The short version of CJC-1295 fits in a sentence. The long version — which is the one that helps — is below.
This page was last updated on 2026-08-01 and is reviewed periodically as new material appears.
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.
CJC-1295 acts at the growth hormone-releasing hormone receptor, a G-protein-coupled receptor found on somatotroph cells in the anterior pituitary. Binding triggers a rise in cyclic AMP and calcium entry, which promotes release of stored growth hormone. Because the peptide mimics the body's own releasing hormone, it amplifies existing secretory pulses rather than driving continuous output. The size of the response therefore depends partly on the subject's own hormonal rhythm and feedback state.
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.
Stability depends heavily on physical state. A lyophilized powder kept dry, desiccated, and shielded from light typically holds its integrity for months to years at minus twenty degrees Celsius, and longer at minus eighty. Once dissolved, the peptide becomes far more vulnerable, since peptide bond hydrolysis, oxidation of susceptible residues, and aggregation all proceed faster in solution. Buffers near neutral pH are generally gentler than strongly acidic or alkaline conditions. Repeated freeze-thaw cycles and exposure to air-liquid interfaces during vigorous mixing cause losses that are easy to overlook.
Verification matters because research peptides vary widely in quality. A certificate of analysis is only as reliable as the method behind it, and a single chromatographic trace reveals little about counter-ions, residual solvents, or water content. Independent laboratories commonly pair mass confirmation with chromatographic purity and, where relevant, quantify water along with acetate or trifluoroacetate content. Reported purity figures are not standardized across suppliers, so a stated value such as ninety-eight percent is not directly comparable unless the analytical method, column, and detection wavelength accompany it.
Characterization of this peptide relies on a small set of routine techniques. Reversed-phase high-performance liquid chromatography separates the target from truncated or oxidized by-products and yields a purity estimate when paired with ultraviolet detection near 214 nanometers. Mass spectrometry, either electrospray coupled to liquid chromatography or matrix-assisted laser desorption, confirms that the observed mass matches the value calculated for the expected sequence. Amino acid analysis, and enzymatic digestion followed by fragment mapping, are used when the sequence itself rather than the mass requires verification.
| Property | Value | Notes |
|---|---|---|
| Primary target | GHRH receptor | G-protein-coupled receptor on pituitary somatotrophs |
| Half-life, long-acting form | Several days | Extended by covalent albumin binding |
| Half-life, short form | About 30 minutes | Cleared rapidly by peptidases and kidneys |
| Route in studies | Subcutaneous injection | Used in the published human trials |
| Main measured effect | Rise in GH and IGF-1 | Surrogate markers rather than clinical endpoints |
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.
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.
The core sequence keeps the receptor-binding region of GHRH while replacing four positions that are vulnerable to dipeptidyl peptidase-4 and other proteases. Substitutions at positions 2, 8, 15, and 27 raise metabolic stability relative to the natural hormone. The N-terminal residues remain essential for activity, so changes there generally lower potency. Molecular weight sits near 3368 daltons for the tetrasubstituted analog without the linker, while the albumin-binding form is heavier because of the added maleimide group.
Studies in this area generally track growth hormone pulses, insulin-like growth factor 1 concentrations, and occasionally body composition endpoints. Most published human data come from early, small trials, and questions about long-term effects remain open. Whether repeated exposure alters pituitary responsiveness over time is not settled. Analytical work relies on immunoassays for the hormones and on mass spectrometry for the peptide itself, because the two measurements answer different questions.
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.
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.
This results in adrenal suppression and atrophy and, upon glucocorticoid discontinuation, temporary adrenal insufficiency. Similarly, CPA both in animals and humans can weakly reduce ACTH and cortisol levels and decrease adrenal gland weight as well as cause adrenal insufficiency with discontinuation. These findings suggest that CPA possesses weak glucocorticoid properties. CPA has been reported to be an antagonist of the glucocorticoid receptor (GR) in vitro and may reduce adrenal cortisol and corticosterone production by weakly inhibiting the enzymes 3β-hydroxysteroid dehydrogenase and 21-hydroxylase. These are antiglucocorticoid actions. However, metabolites of CPA, for instance 15β-hydroxycyproterone acetate, may have differing activities. Both cyproterone and CPA have been found to possess glucocorticoid effects, and based on studies in mice, it has been suggested that CPA has approximately one-fifth of the potency of prednisone as a glucocorticoid. The glucocorticoid effects of CPA in humans appear to be less significant than those in animals. Megestrol acetate, medroxyprogesterone acetate, and chlormadinone acetate are all steroidal progestins of the 17α-hydroxyprogesterone family and close analogues of CPA which similarly possess glucocorticoid properties and the potential for producing adrenal insufficiency upon discontinuation.
=== Biography and papers === His biography, written by John F. Galliher, Wayne H. Brekhus, and David P. Keys, was published in 2004, under the title Laud Humphreys: Prophet of Homosexuality and Sociology. The authors establish the case that Humphreys was an extremely complex person and that he was professionally marginalized in the discipline of sociology. The book also heralds his contributions to the discipline of sociology, as well as his advocacy for African-American civil rights, gay rights, and against war. The University of Southern California houses the Laud Humphreys Papers Collection, as part of the ONE National Gay & Lesbian Archives.
