CJC-1295

10mg Vial

10 July 2026Updated 29 August 2026

CJC-1295

Overview Research0 Mechanism Protocols Safety

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Full range of benefits for CJC-1295

Stimulates endogenous pulsatile growth hormone release

Sustains elevated GH levels via prolonged DAC formulation

Increases circulating IGF-1 concentrations

May support increases in lean body mass

May promote reduction in fat mass through enhanced lipolysis

May enhance protein synthesis and nitrogen retention

Associated with markers of improved bone formation/density

May improve exercise recovery and soft tissue repair

May improve sleep quality and sleep architecture in some studies

Enables less frequent dosing compared with short‑acting GHRH analogs

This peptide's combination-safety and interaction data below always stays visible, regardless of membership.

Warning

Important information. The data compiled from scientific literature is provided for educational purposes. Dosage ranges reflect what is reported in studies and do not constitute a recommendation, prescription, or usage guidance. Health decisions should always be made with a qualified professional.

Peptide Interactions

// 13 known interactions

Synergistic(3)Compatible(3)Monitor(4)Avoid(3)

Generally well-tolerated alongside this peptide

Vitamin D

No direct pharmacologic interaction; vitamin D supplementation is generally compatible and may support bone and musculoskeletal outcomes during GH-axis therapy.

Omega-3 fatty acids

Generally neutral co-administration with no known adverse pharmacologic interaction with CJC-1295 and no requirement for special adjustments.

Statins

Statin therapy is typically compatible with CJC-1295, although clinicians should interpret lipid changes in the context of GH/IGF‑1 effects.

All interaction categories

Synergistic (3)

GHRP-6: A ghrelin receptor agonist that when combined with a GHRH analogue like CJC-1295 produces synergistic increases in the amplitude and frequency of growth hormone (GH) secretion.
GHRP-2: Another growth hormone secretagogue that acts via the ghrelin receptor and, when co-administered with CJC-1295, potentiates GH pulses and IGF‑1 responses.
Ipamorelin: A selective GH secretagogue that synergizes with GHRH analogues to augment GH release with relatively lower effects on ACTH/cortisol compared with older GHRPs.

Compatible (3)

Vitamin D: No direct pharmacologic interaction; vitamin D supplementation is generally compatible and may support bone and musculoskeletal outcomes during GH-axis therapy.
Omega-3 fatty acids: Generally neutral co-administration with no known adverse pharmacologic interaction with CJC-1295 and no requirement for special adjustments.
Statins: Statin therapy is typically compatible with CJC-1295, although clinicians should interpret lipid changes in the context of GH/IGF‑1 effects.

Monitor (4)

Insulin and oral hypoglycaemic agents (e.g., insulin, metformin, sulfonylureas): CJC-1295 increases GH and IGF‑1 which can reduce insulin sensitivity and alter glycaemic control, so blood glucose and antidiabetic dosing should be monitored and adjusted as needed.
Levothyroxine (thyroid hormone replacement): Manipulation of the GH axis can alter peripheral thyroid hormone metabolism and unmask or change requirements for thyroid replacement, so TSH/free T4 should be monitored and doses adjusted accordingly.
Systemic glucocorticoids (e.g., prednisone): Glucocorticoids antagonize GH action and both affect glucose metabolism, so adrenal status, clinical response and glycaemia require monitoring when used together.
Recombinant human growth hormone (rhGH): Concomitant rhGH can produce additive increases in IGF‑1 and risk of GH excess, necessitating monitoring of IGF‑1, glucose homeostasis and clinical signs to guide dosing.

Avoid (3)

IGF‑1 analogs (mecasermin): Combining CJC-1295 with exogenous IGF‑1 analogs may cause excessive growth factor signalling and increase the risk of hypoglycaemia and other adverse effects, so clinician risk–benefit assessment is required.
Active malignancy or concurrent oncology therapies: Activation of the GH/IGF‑1 axis may theoretically stimulate tumour growth or interfere with cancer treatments, so use in patients with active or recent malignancy requires oncology consultation and caution.
Oral estrogen therapy (e.g., ethinyl estradiol, oral HRT): Oral estrogens blunt the hepatic IGF‑1 response to GH stimulation and can alter clinical efficacy of GH secretagogues, so clinicians should evaluate hormone status and consider route/dosing adjustments.