en · de · es · fr · pt
field-notes.peptides6088.com › Wiki › Cjc-1295 Structure And Mechanism — Quick Reference

Cjc-1295 Structure And Mechanism — Quick Reference

By Editorial Desk · published 2026-05-16 · last reviewed 2026-06-06 · Wiki

If you have been reading about drug affinity complex and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.

Updated 2026-06-06. Numbers and descriptions here follow the published literature rather than marketing material.

CJC-1295 Structure And Mechanism

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.

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.

Persistence, Stability and Measurement

Analytical confirmation usually relies on reversed-phase high-performance liquid chromatography for purity and on liquid chromatography coupled to mass spectrometry for identity. Mass data reveal the expected molecular mass and can flag truncated or oxidized species. Amino acid analysis and peptide mapping provide sequence-level verification. Immunoassays are used in some biological matrices, but antibodies raised against one releasing-hormone analog may cross-react with another. Reported purity figures depend heavily on the method used, so comparisons between suppliers require matching the analytical approach.

The two variants differ dramatically in how long they persist in circulation. The form lacking the albumin-binding group has a plasma half-life measured in tens of minutes, comparable to the natural hormone fragment. The version carrying the drug affinity complex binds albumin and shows a half-life of roughly six to eight days in human studies. That figure comes from small trials that tracked hormone levels over extended periods. The physiological consequences of sustained versus pulsatile stimulation are still debated and the literature does not settle the point.

Lyophilized peptide powder is comparatively stable when kept dry, cold, and protected from light. Once dissolved, the molecule is vulnerable to deamidation, oxidation, and aggregation, with the rate depending on pH, buffer composition, and temperature. Alkaline conditions and repeated freeze-thaw cycles accelerate loss of the intact peptide. The methionine present in the native sequence is a known oxidation site, which is one reason it was replaced in the modified fragment. Suppliers typically recommend cold storage of solutions and use within a short window.

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

Background and Receptor Mechanism

Two principal forms appear in the literature and in research supply. One carries a drug affinity complex, a maleimide-based group that forms a covalent bond with circulating albumin. This linkage slows clearance and produces a long-lasting elevation of peptide levels. The other form lacks that group and is often labeled MOD GRF(1-29). It has a much shorter circulation time. Both variants retain the same core receptor-binding sequence. Reported half-lives differ substantially between the two.

At the pituitary, the peptide binds the growth hormone-releasing hormone receptor on somatotroph cells. Receptor activation raises intracellular cyclic AMP and triggers release of stored growth hormone. Somatostatin and other hypothalamic signals modulate this response. Negative feedback from insulin-like growth factor 1 also influences output. The same regulatory architecture operates with the native hormone. Whether the synthetic analog alters feedback dynamics over repeated exposure remains an open question. Most published receptor work uses cell models rather than intact human systems.

CJC-1295 is a synthetic peptide belonging to the growth hormone-releasing hormone analog family. It comprises twenty-nine amino acid residues derived from the N-terminal region of natural GHRH. The molecule incorporates several non-natural substitutions that increase resistance to enzymatic degradation. These modifications extend its activity compared with the native hormone fragment. Researchers use it to study pituitary growth hormone secretion in laboratory and clinical settings. This compound is distinct from native GHRH in its stability profile.

Related pages on this site

Background and Naming Conventions

Four amino acid substitutions separate the modified backbone from the parent GRF(1-29) sequence. These changes reduce recognition by dipeptidyl peptidase IV and related proteases, extending the interval before degradation. Development work in this area sought longer-acting GHRH analogs for endocrine investigation. Published descriptions treat the substitution set as a defining property of the core sequence, while the albumin-binding linker is described separately as an optional addition to that same backbone.

CJC-1295 is a synthetic peptide analog of growth hormone-releasing hormone, constructed on the 29-amino-acid fragment designated GRF(1-29). The name began as an internal development code during the 1990s and later spread through research supply catalogs and discussion forums. The molecule does not occur in nature; its sequence is engineered rather than isolated from tissue. Two related compounds are sold under this single label, and they differ by one appended chemical group that strongly influences how long the peptide remains in circulation.

Receptor Action and Pharmacokinetics

The attached maleimide group explains the unusual duration of the DAC version. After injection it reacts with the thiol of cysteine-34 on serum albumin, forming a stable covalent bond. The resulting conjugate is too large for rapid kidney filtration and is shielded from many peptidases. Reported half-lives for this form reach several days, whereas the version without the group is cleared in roughly half an hour. That gap is the main pharmacological difference between the two.

