Identity a synthetic 44-amino-acid analog of human GHRH (the full-length 44-aa sequence) carrying an N-terminal trans-3-hexenoic acid (hexenoyl) modification that resists DPP-4/enzymatic degradation. Developed by Theratechnologies (Canada). At 44 aa it sits at the upper boundary of the "peptide" range (endogenous GHRH is also 44 aa), and the FDA now regulates it as a biologic (BLA). (CJC-1295 stabilises the shorter 1-29 fragment instead.) ## Development & history - Theratechnologies developed TH9507 as a stabilized GHRH that survives systemic proteases long enough to reach the pituitary.
- Pivotal Phase 3 RCT — Falutz et al., N Engl J Med 2007 — established efficacy in HIV-associated lipodystrophy.
- FDA approval November 2010 as Egrifta, for reduction of excess abdominal (visceral) fat in HIV-infected adults with lipodystrophy — the first and only drug specifically approved for that condition, and the only FDA-approved GHRH analog.
- Reformulated as Egrifta SV (2019) and again as Egrifta WR / F8 (2025) — approvals that keep it a current, actively-marketed medicine (unlike Sermorelin's withdrawn Geref). ## Mechanism (as proposed) a GHRH-receptor agonist on pituitary somatotrophs → pulsatile GH release → hepatic IGF-1 → GH/IGF-1 drive lipolysis preferentially in visceral fat (which expresses more GH receptors than subcutaneous fat), giving the visceral-selective effect documented in the trials. Its short half-life (~26–38 min) preserves the body's natural pulsatile GH rhythm — unlike the sustained "GH bleed" of CJC-1295-DAC.