With some hesitation Fermi agreed to self-censor. But Joliot-Curie did not, and in April 1939 his team in Paris, including Hans von Halban and Lew Kowarski, reported in the journal Nature that the number of neutrons emitted with nuclear fission of uranium was then reported at 3.5 per fission. Szilard and Walter Zinn found "...the number of neutrons emitted by fission to be about two." Fermi and Anderson estimated "a yield of about two neutrons per each neutron captured."
== External links == "P2Y Receptors: P2Y1". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and Clinical Pharmacology. Archived from the original on 2016-03-03. Retrieved 2008-12-09. This article incorporates text from the United States National Library of Medicine, which is in the public domain.
Sources: en.wikipedia.org
Preparing TNP-ATP is a one-step synthesis that is relatively safe and easy. Adenosine's ribose moiety can be trinitrophenylated by 2,4,6-trinitrobenzene-1-sulfonate (TNBS). The resulting compound assumes a bright orange color and has visible absorption characteristics, as is characteristic of a Meiseinheimer spiro complex compound linking. To see the exact method of preparion, please refer to T. Hiratsuka's and K. Uchida's paper "Preparation and Properties of 2'(r 3')-O(2,4,6-trinitrophenyl) Adenosine 5'-triphosphate, an Analog of Adenosine Triphosphate," found in the reference section. To revert TNP-ATP back to its constituent parts, or in other words to hydrolyze TNP-ATP to give equilmolar amounts of picric acid (TNP) and ATP, TNP-ATP should be treated with 1 M HCl at 100 degrees Celsius for 1.5 hours. This is because if TNP-ATP is acidified under mild conditions, it results in the opening of the dioxolane ring attached to the 2’-oxygen, leaving a 3’O-TNP derivative as the only product.
Brunton Medal 1979, Sir Francis Avery Jones research medal of the British Society of Gastroenterology, the highest research award that the national gastroenterology body confers on its researchers. Fellowships: Royal Colleges of Physicians of Glasgow (1975) London (1977) Edinburgh (1981) Royal College of Pathologists (1984) Fellow of the Royal Society of Edinburgh (1990) The Anne Ferguson building at the Western General Hospital, Edinburgh, is named after her. In 1966, she married John Ferguson, a sociology lecturer at the University of Strathclyde, and together they adopted two children, a girl and a boy. John Ferguson died of cancer in 1989. She married Professor Gerald Collee, emeritus Professor of Medical Microbiology at the University of Edinburgh in 1995. In her youth, Ferguson represented the University of Glasgow in athletics as a middle-distance runner. She was also on the Scottish women's basketball team. She enjoyed hill walking and mountaineering, and once visited the Himalayas with her first husband. Ferguson died of pancreatic cancer in Edinburgh on 21 December 1998.
RdRps are highly conserved in viruses and are related to telomerase, though the reason for this was an ongoing question as of 2009. The similarity led to speculation that viral RdRps are ancestral to human telomerase. The most famous example of RdRp is in poliovirus. The viral genome is composed of RNA, which enters the cell through receptor-mediated endocytosis. From there, the RNA acts as a template for complementary RNA synthesis. The complementary strand acts as a template for the production of new viral genomes that are packaged and released from the cell ready to infect more host cells. The advantage of this method of replication is that no DNA stage complicates replication. The disadvantage is that no 'back-up' DNA copy is available. Many RdRps associate tightly with membranes making them difficult to study. The best-known RdRps are polioviral 3Dpol, vesicular stomatitis virus L, and hepatitis C virus NS5B protein. Many eukaryotes have RdRps that are involved in RNA interference: these amplify microRNAs and small temporal RNAs and produce double-stranded RNA using small interfering RNAs as primers. These RdRps are used in defense mechanisms and can be appropriated by RNA viruses. Their evolutionary history predates the divergence of major eukaryotic groups.
However, it indicated a poisoning effect on modification of strontium. Some bismuth alloys, such as Bi35-Pb37-Sn25, are combined with nonsticking materials such as mica, glass, and enamels because they easily wet them, allowing to make joints to other parts. Addition of bismuth to caesium enhances the quantum yield of caesium cathodes. Sintering of bismuth and manganese powders at 300 °C (572 °F) produces a permanent magnet and magnetostrictive material, which is used in ultrasonic generators and receivers working in the 10–100 kHz range and in magnetic and holographic memory devices.
== History == BMS-986122 was first described in 2013, and along with BMS-986121, was the first selective MOR PAM to be discovered. They were identified via high-throughput screening (HTS). Their characterization led to the discovery of a putative conserved allosteric site across the MOR and other opioid receptors.
Sources: en.wikipedia.org
It binds the growth hormone-releasing hormone receptor on pituitary somatotroph cells. Receptor activation raises cyclic AMP and promotes release of stored growth hormone granules. Because the peptide persists longer than natural releasing hormone, stimulation is prolonged rather than brief.
The drug affinity complex links the peptide to serum albumin through a covalent bond. The conjugate is too large to be filtered quickly by the kidneys and is shielded from enzymatic breakdown. This extends the apparent half-life from roughly minutes to several days.
Long-term safety and any clinical benefit are unestablished. Published human data cover small groups over limited periods and focus on hormone levels rather than health outcomes. Whether prolonged elevation of growth hormone and insulin-like growth factor 1 is beneficial or harmful is an open question.
Mass spectrometry establishes whether the observed molecular weight matches the calculated sequence mass. Chromatographic retention and fragment mapping add further confidence about sequence and composition. A single technique alone is rarely treated as sufficient evidence of identity.