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Cjc-1295 Structure And Mechanism — Questions and Answers

By Editorial Desk · published 2025-10-20 · last reviewed 2025-11-09 · Topic

Everything below concerns albumin binding. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.

Last reviewed on 2025-11-09. Where a claim depends on a specific study, the study is described rather than over-claimed.

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.

Structure And Receptor Pharmacology

Two related forms appear under the CJC-1295 name. The simpler analogue, commonly written as modified GRF(1-29), carries the four substitutions but no additional conjugation. The second form attaches a maleimidopropionic acid linker to a lysine residue, a modification frequently called the drug affinity complex. That linker reacts with the free thiol on serum albumin to form a covalent bond. Because albumin has a long residence time in blood, the conjugated peptide stays in circulation far longer than the unconjugated analogue.

Receptor level activity follows the canonical GHRH pathway. The peptide binds the GHRH receptor, a class B G protein coupled receptor on somatotroph cells of the anterior pituitary. Binding raises intracellular cyclic AMP, which promotes calcium entry and the release of growth hormone into the bloodstream. Because the molecule acts at the same receptor as the endogenous hormone, its effect is superimposed on the natural pulsatile rhythm rather than replacing it. Whether sustained receptor occupation leads to desensitization is not fully settled.

CJC-1295 belongs to a class of synthetic peptides modeled on growth hormone releasing hormone, a forty-four amino acid signal produced by the hypothalamus. The compound is built from the first twenty-nine residues of the natural sequence, with four substitutions introduced at positions 2, 8, 15 and 27. These changes were designed to slow enzymatic breakdown while preserving receptor activation. The result is a peptide that is shorter than native GHRH and considerably more resistant to ordinary clearance pathways 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

Molecular Background and Naming

The peptide backbone includes a D-alanine at position two, which resists cleavage by dipeptidyl peptidase IV, and several other substitutions that reduce degradation. Its molecular weight is roughly 3.4 kDa without the linker and about 3.6 kDa with it. The molecule is water soluble and is normally supplied as a lyophilized powder. Precise sequence and mass values depend on which variant is described, so technical documents usually state the exact form being referenced.

CJC-1295 is a synthetic peptide designed as a long-acting analogue of growth hormone-releasing hormone (GHRH). Its structure derives from the first 29 amino acids of native GHRH, a fragment often called GRF(1-29). Four substitutions were introduced to slow enzymatic breakdown and extend activity relative to the natural sequence. The compound was developed by ConjuChem as part of a broader effort to improve the pharmacokinetic profile of peptide hormones. It is studied in laboratory and clinical research settings rather than appearing as a naturally occurring substance.

Two related forms circulate in technical discussion under the same family name. The original version carries a drug affinity complex (DAC) that binds covalently to serum albumin after administration, and this linkage substantially extends circulation time. A second form, frequently written as modified GRF(1-29) or CJC-1295 without DAC, lacks that linker and clears much faster. The naming is a frequent source of confusion because the shorthand CJC-1295 can refer to either form depending on the source. Reports sometimes fail to specify which variant was studied.

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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.

Mechanism and Pharmacokinetics

Binding of the peptide to the growth hormone-releasing hormone receptor on pituitary somatotrophs triggers a G protein coupled cascade that raises cyclic AMP and opens calcium channels. The result is greater secretion of growth hormone into the bloodstream. Because the peptide acts at the same receptor as the natural hypothalamic hormone, its effect is amplified pulse size rather than an entirely separate release pathway. Receptor binding alone does not determine the response, since somatostatin tone and other inputs modulate the final output.

The albumin-binding version stays in circulation for days, because covalent attachment to serum albumin shields the peptide from rapid filtration and degradation. Reported half-lives for this form fall in the range of several days. The version without the linker is cleared in minutes, with estimates often near thirty minutes in animal work. These figures come from small studies and vary with assay method, species, and route, so they are best read as approximate rather than fixed constants.

Further detail

negative supercoiling The supercoiling of a double-stranded DNA molecule in the direction opposite to the turn of the double helix itself (e.g. a left-handed coiling of a helix with a right-handed turn). Contrast positive supercoiling.

