A practical reference on GHRH analog: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2025-09-20 and is reviewed periodically as new material appears.
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.
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.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Class | Synthetic peptide | GHRH receptor agonist |
| Sequence length | 29 amino acids | Derived from human GHRH |
| Molecular weight | About 3368 Da without linker | Albumin-binding form is heavier |
| Appearance | White to off-white lyophilized powder | Common form for research reference material |
| Typical storage | -20 °C or below, desiccated | Protect powder from light and moisture |
The peptide binds GHRH receptors on somatotroph cells within the anterior pituitary, triggering a signalling cascade that increases growth hormone secretion. Its improved resistance to dipeptidyl peptidase IV degradation distinguishes it from the parent hormone. In the DAC-bearing version, a maleimide group reacts with a cysteine residue on serum albumin, forming a covalent bond that keeps the peptide in circulation far longer. That albumin attachment is the central design feature separating the two research variants.
Pharmacokinetic behaviour differs sharply between the two forms. The DAC-bearing peptide shows an extended circulation time measured in days, whereas the version without the complex is cleared within roughly half an hour. This gap shapes how researchers design dosing schedules in animal models. Whether the prolonged presence of the DAC form produces effects meaningfully different from the short-acting variant remains an open question, since comparative human data are scarce.
Reconstitution is typically performed with sterile water or bacteriostatic water, added slowly against the vial wall. The resulting solution should be clear and colorless; cloudiness or visible particles suggest a problem with the material or the diluent. Once in solution, the peptide is less stable than the dry powder. Refrigerated storage at two to eight degrees Celsius is common for short-term holding, while freezing aliquots is described for longer periods.
Purity is most often assessed by reversed-phase high-performance liquid chromatography, reported as a percentage of total peak area. Identity is confirmed by mass spectrometry, which yields a molecular ion consistent with the expected sequence. Amino acid analysis and peptide mapping provide additional characterization. Reported purity values are method-dependent, so figures from different laboratories are not always directly comparable without details of column, gradient, and detection wavelength.
Peptide degradation proceeds mainly through hydrolysis, oxidation of methionine, and deamidation of asparagine or glutamine residues. The maleimide group on the albumin-binding variant can also react with thiols or hydrolyze in aqueous media. Because these pathways accelerate with temperature and pH extremes, handling conditions strongly influence measured stability. Stability data in the public literature are limited and often generated under differing conditions, so general statements about shelf life should be read as approximate.
In 1906, the German expedition team of Albert Grünwedel explored the Kizil Caves. Albert von Le Coq, who worked under the direction Grünwedel, had to leave in June 1906 due to health problems. Grünwedel generally photographed and copied the murals, before removing those he considered essential. Most of the fragments removed are now in Museum of Asian Art (formerly Museum für Indische Kunst) in Dahlem, Berlin. Other explorers removed some fragments of murals, that may now be found in museums in Russia, Japan, Korea and United States. Although the site has been both damaged and looted, around 5000 square metres of wall paintings remain, These murals mostly depict Jataka stories, avadanas, and legends of the Buddha, and are an artistic representation in the tradition of the Hinayana school of the Sarvastivadas. Carbon-testing and stylistical analysis helped determine three main periods in the paintings at Kizil, which cover a period from 300 CE to 650 CE. The early art of Kizil correspond to the Western school of art in the Tarim Basin, and mainly displays influences from Gandhara and the Iranian world, particularly influence from the Hephthalites, and no influence from East Asia. The Kizil Caves were designated by the Germans by a series of names, and have been separately numbered by the Chinese. A correspondence chart has been produced by Rhie. Some very early caves, now numbered 90–17 to 90–24, have been discovered since the 1990s in the lower parts of the cliff at the entrance of the central valley.
=== Team Deathmatch === In the team deathmatch mode, players are organized in two teams, Resistance and Combine, both of them with different characters that appear exactly as they do in Half-Life 2. In the gaming aspect, team deathmatch has almost the same rules as deathmatch mode, except for:
=== EU ban === The EU banned estradiol, progesterone, testosterone, zeranol, melengestrol acetate and trenbolone acetate. The first three are synthetic versions of endogenous hormones that are naturally produced in humans and animals, and in a wide range of foods, whereas the last two are synthetic, designed to mimic the behaviour of endogenous hormones. Zeranol (alpha-zearalanol) is produced semi-synthetically, but occurs naturally in some foods. It is one of several derivatives of zearalenone produced by certain Fusarium. Although its occurrence in animal products can be partly due to ingestion of such feeds, alpha-zearalanol can be produced endogenously in ruminants that have ingested zearalenone and some zearalenone derivatives. The EU did not impose an absolute ban. Under veterinary supervision, cattle farmers were permitted to administer the synthetic versions of natural hormones for cost-reduction and possibly therapeutic purposes, such as synchronising oestrus cycles. All six hormones were licensed for use in the US and in Canada. Under the Agreement on the Application of Sanitary and Phytosanitary Measures, signatories have the right to impose restrictions on health and safety grounds subject to scientific analysis. The heart of the dispute was the fact that risk analysis is statistical, and thus unable to determine with absolute certainty the absence of health risks. While US and Canada beef producers claimed that beef produced with the use of hormones was safe, the EU asserted that it was not safe.
