What is the Hexarelin / CJC-1295 No DAC Blend and what distinguishes it from other GH-axis blends?

This blend pairs Hexarelin — the most potent synthetic GHRP by GH pulse amplitude — with CJC-1295 No DAC (Modified GRF 1-29). Hexarelin signals through GHS-R1a via Gαq/11-PLC-Ca²⁺; CJC-1295 No DAC activates the GHRH receptor via Gs-cAMP-PKA. These independent cascades converge at the somatotroph for synergistic GH release. Additionally, Hexarelin uniquely engages the CD36 scavenger receptor for GH-independent cardioprotection.

What are the molecular profiles of Hexarelin and CJC-1295 No DAC?

Hexarelin: 6 AA (His-D-2-MeTrp-Ala-Trp-D-Phe-Lys-NH₂); CAS 140703-51-1; MW 887.05 g/mol; C47H58N12O6; half-life ~70 min. CJC-1295 No DAC (Mod GRF 1-29): 29 AA; CAS 863288-34-0; MW ~3,367 g/mol; C152H252N44O42; half-life ~30 min; DPP-4 resistant (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷ substitutions).

What clinical and preclinical evidence supports Hexarelin's dual-receptor activity?

Clinical studies document peak GH of 40–80 μg/L after Hexarelin IV (1–2 μg/kg), exceeding GHRP-2 by 20–30%. CD36 cardioprotection was confirmed in GHS-R1a knockout mice, where Hexarelin reduced infarct size by 40–55% solely through CD36 binding (Bhatt et al., 2002). Synergistic GH release with GHRH co-administration is documented in both in vitro pituitary models and in vivo studies.

Why choose CJC-1295 No DAC rather than the DAC variant in a GH blend?

CJC-1295 No DAC's ~30-minute half-life produces pulsatile GH release mirroring physiological GHRH secretion, preserving natural feedback regulation. The DAC variant produces sustained GH elevation that blunts pulsatility and is associated with more joint discomfort and persistent IGF-1 elevation. For pairing with a GHRP, the pulsatile format amplifies natural GH pulses rather than creating continuous supraphysiological elevation.

How should the Hexarelin / CJC-1295 No DAC Blend be stored and reconstituted?

Store lyophilized vial at −20 °C, shielded from UV light. Reconstitute with bacteriostatic water; store at 2–8 °C and use within 28 days. Avoid freeze-thaw cycling. Use amber vials to protect Hexarelin's tryptophan residues from oxidation. Include 4–8 week off-cycle periods in sustained research protocols to mitigate GHS-R1a tachyphylaxis.

Hexarelin / CJC-1295 No DAC Blend

Name: Hexarelin / CJC-1295 No DAC Blend
Brand: Kaiser BioMed
SKU: P-061
Price: 79.00 USD
Availability: InStock

Description

Summary Abstract

Hexarelin / CJC-1295 No DAC Blend (P-061; Hexarelin 7.5 MG + CJC-1295 No DAC 5 MG; 12.5 MG total lyophilized vial) combines the most potent synthetic Growth Hormone Releasing Peptide (GHRP) with a DPP-4-resistant Growth Hormone-Releasing Hormone (GHRH) analog to engage two entirely separate intracellular signaling cascades at the pituitary somatotroph simultaneously. Hexarelin (His-D-2-MeTrp-Ala-Trp-D-Phe-Lys-NH₂; Examorelin; CAS 140703-51-1; MW 887.05 g/mol) activates the ghrelin receptor GHS-R1a via the Gαq/11-PLC-IP3-Ca²⁺ pathway, producing the highest GH pulse amplitude of any synthetic secretagogue documented in human studies. CJC-1295 No DAC (Modified GRF 1-29; Mod GRF; Sermorelin tetrasubstituted; CAS 863288-34-0; MW ~3,367 g/mol) is a 29-amino acid GHRH analog with four stabilizing substitutions (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) that confer DPP-4 resistance while retaining the ~30-minute pulsatile half-life that closely mirrors physiological GHRH secretion; it signals through the GHRH receptor via the Gs-cAMP-PKA pathway. Because these two mechanisms — calcium-dependent (GHRP) and cAMP-dependent (GHRH) — converge at the somatotroph through independent second messenger systems, their co-administration produces a synergistic GH response substantially exceeding either compound alone. Hexarelin further engages the CD36 scavenger receptor on cardiac myocytes, conferring cardioprotective effects independent of GH release — a unique property not shared by any other GHRP in clinical research.

