Research Comparison

CJC-1295 vs IGF-1 DES

CJC-1295 (GHRH analog (long-acting, with Drug Affinity Complex / DAC)) and IGF-1 DES (IGF-1 analog (truncated des(1-3) IGF-1 variant)) are documented as co-studied in the PeptiDex library. This page puts the two entries side by side on class, molecular weight, half-life, origin, mechanism and studied research areas — every value taken from the entry it belongs to.

For research and educational purposes only. This page places two documented library entries next to each other. It is not medical advice, it does not rank one compound above the other or claim either is more effective, and it is not a usage, dosing, or combination recommendation.

Why these two are co-studied

Cross-referenced for research context — not a usage or combination recommendation.

From the IGF-1 DES entryGHRH-driven GH/IGF-1 elevation is studied alongside a direct IGF-1 receptor agonist.

At a glance

Side-by-side reference for CJC-1295 and IGF-1 DES on compound class, research category, length, molecular weight, half-life and origin.
AttributeCJC-1295IGF-1 DES
Compound classGHRH analog (long-acting, with Drug Affinity Complex / DAC)IGF-1 analog (truncated des(1-3) IGF-1 variant)
Research categoryGrowth & GH-AxisGrowth & GH-Axis
Length (amino acids)30 amino acids67 amino acids
Molecular weightApproximately 3647 g/mol (with DAC linker)Approximately 7372 g/mol
Half-lifeSubstantially extended vs native GHRH; reported on the order of days (approximately 6-8 days) due to albumin binding via DACVery short in circulation (minutes), reflecting IGF-1's rapid clearance when not bound to IGFBPs
OriginCJC-1295 (with DAC) is a synthetic long-acting GHRH analog based on a modified GHRH(1-29) sequence, developed by ConjuChem. It incorporates a Drug Affinity Complex (DAC) that binds serum albumin to greatly extend circulating half-life.IGF-1 DES (DES(1-3)IGF-1) is a naturally occurring and synthetically produced truncated variant of insulin-like growth factor 1, lacking the first three N-terminal amino acids (Gly-Pro-Glu) of the 70-residue mature IGF-1.

“Not documented” means the PeptiDex entry records no value for that field. Nothing on this page is estimated, and no figure is carried over from one compound to the other.

How CJC-1295 works

CJC-1295 is a GHRH-receptor agonist that stimulates pulsatile GH secretion from the pituitary. Its GHRH(1-29) backbone carries stabilizing amino-acid substitutions (e.g. at positions 2, 8, 15, 27) that resist DPP-4 degradation, and the DAC group forms a covalent bond with albumin, dramatically prolonging its action. This produces a sustained elevation of GH and IGF-1 rather than sharp discrete pulses.

How IGF-1 DES works

IGF-1 DES is an agonist of the IGF-1 receptor, activating the same anabolic and proliferative signaling as native IGF-1. The removal of the N-terminal tripeptide markedly reduces its binding to IGF-binding proteins (IGFBPs), so a larger fraction remains free and it is reported to be more potent locally than full-length IGF-1. Its reduced IGFBP binding also contributes to a shorter systemic half-life.

Mechanistic descriptions reflect published research-literature understanding and are quoted from each compound's own entry. Much peptide research is preclinical (in-vitro or animal-model); mechanism in humans may differ and is not established for many compounds.

Where each one appears in the literature

The research contexts each entry documents. Listing a research area is not a claim of efficacy or a therapeutic indication, and the two lists are not scored against each other.

CJC-1295

Sustained stimulation of the GH/IGF-1 axis (early-phase clinical and preclinical)Body-composition researchInvestigation of long-acting GHRH analog pharmacokineticsStudies combining GHRH analogs with GHRPs

IGF-1 DES

IGF-1 receptor signaling and tissue growth research (preclinical)Studies on reduced IGFBP binding and enhanced local potencyCell-proliferation and myogenesis researchComparative IGF-1 analog pharmacology

What sets each apart

CJC-1295

The DAC version's albumin binding gives it a far longer half-life (days) than the no-DAC 'Mod GRF 1-29' (minutes), making it the long-acting member of the CJC-1295 family.

IGF-1 DES

IGF-1 DES differs from native and LR3 IGF-1 by its N-terminal truncation (des 1-3), which lowers IGFBP binding and increases local potency but with a short systemic half-life, unlike the long-acting LR3 variant.

Frequently asked questions

What is CJC-1295 (with DAC)?

CJC-1295 is a synthetic long-acting analog of GHRH(1-29). This slug refers to the DAC (Drug Affinity Complex) version, which carries a maleimidopropionic acid linker that covalently binds serum albumin after injection, dramatically extending its circulating half-life to several days.

What is the difference between CJC-1295 with DAC and without DAC?

Both share the same modified 29-amino-acid GHRH core with substitutions that resist DPP-IV cleavage. The DAC version adds an albumin-binding complex giving a half-life of roughly 6-8 days, producing a sustained 'GH bleed,' whereas the no-DAC version (Mod GRF 1-29) has only a ~30 minute half-life and produces discrete pulses.

What does the long half-life mean for research design?

Because CJC-1295 with DAC persists for days, it raises the baseline of GHRH tone rather than producing sharp pulses. In research this is described as elevating overall GH and IGF-1 output; studies often examine how this sustained tone interacts with pulsatile GHRP stimulation.

What is IGF-1 DES?

IGF-1 DES, or DES(1-3) IGF-1, is a truncated analog of insulin-like growth factor-1 that lacks the first three N-terminal amino acids (Gly-Pro-Glu), leaving a 67-amino-acid peptide. It is an IGF-1 receptor agonist studied for its markedly higher per-unit potency than native IGF-1.

How does IGF-1 DES differ from IGF-1 LR3?

Both are IGF-1 analogs with reduced binding to IGF-binding proteins, but they differ sharply in duration: IGF-1 DES has a very short half-life (~20-30 minutes) and is studied for localized, short-acting effects, while IGF-1 LR3 has an extended half-life (~20-30 hours) supporting systemic, less-frequent dosing.

Why is IGF-1 DES more potent than native IGF-1?

Removing the first three N-terminal residues sharply reduces the peptide's affinity for IGF-binding proteins (IGFBPs), leaving more free peptide available to activate the IGF-1 receptor. The research literature reports this yields roughly a 10-fold increase in in-vivo potency per unit dose.

Answers are the ones published on each compound's own PeptiDex entry. They are educational summaries of research-literature context and are not medical advice.

Continue exploring