That promise is null and void if Zverev – and the media – isn't willing to be honest." At the beginning of the 2024 Australian Open, a court official announced that Zverev was scheduled to stand trial before the Tiergarten District Court in Berlin. The timing of the announcement, combined with Zverev's semifinal run at the tournament, brought heightened interest in and scrutiny of the allegations from both the press and the public. The trial began on 31 May 2024. On 7 June 2024, the third day of the trial, the judge agreed to a request by the public prosecution office, endorsed by the alleged victim, to provisionally terminate the proceedings subject to the condition that Zverev pay €200,000, of which €150,000 would go to the German State Treasury and €50,000 to charitable organizations. The trial therefore concluded without a finding of guilt. The prosecutor's request to terminate the proceedings followed an out-of-court agreement between Zverev and the alleged victim, the terms of which were not disclosed. According to his counsel, Zverev entered into the agreement "to put a quick end to the proceedings – above all in the interest of their child", emphasizing that the agreement "includes no determination or admission of guilt".

Liakhov, a vigorous, able, and reactionary officer firmly committed to upholding absolute monarchies whatever in Russia or Iran, transformed the Persian Cossack Brigade into a mounted para-military police force rather than as a combat force. Liakhov was close to the new Shah, Mohammed Ali, who ascended to the Peacock Throne in January 1907, and it was due to the shah's patronage that Liakhov transformed the Persian Cossack Brigade into the main bulwark of the Iranian state. In June 1908, Liakhov led the Cossack Brigade in bombarding the Majlis (Parliament) while being appointed military governor of Tehran as the shah attempted to do away with the constitution his father had been forced to grant in 1906 Reza Khan, who became the first Iranian to command the Cossack Brigade led the coup d'état in 1921 and in 1925 deposed the Qajars to found a new dynasty. After the outbreak of World War I in August 1914, Cossacks became a key component in the cavalry of the Imperial Russian Army. The mounted Cossacks made up 38 regiments, plus some infantry battalions and 52 horse artillery batteries. Initially, each Russian cavalry division included a regiment of Cossacks in addition to regular units of hussars, lancers, and dragoons. By 1916, the Cossacks' wartime strength had expanded to 160 regiments, plus 176 independent sotnias (squadrons) employed as detached units. The importance of cavalry in the frontlines faded after the opening phase of the war settled into a stalemate.

=== Singapore === The TCM Practitioners Act was passed by Parliament in 2000 and the TCM Practitioners Board was established in 2001 as a statutory board under the Ministry of Health, to register and regulate TCM practitioners. The requirements for registration include possession of a diploma or degree from a TCM educational institution/university on a gazetted list, either structured TCM clinical training at an approved local TCM educational institution or foreign TCM registration together with supervised TCM clinical attachment/practice at an approved local TCM clinic, and upon meeting these requirements, passing the Singapore TCM Physicians Registration Examination (STRE) conducted by the TCM Practitioners Board. In 2024, Nanyang Technological University will offer the four-year Bachelor of Chinese Medicine programme, which is the first local programme accredited by the Ministry of Health.