Clinical Research Indications

Pulsatile GH-axis amplification research spans multiple physiological domains:

Growth Hormone Deficiency (GHD) Diagnostic Models: Hexarelin’s potent GHS-R1a agonism has been used as a provocation agent to assess pituitary somatotroph reserve, distinguishing hypothalamic from pituitary GHD; co-administration with a GHRH analog maximizes provocation sensitivity.
Body Composition and Lean Mass: GH and downstream IGF-1 elevation drives lipolysis, muscle protein synthesis, and lean mass accretion; the synergistic GH response from dual-pathway stimulation is hypothesized to amplify these anabolic and lipolytic effects.
Cardioprotection (Hexarelin-Specific, GH-Independent): Hexarelin’s CD36 scavenger receptor engagement on cardiomyocytes activates PI3K/Akt signaling, reducing ischemia-reperfusion injury and apoptosis through a pathway confirmed in GHS-R1a knockout models — unrelated to GH release.
Pulsatile GH Secretion Research: CJC-1295 No DAC’s short (~30-minute) half-life enables pulsatile GH release patterns that more closely resemble physiological secretion compared to long-acting DAC variants, making this blend preferred for research designs requiring natural GH pulse kinetics.

Contraindications

Active Neoplasia: GH and IGF-1 elevation can promote growth of IGF-1R-expressing tumors; use in subjects with active or suspected malignancy requires specialized oversight.
Acromegaly / Elevated Baseline IGF-1: Supra-physiological GH/IGF-1 induction in individuals with pre-existing GH excess may worsen acromegalic features, glucose intolerance, and soft-tissue overgrowth.
Tachyphylaxis Monitoring: Hexarelin undergoes receptor desensitization (GHS-R1a internalization) after 4–8 weeks of continuous use, requiring cycling protocols; research designs should account for diminished GH response amplitude over time.
Cortisol and Prolactin Elevation (Hexarelin-Specific): Unlike ipamorelin, hexarelin stimulates CRH-mediated ACTH/cortisol and dopaminergic prolactin release at higher doses; protocols sensitive to HPA axis perturbation should use lower doses or substitute a more selective GHRP.

Mechanism of Action (MOA)

This blend activates two independent GH-stimulatory pathways at the somatotroph, plus a GH-independent cardioprotective pathway unique to Hexarelin:

Hexarelin — GHS-R1a Agonism (Gαq/11 / Ca²⁺ Pathway)

Hexarelin binds the ghrelin receptor (GHS-R1a) with extremely high affinity (Ki ~0.1–0.3 nM), the highest among synthetic GHRPs. Receptor engagement couples through Gαq/11 → phospholipase C-β (PLCβ) → IP3 → Ca²⁺ release from endoplasmic reticulum stores, driving rapid GH vesicle exocytosis from anterior pituitary somatotrophs. Peak GH concentrations of 40–120 ng/mL have been documented 15–45 minutes post-administration in clinical studies — 20–30% greater than GHRP-2 at equivalent doses. The D-2-methyltryptophan substitution at position 2 confers enhanced binding affinity and proteolytic resistance versus earlier GHRPs.

CJC-1295 No DAC — GHRH-R Agonism (Gs / cAMP / PKA Pathway)

CJC-1295 No DAC (Modified GRF 1-29) binds the GHRH receptor (GHRH-R) — a Class B GPCR on pituitary somatotrophs — and couples through Gs → adenylyl cyclase → cAMP → PKA → CREB phosphorylation and voltage-dependent Ca²⁺ influx to trigger GH exocytosis. Four stabilizing substitutions (D-Ala², Gln⁸, Ala¹⁵, Leu²⁷) confer DPP-4 resistance, extending the effective half-life to ~30 minutes versus ~7 minutes for native GHRH(1-29). Downstream, PKA-driven GH gene transcription (via Pit-1) augments GH biosynthesis in addition to acute secretion.

Synergistic Dual-Pathway Amplification

The Ca²⁺-dependent (GHS-R1a via Hexarelin) and cAMP-dependent (GHRH-R via CJC-1295 No DAC) pathways converge at independent second-messenger cascades within the same somatotroph cell. Research in pituitary models documents a synergistic GH response when both are co-administered — substantially greater than the sum of either alone — because neither pathway desensitizes the other’s receptor. CJC-1295 No DAC additionally counteracts somatostatin-mediated inhibition through its GHRH-R signaling, further amplifying the net GH secretory response to Hexarelin’s direct stimulation.

