °C, protect from light |
Frequently Asked Questions
Why combine CJC-1295 with Ipamorelin?
CJC-1295 activates the GHRH receptor (baseline GH stimulation, Gs/cAMP signalling); Ipamorelin activates GHS-R1a (GH pulse amplification, Gq/PLC signalling). The two receptors are on the same pituitary somatotroph cells but engage different downstream pathways — co-activation enables research into combined GH-axis pharmacology.
What does DAC mean in CJC-1295?
DAC (drug-affinity complex) refers to the modification that enables non-covalent albumin binding, extending the preclinical half-life of the underlying GHRH 1-29 sequence from minutes to substantially longer time windows.
Why is Ipamorelin selective?
Ipamorelin is engineered for selective GHS-R1a agonism with substantially reduced engagement of receptor systems driving cortisol and prolactin release — a major advantage over earlier non-selective GHRPs including GHRP-6 and GHRP-2.
Is this stack approved for human use?
Advanced Peptide Science supplies the CJC-1295 + Ipamorelin Blend exclusively for in vitro and in vivo scientific research. Not for human consumption. Research use only.
For Research Use Only. Not for human consumption. Not intended to diagnose, treat, cure, or prevent any disease.
