Synthetic analog of growth hormone releasing hormone whose short half-life leaves GH secretion pulsatile, in patterns resembling natural physiology. Where CJC-1295 with DAC elevates GH continuously, this version keeps the natural pulsatility.
Growth hormone releasing hormone, modified with albumin-binding technology so that duration extends. Binding of the DAC to albumin lengthens half-life and holds GHRH receptor stimulation continuous.
Polypeptide hormone of 191 amino acids, also called somatropin, with FDA approval covering growth hormone deficiency in children and adults, HIV-associated wasting, and other conditions. Anabolic effects arrive by two routes, direct and indirect through IGF-1.
Analog of insulin-like growth factor-1, truncated: three N-terminal amino acids are absent from the start of the chain. Binding to IGF binding proteins (IGFBPs) is eliminated by that change, so no part of the peptide is sequestered in circulation and 100% stays bioactive. Potency then runs approximately 10x native IGF-1, against a half-life that is extremely short — 20–30 minutes. The short duration is considered a feature, not a limitation: injection can be placed at a specific site in the target muscle immediately after a workout, so growth stays localized and systemic exposure is reduced.
Selective GHRP that raises natural GH production from the pituitary while disruption of cortisol and prolactin stays minimal. It is known for a clean safety profile and for consistent GH pulses, free of the significant side effects common to other growth hormone releasing peptides.
Analog of human growth hormone-releasing hormone, synthetic, 29 amino acids long. Growth hormone production rises naturally under it while the physiological pulsatile pattern holds. The FDA approved it in 1997 for GH deficiency in children; discontinuation followed in 2008, for manufacturing reasons and not safety concerns.
Synthetic GHRH analog with FDA approval, designed for HIV-associated lipodystrophy. Visceral fat is targeted selectively — clinical trials record 15–20% visceral fat reduction — while subcutaneous fat is preserved.
Soluble form of the activin type IIB receptor (ActRIIB) fused to an IgG1 Fc domain. As a decoy receptor it binds and neutralizes myostatin along with other TGF-beta superfamily members that ordinarily limit muscle growth. Acceleron Pharma developed it for Duchenne muscular dystrophy (DMD) and took it to Phase 2 clinical trials, where vascular side effects — nosebleeds and telangiectasia among them — halted development. A single dose in healthy volunteers produced significant gains in lean mass and drops in fat mass within 29 days.
Synthetic growth hormone secretagogue that prompts the pituitary gland to release growth hormone. Among the GHRP family it ranks with the most potent, 2–3 times as effective as GHRP-6 at stimulating GH release. Its original role was diagnostic, for growth hormone deficiency; the mechanism is mimicry of ghrelin and binding at the GHS-R1a receptor.
Synthetic growth hormone secretagogue that prompts the pituitary gland to release growth hormone. It was among the first GHRPs developed and binds the ghrelin receptor (GHS-R1a). Rather than supply GH directly as an injection would, it raises the body's own GH production while negative feedback mechanisms stay balanced. Appetite stimulation is its noted potent effect.
Among synthetic growth hormone secretagogues, one of the most potent available. Binding at the GHS-R1a receptor of the hypothalamus and pituitary mimics ghrelin and releases GH. With GHRH the effect is synergistic: the GH response comes out greater than the arithmetic sum of the two given separately. Cardioprotective properties unique to it are mediated by the CD36 receptor.
Synthetic 83-amino acid analog of insulin-like growth factor-1, never approved for human use. An N-terminal extension and the R3 substitution cut interaction with binding proteins, so free circulating levels stay elevated and potency runs about 3x that of native IGF-1.
IGF-1 splice variant without pegylation, produced locally in muscle tissue after mechanical stress. Its half-life is very short next to PEG-MGF, so administration must be more frequent, or localized by injection.
IGF-1 variant carrying a PEG attachment, which stretches half-life from minutes into hours. Muscle satellite cells are activated after mechanical stress or injury.