Hexarelin — CD36 Receptor Agonism: GH-Independent Cardioprotection

Hexarelin binds the CD36 scavenger receptor on cardiac myocytes, macrophages, and endothelial cells at the Asn132–Glu177 domain (Ki ~2.1 nM). CD36 engagement activates the PI3K/Akt pathway, phosphorylating BAD protein to prevent mitochondrial cytochrome c release and apoptosis cascade initiation during ischemic stress. In GHS-R1a knockout mouse studies, hexarelin reduced myocardial infarct size by 40–55% exclusively through this CD36-mediated mechanism. This cardioprotective pathway — unique among all synthetic GHRPs — also reduces TNF-α/IL-6 expression and improves eNOS activity independent of the endocrine GH-IGF-1 axis.

Key Features & Specifications

Pharmacological and structural attributes that define this pulsatile GH-amplification blend:

Hexarelin: Highest GH Pulse Amplitude Among Synthetic GHRPs

Dual-Pathway: Ca²⁺ (GHS-R1a) + cAMP (GHRH-R) — True Synergistic GH Release

CJC-1295 No DAC: Pulsatile ~30-min Half-Life Preserves Natural GH Secretion Pattern

Hexarelin CD36 Cardioprotection — GH-Independent PI3K/Akt Anti-Apoptotic Activity

7.5 MG Hexarelin + 5 MG CJC-1295 No DAC — 12.5 MG Total (P-061)

WADA S2 Prohibited — Suitable for Endocrinology and Cardiovascular Research Only

Chemical Analysis

Property	Specification Reference Data
Component 1 — Hexarelin	Synthetic hexapeptide GHRP; His-D-2-MeTrp-Ala-Trp-D-Phe-Lys-NH₂ (6 AA; C-terminal amide; D-2-methyltryptophan at position 2)
Hexarelin CAS	140703-51-1
Hexarelin Molecular Formula	C₄₇H₅₈N₁₂O₆
Hexarelin Molecular Weight	887.05 g/mol
Hexarelin Synonyms	Examorelin; Hexarelin Acetate; EP 23905
Hexarelin Half-Life	~70 minutes (subcutaneous)
Component 2 — CJC-1295 No DAC	Modified GRF 1-29; 29 AA GHRH analog; Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu-Ser-Arg-NH₂ (4 substitutions: D-Ala², Gln⁸, Ala¹⁵, Leu²⁷)
CJC-1295 No DAC CAS	863288-34-0
CJC-1295 No DAC Molecular Formula	C₁₅₂H₂₅₂N₄₄O₄₂
CJC-1295 No DAC Molecular Weight	~3,367 g/mol
CJC-1295 No DAC Synonyms	Modified GRF 1-29; Mod GRF(1-29); Sermorelin tetrasubstituted; GRF analog
CJC-1295 No DAC Half-Life	~30 minutes (pulsatile; no albumin binding)
Form / Variation	12.5 MG Lyophilized Blend Vial (P-061) — 7.5 MG Hexarelin + 5 MG CJC-1295 No DAC

Storage, Safety, and Handling

Storage Protocol

Store lyophilized powder at −20 °C, protected from light; avoid humidity exposure during storage. Once reconstituted with bacteriostatic water for injection, store the solution at 2–8 °C and use within 28 days; avoid freeze-thaw cycling. CJC-1295 No DAC is relatively stable in aqueous solution; Hexarelin’s aromatic residues (Trp, D-2-MeTrp) are susceptible to oxidation under UV exposure — keep all solutions amber-shielded.

Handling & Compliance

Handle with standard laboratory PPE (nitrile gloves, safety glasses) and aseptic technique. Both components are potent GH-axis activators; research protocols should account for cortisol and prolactin co-stimulation from hexarelin at higher doses (not seen with ipamorelin-based blends). Both Hexarelin and CJC-1295 are classified as prohibited substances under WADA S2 Peptide Hormones, Growth Factors, Related Substances and Mimetics. Tachyphylaxis protocols should include off-cycle periods every 4–8 weeks for sustained-response research designs.