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Cjc-1295 Structure And Mechanism — Quick Reference

By Editorial Desk · published 2026-05-13 · last reviewed 2026-06-03 · Guide

A practical reference on GHRH analog: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.

Reviewed 2026-06-03. Anything still debated is marked as such rather than presented as settled.

CJC-1295 Structure And Mechanism

CJC-1295 is a synthetic analogue of growth hormone-releasing hormone, built on the 29-amino-acid GHRH(1-29) fragment. Four substitutions distinguish it from the natural sequence: D-alanine at position 2, glutamine at position 8, alanine at position 15, and leucine at position 27. These changes reduce enzymatic cleavage and extend the peptide's persistence in circulation. The compound is discussed in two forms, one carrying a drug affinity complex and one without it.

The drug affinity complex is a maleimidopropionic acid group attached to a lysine side chain. It reacts with the free thiol of cysteine-34 on circulating albumin, forming a covalent bond. This conjugation keeps the peptide in the bloodstream and shields it from rapid renal filtration and proteolysis. Reported circulation half-lives for the albumin-bound form fall in the range of roughly six to nine days in early human studies.

Binding to GHRH receptors on pituitary somatotroph cells triggers cyclic AMP signaling and stimulates growth hormone synthesis and release. Because the peptide acts upstream of the pituitary, effects are mediated through endogenous growth hormone rather than direct receptor activation in peripheral tissues. Increases in insulin-like growth factor 1 are generally described as a downstream consequence. Most published human exposure data come from small early-stage studies, and the clinical significance of the pharmacokinetic profile remains incompletely characterized.

Identity and Naming History

The peptide backbone corresponds to GRF(1-29), the first 29 residues of native growth hormone-releasing hormone, which retains most of the receptor-activating activity of the full-length molecule. Four substitutions distinguish the analog from the natural sequence: D-alanine at position 2, glutamine at position 8, alanine at position 15, and leucine at position 27. These changes slow cleavage by dipeptidyl peptidase IV, the enzyme that degrades native hormone in plasma within minutes. The outcome is improved enzymatic stability combined with a still brief residence time when no additional modification is present.

Naming in this area is inconsistent, and readers should treat product labels with care. In much of the literature and in vendor catalogs, the unqualified term refers to the albumin-binding version, while the version lacking the DAC group appears as modified GRF(1-29), mod GRF(1-29), or the same name with a without-DAC qualifier. Because one abbreviation has been applied to both materials, the only reliable way to identify a sample is to check the stated sequence and the presence of the linker.

CJC-1295 is the name used for a synthetic peptide modeled on growth hormone-releasing hormone, the hypothalamic signal that prompts the pituitary to release growth hormone. The compound was described by a Canadian drug discovery company in the mid-2000s as a long-acting research tool. Two closely related molecules share the name in practice: one carries a drug affinity complex, or DAC, group, and one does not. The distinction matters because the two behave differently in circulation.

Cjc-1295 at a glance

PropertyValueNotes
Physical formLyophilized white powderSupplied as a freeze-dried solid for research use
Molecular weightApproximately 3,647 Da (DAC form)Lower for the variant lacking the albumin-binding moiety
SolubilitySoluble in water and aqueous bufferTypically dissolved in sterile or bacteriostatic water
Typical storage temperature−20 °C or belowDry powder, desiccated and protected from light
Common analytical methodReversed-phase HPLC with mass spectrometryUsed for purity estimation and identity confirmation

Handling, Stability and Analysis

Reported half-lives differ widely between the two variants and between species. Values for the albumin-binding form are usually expressed in days, while the unconjugated form is measured in minutes to a few hours. Sampling schedules, assay sensitivity, and route of administration all influence the numbers, which limits direct comparison across studies. Whether sustained receptor occupancy produces different downstream effects from pulsatile stimulation remains an open question in the published work. Claims about relative potency should therefore be read alongside the specific study design that produced them.

Lyophilised powder is the usual supplied form. The material is hygroscopic, so vials are typically equilibrated to room temperature before opening in order to prevent condensation on the contents. Long-term storage is generally described at minus twenty degrees Celsius or colder, protected from light and moisture. Repeated freeze-thaw cycles are avoided because they promote aggregation and loss of soluble material. A reconstituted solution is considerably less stable than the dry powder and is normally kept refrigerated for short periods only.