Sources: en.wikipedia.org
== History == The first low-cost spectrophotometer capable of recording an infrared spectrum was the Perkin-Elmer Infracord produced in 1957. This instrument covered the wavelength range from 2.5 μm to 15 μm (wavenumber range 4,000 cm−1 to 660 cm−1). The lower wavelength limit was chosen to encompass the highest known vibration frequency due to a fundamental molecular vibration. The upper limit was imposed by the fact that the dispersing element was a prism made from a single crystal of rock-salt (sodium chloride), which becomes opaque at wavelengths longer than about 15 μm; this spectral region became known as the rock-salt region. Later instruments used potassium bromide prisms to extend the range to 25 μm (400 cm−1) and caesium iodide 50 μm (200 cm−1). The region beyond 50 μm (200 cm−1) became known as the far-infrared region; at very long wavelengths it merges into the microwave region. Measurements in the far infrared needed the development of accurately ruled diffraction gratings to replace the prisms as dispersing elements, since salt crystals are opaque in this region. More sensitive detectors than the bolometer were required because of the low energy of the radiation. One such was the Golay detector. An additional issue is the need to exclude atmospheric water vapour because water vapour has an intense pure rotational spectrum in this region. Far-infrared spectrophotometers were cumbersome, slow and expensive.
Benazepril (Lotensin) Cilazapril (Inhibace) Enalapril (Vasotec/Renitec/Berlipril/Enap/Enalapril Profarma) Imidapril (Tanatril) Lisinopril (Listril/Lopril/Novatec/Prinivil/Zestril, Lisidigal) Moexipril (Univasc) Perindopril (Coversyl/Aceon/Perindo) Quinapril (Accupril) Ramipril (Altace/Prilace/Ramace/Ramiwin/Triatec/Tritace/Ramitac) Trandolapril (Mavik/Odrik/Gopten) Ceronapril (never marketed) Fosinopril (Fositen/Monopril) ACE inhibitor peptides can be derived from natural sources such as algae, fruit, seeds, dairy and animal products. A comprehensive resource on anti-hypertensive peptides is available in the form of a database. It contains around 1700 unique antihypertensive peptides. Arfalasin (HOE 409) is an angiotensin antagonist.
The MCM6 gene, MCM6, is expressed at very high level. MCM6 contains 18 introns. There are 2 non overlapping alternative last exons. The transcripts appear to differ by truncation of the 3' end, presence or absence of 2 cassette exons, common exons with different boundaries. MCM6 produces, by alternative splicing, 3 different transcripts, all with introns, putatively encoding 3 different protein isoforms. MCM6 contains two of the regulatory regions for LCT, the gene encoding the protein lactase, located in two of the MCM6 introns, approximately 14 kb and 22 kb upstream of LCT. A substitution of thymine for cytosine in the first region (at -13910), in particular, has been shown to function in vitro as an enhancer element capable of differentially activating transcription of LCT promoter. Mutations in these regions are associated with lactose tolerance into adult life. MCM6 has been shown to interact with: Mini Chromosome Maintenance
Dexatrim has been on the market for more than 45 years. The brand was originally owned by Thompson Medical, which was acquired by Chattem in 1998. It is now part of Sanofi. Dexatrim formula has changed considerably over the years. In prior formulations, Dexatrim contained the decongestant phenylpropanolamine (PPA) and the amphetamine-like compound ephedra. A 2000 study by Yale University School of Medicine showed an increased risk of hemorrhagic stroke with taking PPA. A case of myocardial injury was also reported using Dexatrim (with PPA) at doses recommended for weight control. In 2000, following the request of the FDA to discontinue marketing drug products containing PPA, Dexatrim dropped PPA from its formula. In 2004, FDA banned a second Dexatrim ingredient, ephedra. Although ephedra showed some effectiveness for short-term weight loss, it was linked to raising blood pressure and increasing the risk of heart problems and stroke. In March 2014, Chattem sold Dexatrim to NVE Pharmaceuticals.
Sources: en.wikipedia.org
Natural GHRH is degraded quickly by dipeptidyl peptidase-4 and related enzymes, giving it a half-life measured in minutes. CJC-1295 carries substitutions that slow that breakdown, so it stays intact longer. Both act at the same pituitary receptor and produce the same class of signal.
The label was first attached to the albumin-binding form during early development work. A shorter analog without the linker later became known by the same name in informal use. Published papers normally state which version was studied, so the methods section resolves the ambiguity.
It is a synthetic peptide rather than a steroid, and it does not occur naturally in the body. Its sequence is derived from a hypothalamic hormone called growth hormone-releasing hormone. It works as a receptor agonist rather than as a replacement for that 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.