Sources: en.wikipedia.org

Background from the literature

Adult T-cell leukemia/lymphoma Angiocentric lymphoma (extranodal natural killer cell lymphoma, nasal-type NK lymphoma, NK/T-cell lymphoma, polymorphic/malignant midline reticulosis) Angioimmunoblastic T-cell lymphoma (angioimmunoblastic lymphadenopathy with dysproteinemia) Blastic NK-cell lymphoma CD30+ cutaneous T-cell lymphoma (primary cutaneous anaplastic large cell lymphoma) Cutaneous lymphoid hyperplasia (borrelial lymphocytoma, lymphadenosis benigna cutis, lymphocytoma cutis, pseudolymphoma, pseudolymphoma of Spiegler and Fendt, sarcoidosis of Spiegler and Fendt, Spiegler–Fendt lymphoid hyperplasia, Spiegler–Fendt sarcoid) Cutaneous lymphoid hyperplasia with bandlike and perivascular patterns Cutaneous lymphoid hyperplasia with nodular pattern (nodular pattern of cutaneous lymphoid hyperplasia) Diffuse large B-cell lymphoma (primary cutaneous large B-cell lymphoma) Granulocytic sarcoma (chloroma, myeloid sarcoma) Granulomatous slack skin Hairy-cell leukemia Hodgkin's disease Ichthyosis acquisita (acquired ichthyosis) IgG4-related skin disease Intravascular large B-cell lymphoma (angiotropic large cell lymphoma, intralymphatic lymphomatosis, intravascular lymphomatosis, malignant angioendotheliomatosis) Jessner lymphocytic infiltrate of the skin (benign lymphocytic infiltration of the skin, Jessner lymphocytic infiltration of the skin, Jessner–Kanof lymphocytic infiltration of the skin, lymphocytic infiltrate of Jessner) Kikuchi's disease (histiocytic necrotizing lymphadenitis) Large plaque parapsoriasis (parapsoriasis en plaques) Lennert lymphoma (lymphoepitheliod lymphoma) Leukemia cutis Lymphoma cutis Lymphomatoid granulomatosis Lymphomatoid papulosis Malignant histiocytosis (histiocytic medullary reticulosis) Marginal zone B-cell lymphoma Mucosa-associated lymphoid tissue lymphoma Mycosis fungoides Non-mycosis fungoides CD30− cutaneous large T-cell lymphoma Nonspecific cutaneous conditions associated with leukemia (leukemid) Pagetoid reticulosis (acral mycoses fungoides, localized epidermotropic reticulosis, mycosis fungoides palmaris et plantaris, unilesional mycosis fungoides, Woringer–Kolopp disease) Pityriasis lichenoides chronica (chronic guttate parapsoriasis, chronic pityriasis lichenoides, dermatitis psoriasiformis nodularis, parapsoriasis chronica, parapsoriasis lichenoides chronica) Pityriasis lichenoides et varioliformis acuta (acute guttate parapsoriasis, acute parapsoriasis, acute pityriasis lichenoides, Mucha–Habermann disease, parapsoriasis acuta, parapsoriasis lichenoides et varioliformis acuta, parapsoriasis varioliformis) Plasmacytoma Plasmacytosis Pleomorphic T-cell lymphoma (non-mycosis fungoides CD30− pleomorphic small/medium-sized cutaneous T-cell lymphoma) Polycythemia vera (erythremia) Primary cutaneous follicular lymphoma (follicular center cell lymphoma, follicular center lymphoma) Primary cutaneous immunocytoma Primary cutaneous marginal zone lymphoma Retiform parapsoriasis Secondary cutaneous CD30+ large cell lymphoma Sézary syndrome Sinus histiocytosis with massive lymphadenopathy (Rosai–Dorfman disease) Subcutaneous T-cell lymphoma (panniculitis-like T-cell lymphoma) Vesiculopustular eruption and leukemoid reaction in Down syndrome

== Pharmacokinetics == Most of the research on creatine so far has focused on its pharmacological properties. There has been less research into the pharmacokinetics of creatine. Studies have not established pharmacokinetic parameters for clinical usage of creatine such as volume of distribution, clearance, bioavailability, mean residence time, absorption rate, and half life. A clear pharmacokinetic profile would need to be established prior to determine optimal clinical dosing.

== Interactions == The drug transfers into breast milk. There is no evidence that its use during pregnancy is harmful to the developing fetus and its use is not contraindicated in pregnancy. The concurrent use of hydroxychloroquine and the antibiotic azithromycin appears to increase the risk for certain serious side effects with short-term use, such as an increased risk of chest pain, congestive heart failure, and mortality from cardiovascular causes. Care should be taken if combined with medication altering liver function as well as aurothioglucose (Solganal), cimetidine (Tagamet) or digoxin (Lanoxin). Hydroxychloroquine can increase plasma concentrations of penicillamine which may contribute to the development of severe side effects. It enhances hypoglycemic effects of insulin and oral hypoglycemic agents. Dose altering is recommended to prevent profound hypoglycemia. Antacids may decrease the absorption of hydroxychloroquine. Both neostigmine and pyridostigmine antagonize the action of hydroxychloroquine. While there may be a link between hydroxychloroquine and hemolytic anemia in those with glucose-6-phosphate dehydrogenase deficiency, this risk may be low in those of African descent. Specifically, the US Food and Drug Administration's (FDA) drug label for hydroxychloroquine lists the following drug interactions:

=== T-cell receptors === In addition to acting through HLA proteins to bind with a T-cell receptor, a drug or its metabolite may bypass HLA proteins to bind directly to a T-cell receptor and thereby stimulate CD8+ T or CD4+ T cells to initiate autoimmune responses. In either case, this binding appears to develop only on certain T cell receptors. Since the genes for these receptors are highly edited, i.e. altered to encode proteins with different amino acid sequences, and since the human population may express more than 100 trillion different (i.e. different amino acid sequences) T-cell receptors while an individual express only a fraction of these, a drug's or its metabolite's ability to induce the DRESS syndrome by interacting with a T cell receptor is limited to those individuals whose T cells express a T cell receptor(s) that can interact with the drug or its metabolite. Thus, only rare individuals are predisposed to develop SJS in response to a particular drug on the bases of their expression of specific T-cell receptor types. While the evidence supporting this T-cell receptor selectivity is limited, one study identified the preferential presence of the TCR-V-b and complementarity-determining region 3 in T-cell receptors found on the T cells in the blisters of patients with allopurinol-induced DRESS syndrome. This finding is compatible with the notion that specific types of T cell receptors are involved in the development of specific drug-induced SCARs.

== Pharmacokinetics == Intramuscular cefodizime bioavailability ranges from 90% to 100%. It distributes into many tissues and is approximately 81% bound to plasma proteins, chiefly albumin. The drug reaches minimum inhibitory concentrations approximately 2–3 hours after administration, maintaining it for several hours afterwards. Clearance of cefodizime from the body is predominantly renal, with the majority of the drug excreted unchanged within the first 12 hours. More specifically, cefodizime is mainly cleared via glomerular filtration in the kidney, in addition to some tubular secretion. In patients with normal renal function, the terminal phase elimination half-life is approximately 3.5 hours.

Sources: en.wikipedia.org

Reference notes

Pu-239 (also known as The Half Life of Timofey Berezin) is a 2006 British drama film written and directed by Hollywood producer Scott Z. Burns in his feature directorial debut, which was based on the book Pu-239 and Other Russian Fantasies written by Ken Kalfus. The film was shown twice at the 2006 Toronto International Film Festival under the title The Half Life of Timofey Berezin before being distributed by HBO Films under its original working title. Pu-239 is the chemical symbol for plutonium-239 (239Pu), the most readily fissile isotope of the element plutonium.

== Transportation == SST class blimp Supersonic transport, aircraft Training Submarines, (US Navy hull classification symbol: SST) Mitsubishi SST, a concept car by Mitsubishi Twin Clutch SST, a twin-clutch transmission developed by Mitsubishi Safe Secure Trailer, see US Office of Secure Transportation SST, the National Rail station code for Stansted Mountfitchet railway station, Essex, England

The Greater Poland uprising of 1918–1919, or Wielkopolska uprising of 1918–1919 (Polish: powstanie wielkopolskie 1918–1919 roku; German: Großpolnischer Aufstand) or Poznań War was a military insurrection of Poles in the Greater Poland region (German: Grand Duchy of Posen or Provinz Posen) against German rule. The uprising had a significant effect on the Treaty of Versailles, which granted a reconstituted Second Polish Republic the area won by the Polish insurrectionists. The region had been part of the Kingdom of Poland and then Polish–Lithuanian Commonwealth before the 1793 Second Partition of Poland when it was annexed by the German Kingdom of Prussia. It had also, following the 1806 Greater Poland uprising, been part of the Duchy of Warsaw (1807–1815), a French client state during the Napoleonic Wars.

== Prognosis == The life expectancy of patients with homocystinuria is reduced only if untreated. It is known that before the age of 30, almost one quarter of patients die as a result of thrombotic complications (e.g., heart attack).

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 CJC-1295 the same as modified GRF(1-29)?

The names are often used interchangeably in casual writing, but they are not strictly identical. Modified GRF(1-29) refers to the unconjugated analogue carrying only the four substitutions. The version sold as CJC-1295 with DAC includes the albumin binding linker and clears much more slowly.

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