Identity and purity are assessed mainly by reversed-phase high-performance liquid chromatography combined with mass spectrometry. The chromatographic separation resolves the target peptide from truncation products and from species carrying oxidised residues, while mass measurement confirms the expected molecular mass. Because the two common variants differ by roughly 280 daltons, a mass determination distinguishes them unambiguously. Purity is often quoted as a percentage of total peak area, although that figure depends on the detection wavelength and the integration method applied.

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Compound Identity and Development History

The compound emerged from work at a Canadian biotechnology firm in the early 2000s. Early human studies examined its effect on growth hormone and insulin-like growth factor 1 in healthy volunteers and in people with HIV-associated fat redistribution. Reports described sustained increases in both markers after a single injection. Development did not advance to regulatory approval, and the clinical programme was later discontinued. The molecule is now encountered mainly as a research chemical rather than a marketed medicine.

Two forms circulate in research settings and are frequently confused. One carries the drug affinity complex and is often written as CJC-1295 with DAC; the other lacks that group and is usually called modified GRF(1-29). The two share the same core sequence but differ sharply in how long they persist in blood. Products labelled only as CJC-1295 normally refer to the version carrying the complex. Documentation that omits the distinction leaves the intended molecule ambiguous.

Notes from published material

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Sources: en.wikipedia.org

Further detail

Congenital hereditary endothelial dystrophy (CHED): There are 2 forms of congenital hereditary endothelial dystrophy (CHED). Commonest is an autosomal recessive form, which is present at birth, but nonprogressive. Nystagmus is seen in association with this form. Another is an autosomal dominant form that occurs within the first few years of life. This form is progressive, but nystagmus is not seen. Deafness and CHED are seen in Harboyan syndrome. The histologic findings are very similar to those seen in pseudophakic/ aphakic bullous keratopathy. The appearance of the cornea is similar to that in congenital glaucoma but without increased corneal diameter and elevated intraocular pressure. Posterior polymorphous corneal dystrophy (PPMD, PPCD): PPCD, also known as Schlichting dystrophy, is an autosomal dominant disorder of the corneal endothelium and Descemet's membrane. It is usually present in the second or third decade of life. It has the same entity as the first form of CHED. Most cases of PPMD are asymptomatic, and these cases generally do not require treatment. PPMD patients with bilateral, corneal opacities that can affect vision, descemet's membrane endothelial keratoplasty or penetrating keratoplasty are the treatments of choice to improve vision and to avoid amblyopia. Congenital hereditary stromal dystrophy (CHSD): CHSD is also known as Congenital stromal corneal dystrophy or Congenital stromal dystrophy of the cornea. It is a rare autosomal dominant disease caused by mutations in the DCN gene.

== Genetics == The VWF gene is located on the short arm p of chromosome 12 (12p13.2). It has 52 exons spanning 178 kbp. Types 1 and 2 are inherited as autosomal dominant traits. Occasionally, type 2 also inherits recessively. Type 3 is inherited as autosomal recessive. However, some individuals heterozygous for type 3 may be diagnosed with VWD type 1, indicating an intermediate inheritance in those cases. VWD occurs in approximately 1% of the population and affects men and women equally. Genetic testing is typically not part of the initial workup for von Willebrand disease, and is not needed for people diagnosed with type 1 VWD based on clinical history and laboratory tests. It is mainly useful for:

250No In 2003, scientists at the FLNR reported that they had been able to synthesise 249No, which decayed by SF with a half-life of 54 μs. Further work in 2006 by scientists at the ANL showed that the activity was actually due to a K-isomer in 250No. The ground state isomer was also detected with a very short half-life of 3.7 μs.

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Sources: en.wikipedia.org

Frequently asked questions

How does CJC-1295 differ from modified GRF(1-29)?

The two share the same 29-amino-acid backbone. CJC-1295 carries an additional albumin-binding moiety that markedly extends its residence time in circulation, while the form without that moiety clears faster. Literature sometimes applies the name loosely to either variant.

Is CJC-1295 an approved medicine?

It has not been approved by major regulatory agencies for any therapeutic indication. Material sold under this name is typically distributed for laboratory research only. Clinical use is not supported by large controlled trials.

What is known about its half-life?

Early human studies of the albumin-binding form reported circulation half-lives on the order of several days. The value depends on assay method and study design. Estimates for the form without the binding moiety are considerably shorter.

Is this compound a naturally occurring hormone?

No. It is a laboratory-made analog of growth hormone-releasing hormone. The natural hormone is a 44-residue peptide, while the analog is built on a shorter 29-residue fragment.

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