Select Strength — 10mg
For in vitro laboratory research use only. Not for human consumption, diagnostic, or therapeutic use.
Research Data
Mechanisms of Action
Data presented from peer-reviewed in vitro studies. All findings are laboratory observations only.
CJC-1295 activates GHRH-R (the synthesis/release signal), while Ipamorelin activates GHSR-1a (the amplification signal that simultaneously inhibits somatostatin). This dual-pathway activation produces synergistic GH release.
Ipamorelin's GHSR-1a selectivity produces GH stimulation without the cortisol, prolactin, or ACTH elevation associated with other GHRP compounds — making it the preferred GHRP for research requiring isolated GH axis effects.
The amplified GH pulses produced by the stack drive proportionally greater hepatic IGF-1 production via JAK2-STAT5, activating downstream anabolic signalling pathways in muscle, bone, and connective tissue cell cultures.
CJC-1295 (GHRH-R agonist) and Ipamorelin (GHSR-1a agonist) activate GH release through independent receptor systems. Combined, they produce a synergistic GH pulse significantly greater than either compound alone.
Analytical Data
| Specification | Value |
|---|---|
| CAS Number | 863288-34-0 / 170851-70-4 |
| Molecular Formula | C₁₄₉H₂₄₄N₄₂O₄₂S / C₃₈H₄₉N₉O₅ |
| Molecular Weight | 3367.90 / 711.86 g/mol |
| Purity (HPLC) | 99.1% |
| Appearance | White lyophilised powder (dual-vial kit) |
| Solubility | Both: Soluble in water |
| Storage | −20°C long-term / 2–8°C short-term (store vials separately) |
| Shelf Life | 24 months from production date |
| Research Grade | Yes — For In Vitro Use Only |
What Research Has Shown
Comparative In Vitro Pituitary Cell Studies
Combined GH Release vs. Untreated Control
Comparative Activity Profile
In Vitro Safety Data
Both components have clean preclinical safety profiles. Ipamorelin is considered the most selective GHRP available — no cortisol, prolactin, or off-target receptor binding.
Observed Adverse Indicators
Cytotoxicity (either compound)
NoneCortisol or prolactin elevation
NoneSynergistic GH axis activation
ExpectedOff-target receptor binding
None⚠️ Theoretical Concern
The synergistic combination produces substantially greater GH release than either compound alone. Researchers should account for this amplified downstream IGF-1 axis activity in experimental designs.
Researcher Reference
CJC-1295 (No DAC) activates the GHRH receptor on pituitary somatotrophs — this is the "accelerator" signal for GH synthesis and release. Ipamorelin activates the ghrelin receptor (GHSR-1a) on the same cells — this is the "amplifier" signal that simultaneously inhibits somatostatin (the GH inhibitory hormone). Together, one compound pushes GH release while the other removes the brake, producing a synergistic pulse greater than either alone.
Among all GHRP compounds (GHRP-2, GHRP-6, Hexarelin, Ipamorelin), Ipamorelin has the most selective receptor binding profile. GHRP-2 and GHRP-6 elevate cortisol and prolactin alongside GH. Hexarelin causes cardiac receptor binding. Ipamorelin's GHSR-1a selectivity produces GH elevation with no cortisol, prolactin, or significant off-target receptor binding in published models.
In published research protocols, CJC-1295 and Ipamorelin are typically reconstituted separately and can be drawn into the same syringe immediately prior to experimental use, as they are compatible in aqueous solution. Do not pre-mix and store combined solutions.
Published in vitro pituitary cell data show GH pulse amplitudes of 5–6× above baseline with the combination, compared to 2.8–3× for individual compounds. Downstream IGF-1 elevation is proportional to GH pulse amplitude and duration.
Peer-Reviewed Literature
All citations refer to published peer-reviewed in vitro research. Data presented for scientific reference only. No claims made regarding human therapeutic use.
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