This is a working overview of GHRH analog, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2025-11-08 and is reviewed periodically as new material appears.
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.
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 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.
| Property | Value | Notes |
|---|---|---|
| Molecular weight, DAC form | About 3647 Da | Varies with salt form |
| Molecular weight, non-DAC form | About 3358 Da | MOD GRF(1-29) |
| Solubility class | Water soluble | Also dissolves in polar solvents |
| Reported half-life, DAC form | About five to eight days | Values from human studies |
| Common synonyms | CJC-1295; MOD GRF(1-29) | Name depends on variant |
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.
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.
Once in circulation, the peptide binds the growth hormone-releasing hormone receptor displayed on pituitary somatotroph cells. Receptor activation couples to Gs proteins, elevates intracellular cyclic AMP, and drives protein kinase A signaling inside the cell. That cascade increases discharge of growth hormone into the bloodstream. The analog therefore operates through a receptor pathway that already exists for the body's own releasing hormone, rather than through an engineered artificial target.
Clearance profiles diverge sharply between the two versions. The albumin-binding molecule stays in plasma for several days, whereas the unmodified analog is largely gone within about half an hour in reported work. Cleavage by dipeptidyl peptidase IV is a major contributor to the short life of the unmodified sequence. These gaps mean the two versions cannot be substituted for each other in study design or in reading results side by side.
Reports on this compound commonly follow serum growth hormone and insulin-like growth factor 1 across defined time windows. Protocols differ in sampling frequency, assay platform, and participant characteristics, which makes direct comparison between publications difficult. Some work focuses on pulsatile release patterns instead of average concentrations. Whether repeated exposure alters endogenous hormone rhythms over long periods remains an open question, and the formal literature is thinner than the volume of informal commentary implies.
Light output is approximately proportional to V 3.4 Power consumption is approximately proportional to V 1.6 Lifetime is approximately proportional to V −16 Color temperature is approximately proportional to V 0.42 A 5% reduction in voltage will double the life of the bulb, but reduce its light output by about 16%. Long-life bulbs take advantage of this trade-off in applications such as traffic signal lamps. Since electric energy they use costs more than the cost of the bulb, general service lamps emphasize efficiency over long operating life. The objective is to minimize the cost of light, not the cost of lamps. Early bulbs had a life of up to 2500 hours, but in 1924 the Phoebus cartel agreed to limit life to 1000 hours. When this was exposed in 1953, General Electric and other leading American manufacturers were banned from limiting the life. The relationships above are valid for only a few percent change of voltage around standard rated conditions, but they indicate that a lamp operated at low voltage could last much longer than at rated voltage, albeit with greatly reduced light output. The "Centennial Light" is a light bulb that is accepted by the Guinness Book of World Records as having been burning almost continuously at a fire station in Livermore, California, since 1901. However, the bulb emits the equivalent light of a four watt bulb. A similar story can be told of a 40-watt bulb in Texas that has been illuminated since 21 September 1908.
Carbonylation of alcohols as illustrated by the Cativa process for the production of acetic acid. Formic acid is prepared by a different carbonylation pathway, also starting from methanol. Oxidation of aldehydes with air using cobalt and manganese catalysts. The required aldehydes can be obtained from alkenes by hydroformylation. Oxidation of hydrocarbons using air. For simple alkanes, this method is inexpensive but not selective enough to be useful. Allylic and benzylic compounds undergo more selective oxidations. Alkyl groups on a benzene ring are oxidized to the carboxylic acid, regardless of its chain length. Benzoic acid from toluene, terephthalic acid from para-xylene, and phthalic acid from ortho-xylene are illustrative large-scale conversions. Acrylic acid is generated from propene. Hydrocarboxylation of alkenes. This method is effective for alkenes that generate secondary and tertiary carbocations, e.g. isobutylene to pivalic acid. In the Koch reaction, the addition of water and carbon monoxide to alkenes or alkynes is catalyzed by strong acids. Hydrocarboxylations involve the simultaneous addition of water and CO. Such reactions are sometimes called "Reppe chemistry." HC≡CH + CO + H2O → CH2=CH−CO2H Hydrolysis of esters. Triglycerides, obtained from plant or animal oils, are precursors to long-chain carboxylic acids are related to soap making. Fermentation of ethanol. This method is used in the production of vinegar. Carbonation, such as the Kolbe–Schmitt reaction as a route to salicylic acid, precursor to aspirin.
