A practical reference on MOD GRF 1-29: what it is, how it behaves, what the literature reports, and where the honest uncertainties sit.
This page was last updated on 2026-05-19 and is reviewed periodically as new material appears.
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.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular class | Synthetic peptide | GHRH analog, not a steroid |
| Backbone length | 29 amino acids | Based on GRF(1-29) |
| Substitutions | Four positions | D-Ala2, Gln8, Ala15, Leu27 |
| Appearance | White to off-white powder | Typical lyophilized research material |
| Common synonyms | Modified GRF(1-29) | Usage varies between sources |
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.
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.
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.
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.
Metopon (5-methylhydromorphone, CAS number 124-92-5) is an opioid analogue that is a methylated derivative of hydromorphone which was invented in 1929 as an analgesic. Metopon is sometimes used in medicine. Although longer acting than hydromorphone, metopon is less potent and its oral bioavailability is fairly low. Generally, metopon has few advantages to distinguish it from other, more commonly used opioid analgesics, although it does have a slightly lower tendency to produce nausea and respiratory depression compared to morphine. In Canada, as of 1948, the hydrochloride of metopon (free base conversion ratio 0.891, molecular weight 335.8) was available only for oral administration for malignant pain and for maintenance of those habituated to morphine; the only dosage form available was singly scored 8 mg tablets. It was manufactured by Parke, Davis, & Co., and was only for sale to doctors and hospitals. Parke, Davis & Co. did not sell metopon to pharmacies. It is unknown whether metopon tablets are still manufactured and sold in Canada. Metopon tablets, ampoules, and suppositories are available in Switzerland, Austria, Germany, and other countries in Continental Europe and the drug is used in Patient Controlled Analgesia pumps for severe chronic pain in particular. Metopon is listed under Schedule II of the US Controlled Substances Act 1970, meaning it has an accepted medical use, but at this time it is not produced commercially and is seen only in laboratory research. It did see some use in medicine — oncology in particular — in the US in the 1950s.
=== Pharmacodynamics === Lasofoxifene selectively binds to both ERα and ERβ with high affinity. Its IC50 for ERα (1.5 nM) is similar to that of estradiol (4.8 nM) and is at least 10-fold higher than those of tamoxifen.
Acetylsalicylic acid/atorvastatin/ramipril (acetylsalicylic acid + atorvastatin + ramipril) Acetylsalicylic acid/simvastatin/ramipril/atenolol/hydrochlorothiazide (acetylsalicylic acid + simvastatin + ramipril + atenolol + hydrochlorothiazide) Atorvastatin/perindopril/amlodipine (atorvastatin + perindopril + amlodipine)
Sources: en.wikipedia.org
== Side effects == The most common side effects of sulfamethoxazole are gastrointestinal disturbances (nausea, vomiting, anorexia) and allergic skin reactions (such as rash and urticaria). There have been rare instances where severe adverse reactions have resulted in fatalities. These include Stevens–Johnson syndrome (SJS), toxic epidermal necrolysis, fulminant hepatic necrosis, agranulocytosis, aplastic anemia, and other blood dyscrasias. Allergic reactions to Sulfonamides have been shown to include the entire Gel-Coombs spectrum of hyperactivity reactions. Type 1 reactions include immunoglobulin E (IgE)-mediated reactions such as urticaria, angioedema, and anaphylaxis. In contrast, non-type 1 hypersensitivities are believed to be caused by metabolites of sulfonamides. Therefore, the liver and kidney are the determining factors of these other hypersensitivity reactions; alterations in kidney or liver functions may increase or decrease the frequencies of these reactions. One study has shown the allergic reaction rate to be about 3.0% over 359 courses of therapy. Of the allergic reactions, skin rashes, eosinophilia and drug fever were the most common, while serious reactions were less common. Sulfamethoxazole is contraindicated in people with a known hypersensitivity to trimethoprim or sulfonamides.
In pharmacokinetics, a loading dose is an initial higher dose of a drug that may be given at the beginning of a course of treatment before dropping down to a lower maintenance dose. A loading dose is most useful for drugs that are eliminated from the body relatively slowly, i.e., which have a long systemic half-life. Such drugs need only a low maintenance dose in order to keep the amount of the drug in the body at the appropriate therapeutic level, but this also means that, without an initial higher dose, it would take a long time for the amount of the drug in the body to reach that level. Drugs which may be started with an initial loading dose include digoxin, teicoplanin, voriconazole, procainamide and fulvestrant. One or a series of doses may be given at the onset of therapy with the aim of achieving the target concentration rapidly.
=== Purge gas === Purge gas is used to control the sample environment, in order to reduce signal noise and to prevent contamination. Mostly nitrogen is used and for temperatures above 600 °C, argon can be utilized to minimize heat loss due to the low thermal conductivity of argon. Air or pure oxygen can be used for oxidative tests like oxidative induction time and He is used for very low temperatures due to the low boiling temperature (~4.2K at 101.325 kPa ).
=== Herbal Medicine === There are herbs that kill or interrupt the lifecycle of scabies mites both in the lab and when topically applied to living people. Despite this, curing the condition solely with herbal medicine is difficult and often not recommended, even by advocates of herbal medicine. There are many natural chemicals that are insecticides (bug killing), acaricides (tick and mite killing), miticides (mite killing), and/or scabicides (Scabies mite killing). Many herbal recepies exist to fight mite-caused diseases including the highly-related sarcoptic mange in other animals but they may claim only to treat symptoms, lessen severity, or prevent new infections. Interest in herbal and hybrid treatments is partially driven by concerns about drug-resistance. Herbs with documented scabicidal effects include thyme, majoram, clove, camphor tree, geranium, tea tree, rosemary, oregano, neem, and coconut. Herbal medicines that kill mites in lab settings may not be safe to apply topically at that concentration. These medicines may also not absorb through the skin well enough to kill mites in pustules, nodules, or burrows.
Sources: en.wikipedia.org
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.
The original material included a linker that binds serum albumin. A later variant removed that linker to reduce the duration of action. Catalogs and papers did not consistently adopt separate names, so both remain widely labeled with the same term.
The amino acid sequence and the presence or absence of the linker group. Mass measured by spectrometry gives an independent check that separates the two forms.
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.