CJC-1295 without DAC, also called Mod-GRF 1-29, is a short-acting GHRH analog studied for growth-hormone-axis signalling in research.
CJC-1295 without DAC, commonly known as Mod-GRF 1-29, is a modified GHRH analog that lacks the albumin-binding drug-affinity complex, resulting in a shorter half-life. It is studied in research related to the growth-hormone axis and GHRH receptor signalling, with a focus on more transient receptor engagement.
GHRH-analog research generally examines effects on growth-hormone pulsatility, downstream IGF-1 signalling, and receptor activity. The non-DAC form is investigated for its shorter action profile, often compared against DAC-modified analogs in preclinical research.
Studied for GHRH receptor effects on growth-hormone-axis activity in research models.
Investigated for shorter, more transient receptor engagement compared to DAC-modified analogs.
Examined for downstream IGF-1 signalling associated with GHRH receptor stimulation in research.
Characterized through assays defining its GHRH receptor agonism and signalling profile.
Bring the vial (10 mg) and bacteriostatic water to room temperature.
Add bacteriostatic water slowly along the glass wall — the volume you add sets the concentration.
Swirl gently (do not shake) until fully clear, then refrigerate at 2–8 °C.
Studied together combining GHRH and GH-secretagogue pathways in growth-axis research models.
Explored in research examining GHRH signalling alongside local IGF-receptor activity.
Links open a PubMed search for the topic. They point to independent literature and are provided for orientation in a research context only.
Also called Mod-GRF 1-29, it is a GHRH analog lacking the drug-affinity complex, giving it a shorter half-life. It is studied for growth-hormone-axis signalling in research.
Without the albumin-binding DAC, it has a shorter circulating time, so it is studied for a more transient action profile compared to CJC-1295 with DAC.
It is studied in the context of GHRH receptor activity, growth-hormone-axis signalling, and downstream IGF-1 pathways within preclinical research models.
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