While Thatcher won the contest, winning the votes of 85% of Conservative MPs, the next day's Glasgow Herald reported that Heseltine's supporters predicted that unless she changed "her style of leadership", she would "be on her way out next year". In spring 1990 Thatcher's political fortunes were looking weaker, as the Conservatives were badly defeated at the Mid Staffordshire by-election and the Poll tax riots took place. But despite Conservative losses at the local elections, Party Chairman Kenneth Baker spun the result as a success by pointing to the Conservative hold of Westminster and Wandsworth Councils, where the poll tax was low. In May 1990, following the elections, Heseltine wrote an article in The Times proposing reform of the poll tax – he called for the tax to be banded according to income, for councils which spent more than a certain level to face mandatory elections, for elected local mayors and for the restoration of the unitary county boroughs (i.e. making smaller cities into counties in their own right, so ending the confusion as to whether county or district council were responsible for high spending) which he himself had abolished. However, the Iraqi invasion of Kuwait in August 1990, which made war seem likely, boosted Thatcher's popularity.
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==== Cancer ==== While traditional chemotherapy can effectively kill cancer cells, lack of specificity for discriminating normal cells and cancer cells in these treatments usually cause severe side effects. Numerous studies have demonstrated that RNAi can provide a more specific approach to inhibit tumor growth by targeting cancer-related genes (i.e., oncogene). It has also been proposed that RNAi can enhance the sensitivity of cancer cells to chemotherapeutic agents, providing a combinatorial therapeutic approach with chemotherapy. Another potential RNAi-based treatment is to inhibit cell invasion and migration. Compared with chemotherapy or other anti-cancer drugs, there are a lot of advantages of siRNA drug. SiRNA acts on the post-transcriptional stage of gene expression, so it does not modify or change DNA in a deleterious effect. SiRNA can also be used to produce a specific response in a certain type of way, such as by downgrading suppression of gene expression. In a single cancer cell, siRNA can cause dramatic suppression of gene expression with just several copies. This happens by silencing cancer-promoting genes with RNAi, as well as targeting an mRNA sequence. RNAi drugs treat cancer by silencing certain cancer promoting genes. This is done by complementing the cancer genes with the RNAi, such as keeping the mRNA sequences in accordance with the RNAi drug. Ideally, RNAi is should be injected and/or chemically modified so the RNAi can reach cancer cells more efficiently. RNAi uptake and regulation is controlled by the kidneys.
Puberty is the process of physical changes through which a child's body matures into an adult body capable of sexual reproduction. It is initiated by hormonal signals from the brain to the gonads: the ovaries in a female, the testicles in a male. In response to the signals, the gonads produce hormones that stimulate libido and the growth, function, and transformation of the brain, bones, muscle, blood, skin, hair, breasts, and sex organs. Physical growth—height and weight—accelerates in the first half of puberty and is completed when an adult body has been developed. Before puberty, the external sex organs, known as primary sexual characteristics, are sex characteristics that distinguish males and females. Puberty leads to sexual dimorphism through the development of the secondary sex characteristics, which further distinguish the sexes. On average, females begin puberty at age 10½ and complete puberty at ages 15–17; males begin at ages 11½–12 and complete puberty at ages 16–17. The major landmark of puberty for females is menarche, the onset of menstruation, which occurs on average around age 12½. For males, first ejaculation, spermarche, occurs on average at age 13. In the 21st century, the average age at which children, especially females, reach specific markers of puberty is lower compared to the 19th century, when it was 15 for females and 17 for males (with age at first periods for females and voice-breaks for males being used as examples).
== History == From 1946 to 1948, the eleven states formed a single British crown colony known as the Malayan Union. Due to opposition from Malay nationalists, the Union was disbanded and replaced by the Federation of Malaya, which restored the symbolic positions of the rulers of the Malay states and introduced greater restrictions on the attainment of citizenship status. Within the Federation, while the Malay states were protectorates of the United Kingdom, Penang and Malacca remained British colonial territories. Like the Malayan Union before it, the Federation did not include Singapore, despite its traditional connections with Malaya. The Malaya Agreement was formulated by the British–Malay Pleno Conference between June and December 1946. At the end of the meeting, the Pleno Conference produced a 100-page "Blue Book." It was signed on 21 January 1948 at King House by the Malay rulers, and by Sir Edward Gent as the representative of the British government. The Agreement superseded the Agreement creating the Malayan Union, and prepared for the establishment of the Federation of Malaya on 1 February 1948. The position of the Malay rulers was also restored. The Federation became independent from British colonial rule and became an independent member of the Commonwealth of Nations on 31 August 1957. In 1963, the Federation was reconstituted as "Malaysia" when it federated with the British territories of Singapore, Sarawak, and North Borneo; a claim to the latter territory was maintained by the Philippines.
Sources: en.wikipedia.org
It is a synthetic peptide modeled on growth hormone-releasing hormone. The molecule is used in research on pituitary growth hormone secretion. It differs from the natural hormone through several stabilizing substitutions.
The DAC form carries a maleimide group that binds albumin and extends circulation time. The non-DAC form lacks this group and clears much faster. Both share the same receptor-binding core.
It targets the growth hormone-releasing hormone receptor on pituitary somatotroph cells. Activation raises cyclic AMP and promotes growth hormone release. Normal feedback pathways remain part of the response.
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.