Downstream of growth hormone, the liver and other tissues increase production of insulin-like growth factor 1, a mediator of many growth-promoting effects. Studies have documented elevated levels of both hormones after dosing, and the rise from the long-acting form persists longer than that produced by shorter-acting analogues. What remains unclear is whether sustained elevation of these markers translates into meaningful clinical benefit, and whether prolonged exposure carries risks that short trials could not detect.

Background and Molecular Features

CJC-1295 is a synthetic peptide modeled on growth hormone-releasing hormone, the hypothalamic signal that prompts the pituitary to release growth hormone. Its sequence corresponds to the first twenty-nine residues of human GHRH, with four substitutions that slow enzymatic breakdown. Early descriptions placed the compound in research on growth hormone deficiency and related conditions, and later literature groups it with the long-acting GHRH analogs. The name appears in both laboratory and popular fitness writing, where it sometimes labels chemically different peptides.

Two related peptides circulate under the CJC-1295 label, and they differ mainly in how long they persist in circulation. The version carrying a drug affinity complex includes a maleimidopropionic acid linker that forms a covalent bond with serum albumin. The other version, usually written as modified GRF(1-29) or tetrasubstituted GRF(1-29), lacks that linker and is cleared quickly. Mixing the two produces inconsistent readings of published half-life values, because the linker rather than the receptor-facing sequence drives most of the difference.

Background from the literature

==== Glycoside hydrolases ==== Another important group of thermostable enzymes are glycoside hydrolases. These enzymes are responsible of the degradation of the major fraction of biomass, the polysaccharides present in starch and lignocellulose. Thus, glycoside hydrolases are gaining great interest in biorefining applications in the future bioeconomy. Some examples are the production of monosaccharides for food applications as well as use as carbon source for microbial conversion in fuels (ethanol) and chemical intermediates, production of oligosaccharides for prebiotic applications and production of surfactants alkyl glycoside type. All of these processes often involve thermal treatments to facilitate the polysaccharide hydrolysis, hence give thermostable variants of glycoside hydrolases an important role in this context.

This results in the Fe2+ ion switching to a low-spin configuration, resulting in a 20% decrease in ionic radius so that now it can fit into the porphyrin ring, which becomes planar. (Additionally, this hydrogen bonding results in the tilting of the oxygen molecule, resulting in a Fe–O–O bond angle of around 120° that avoids the formation of Fe–O–Fe or Fe–O2–Fe bridges that would lead to electron transfer, the oxidation of Fe2+ to Fe3+, and the destruction of hemoglobin.) This results in a movement of all the protein chains that leads to the other subunits of hemoglobin changing shape to a form with larger oxygen affinity. Thus, when deoxyhemoglobin takes up oxygen, its affinity for more oxygen increases, and vice versa. Myoglobin, on the other hand, contains only one heme group and hence this cooperative effect cannot occur. Thus, while hemoglobin is almost saturated with oxygen in the high partial pressures of oxygen found in the lungs, its affinity for oxygen is much lower than that of myoglobin, which oxygenates even at low partial pressures of oxygen found in muscle tissue. As described by the Bohr effect (named after Christian Bohr, the father of Niels Bohr), the oxygen affinity of hemoglobin diminishes in the presence of carbon dioxide.

Adverse human health effects have been associated with a compound. There is an established relationship between the positive and negative effect(s) of the compound. Emerging contaminants are those which have not previously been detected through water quality analysis, or have been found in small concentrations with uncertainty as to their effects. The risk they pose to human or environmental health is not fully understood.

=== Inositol depletion hypothesis === Lithium treatment has been found to inhibit the enzyme inositol monophosphatase, involved in degrading inositol monophosphate to inositol required in PIP2 synthesis. This leads to lower levels of inositol triphosphate, created by decomposition of PIP2. This effect has been suggested to be further enhanced with an inositol triphosphate reuptake inhibitor. Inositol disruptions have been linked to memory impairment and depression. It is known with good certainty that signals from the receptors coupled to the phosphoinositide signal transduction are affected by lithium. Myo-inositol is also regulated by the high affinity sodium mI transport system (SMIT). Lithium is hypothesized to inhibit mI entering the cells and mitigate the function of SMIT. Reductions of cellular levels of myo-inositol results in the inhibition of the phosphoinositide cycle.

American Bells - A guide to the species in subgenus Viorna American Clematis Society Clematis viorna images at bioimages.vanderbilt.edu Clematis virginiana images at bioimages.vanderbilt.edu International Clematis Society "Clematis" . The American Cyclopædia. 1879. The Clematis., one of the Flowers of Loveliness for 1838 with an illustration (Clematis) by Thomas Uwins combined with poetry (The Clematis) by Letitia Elizabeth Landon.

Sources: en.wikipedia.org

Reference notes

Impact factor data ... have a strong influence on the scientific community, affecting decisions on where to publish, whom to promote or hire, the success of grant applications, and even salary bonuses. More targeted research has begun to provide firm evidence of how deeply the impact factor is embedded within formal and informal research assessment processes. A review in 2019 studied how often the JIF featured in documents related to the review, promotion, and tenure of scientists in US and Canadian universities. It concluded that 40% of universities focused on academic research specifically mentioned the JIF as part of such review, promotion, and tenure processes. A 2017 study of how researchers in the life sciences behave concluded that "everyday decision-making practices as highly governed by pressures to publish in high-impact journals." It has been argued that the deeply embedded nature of such indicators not only affects research assessment, but the more fundamental issue of what research is actually undertaken: "Given the current ways of evaluation and valuing research, risky, lengthy, and unorthodox project rarely take center stage."

=== Transdermal administration === Transdermal estradiol is available in the forms of patches, gels, emulsions, and sprays. In the case of gels, emulsions, and sprays, the route is sometimes referred to as topical rather than as transdermal. Topical administration can also refer to vaginal administration of gels and creams however. Estradiol has moderate skin permeability, which is based on the lipophilicity and hydrophilicity of a compound. In general, the more polar groups, such as hydroxyl groups, that are present in a steroid, and hence the more hydrophilic and less lipophilic it is, the lower its skin permeability. For this reason, estrone and progesterone have higher skin permeability, while estriol and cortisol have lower skin permeability. The transdermal bioavailability of estradiol in an alcohol solution is approximately 10%. Transdermal estradiol reservoir patches have been reported to have a bioavailability of 3 to 5%. Estradiol is a highly potent compound and circulates at picomolar concentrations (pg/mL), which makes it ideal for transdermal application as only small amounts of substance need to be delivered across the skin. Conversely, progesterone, which circulates at levels in the nanomolar range and requires a far higher quantity of substance for biological effect, is not well-suited for transdermal delivery.

==== Genetic defects ==== Genetically confirmed diagnoses of diseases affecting vitamin B6 metabolism (ALDH7A1 deficiency, pyridoxine-5'-phosphate oxidase deficiency, PLP binding protein deficiency, hyperprolinaemia type II and hypophosphatasia) can trigger vitamin B6 deficiency-dependent epileptic seizures in infants. These are responsive to pyridoxal 5'-phosphate therapy.

== Bibliography == Biko, Steve (1979). Steve Biko: Black Consciousness in South Africa; Biko's Last Public Statement and Political Testament. Random House. ISBN 978-0-394-72739-4. Biko, Steve (2002). I Write What I Like: Selected Writings. University of Chicago Press. ISBN 978-0-226-04897-0. Clarke, Anthony J.; Fiddes, Paul S., eds. (2005). Flickering Images: Theology and Film in Dialogue. Regent's Study Guides. Vol. 12. Macon, GA: Smyth & Helwys Publishing. ISBN 1-57312-458-3. Goodwin, June (1995). Heart of Whiteness: Afrikaners Face Black Rule In the New South Africa. Scribner. ISBN 978-0-684-81365-3. Harlan, Judith (2000). Mamphela Ramphele. The Feminist Press at CUNY. ISBN 978-1-55861-226-6. Juckes, Tim (1995). Opposition in South Africa: The Leadership of Z. K. Matthews, Nelson Mandela, and Stephen Biko. Praeger Publishers. ISBN 978-0-275-94811-5. Magaziner, Daniel (2010). The Law and the Prophets: Black Consciousness in South Africa, 1968–1977. Ohio University Press. ISBN 978-0-8214-1918-2. Malan, Rian (2000). My Traitor's Heart: A South African Exile Returns to Face His Country, His Tribe, and His Conscience. Grove Press. ISBN 978-0-8021-3684-8. Omand, Roger (1989). Steve Biko and Apartheid (People & Issues). Hamish Hamilton Limited. ISBN 978-0-241-12640-0. Paul, Samuel (2009). The Ubuntu God: Deconstructing a South African Narrative of Oppression. Pickwick Publications. ISBN 978-1-55635-510-3. Pityana, Barney (1992). Bounds of Possibility: The Legacy of Steve Biko & Black Consciousness. D. Philip. ISBN 978-1-85649-047-4. Price, Linda (1992).

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.

What is the difference between the forms with and without a drug affinity complex?

The version carrying the affinity complex bears a maleimide group that binds serum albumin, which extends its circulation time to several days. The version without it lacks this group and clears within roughly half an hour. The two are chemically related but behave very differently once in the body.

Network