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Last reviewed on 2026-06-25. Where a claim depends on a specific study, the study is described rather than over-claimed.
CJC-1295 is a synthetic peptide analog of growth hormone-releasing hormone, constructed on the 29-amino-acid fragment designated GRF(1-29). The name began as an internal development code during the 1990s and later spread through research supply catalogs and discussion forums. The molecule does not occur in nature; its sequence is engineered rather than isolated from tissue. Two related compounds are sold under this single label, and they differ by one appended chemical group that strongly influences how long the peptide remains in circulation.
The dividing feature between the two forms is a maleimide-based drug affinity complex, abbreviated DAC. In the DAC-bearing version, a linker attaches the peptide to serum albumin after administration, and that association slows removal from plasma. The version lacking DAC appears in catalogs as MOD GRF(1-29) or tetrasubstituted GRF(1-29). Because informal writing treats both as one item, comparisons drawn from such sources routinely blend measurements taken from two molecules with substantially different behavior.
Four amino acid substitutions separate the modified backbone from the parent GRF(1-29) sequence. These changes reduce recognition by dipeptidyl peptidase IV and related proteases, extending the interval before degradation. Development work in this area sought longer-acting GHRH analogs for endocrine investigation. Published descriptions treat the substitution set as a defining property of the core sequence, while the albumin-binding linker is described separately as an optional addition to that same backbone.
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.
| Property | Value | Notes |
|---|---|---|
| Molecular class | Synthetic peptide | Analog of growth hormone-releasing hormone |
| Chain length | 29 amino acids | Based on the GRF(1-29) fragment |
| Appearance | White to off-white lyophilized powder | Common research supply form |
| Solubility | Soluble in water and aqueous buffers | Powder requires reconstitution before use |
| Typical storage | −20 °C or below | Kept away from light and moisture |
The two variants differ dramatically in how long they persist in circulation. The form lacking the albumin-binding group has a plasma half-life measured in tens of minutes, comparable to the natural hormone fragment. The version carrying the drug affinity complex binds albumin and shows a half-life of roughly six to eight days in human studies. That figure comes from small trials that tracked hormone levels over extended periods. The physiological consequences of sustained versus pulsatile stimulation are still debated and the literature does not settle the point.
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.
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.
Binding to GHRH receptors on pituitary somatotroph cells triggers cyclic AMP signaling and stimulates growth hormone synthesis and release. Because the peptide acts upstream of the pituitary, effects are mediated through endogenous growth hormone rather than direct receptor activation in peripheral tissues. Increases in insulin-like growth factor 1 are generally described as a downstream consequence. Most published human exposure data come from small early-stage studies, and the clinical significance of the pharmacokinetic profile remains incompletely characterized.
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.
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palindromic sequence Also palindrome. A nucleic acid sequence of a double-stranded DNA or RNA molecule in which the unidirectional sequence (e.g. 5' to 3') of nucleobases on one strand is identical to the sequence in the same direction (e.g. 5' to 3') on the complementary strand. In other words, a sequence is said to be palindromic if it is equal to its own reverse complement. Palindromic motifs are common recognition sites for restriction enzymes.
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== Calculation of Amino Acid Residue Volume == Because of the van der Waals force, atoms occupy space, which prevents other atoms from passing through each other. This 3D space or volume is called the excluded volume. Excluded volume is defined as the volume occupied by an atom or residue as determined by its atomic radii and its nearest neighbors. Excluded volume it is typically given in units of cubic Angstroms. In VADAR the excluded volume for each amino acid residue is listed under two different column headers: RES VOL (residue volume) and FRAC VOL (fractional volume). Residue volume is presented in cubic Angstraoms and calculated using the Voronoi polyhedra algorithm that was first introduced by Dr. Frederic Richards. In VADAR the number listed under the RES VOL header corresponds to the excluded volume (in cubic Angstroms) while the value under the FRAC VOL header corresponds to the fractional volume (which ranges from 0 to 1.0 or more). If a protein is efficiently packed, all of its residues should have fractional volumes close to 1.0 (+/- 0.1). In certain circumstances, if an amino acid residue is located in an interior cavity (or it has been placed improperly through poor refinement) it could have a fractional volume greater than 1.20. An amino acid residue located in a compressed region or a poorly refined region will have a fractional volume less than 0.80. Structural biologists often use excluded volume to help them find cavities, water-binding pockets, unexpected atomic overlaps or to identify problem areas in a protein structure.
Sources: en.wikipedia.org
== Discovery == In 1902, Léon Teisserenc de Bort from France and Richard Assmann from Germany, in separate but coordinated publications and following years of observations, published the discovery of an isothermal layer at around 11–14 km (6.8-8.7 mi), which is the base of the lower stratosphere. This was based on temperature profiles from mostly unmanned and a few manned instrumented balloons.
=== Pharmacodynamics === Dutasteride belongs to a class of drugs called 5α-reductase inhibitors, which block the action of the 5α-reductase enzymes that convert testosterone into DHT. It inhibits all three forms of 5α-reductase, and can decrease DHT levels in the blood by up to 98%. Specifically it is a competitive, mechanism-based (irreversible) inhibitor of all three isoforms of 5α-reductase, types I, II, and III (IC50Tooltip Half-maximal inhibitory concentration values are 3.9 nM for type I and 1.8 nM for type II). This is in contrast to finasteride, which is similarly an irreversible inhibitor of 5α-reductase but only inhibits the type II and III isoenzymes. As a result of this difference, dutasteride is able to achieve a reduction in circulating DHT levels of up to 98%, whereas finasteride is able to achieve a reduction of only 65 to 70%. In spite of the differential reduction in circulating DHT levels, the two drugs decrease levels of DHT to a similar extent of approximately 85 to 90% in the prostate gland, where the type II isoform predominates. Since 5α-reductases degrade testosterone to DHT, the inhibition of these enzymes could theoretically cause an increase in testosterone. A 2018 review found that initiation of 5α-reductase inhibitors did not result in a consistent increase in testosterone levels. Among the studies analyzed, there was no statistically significant change in testosterone levels from 5α-reductase inhibitors overall, though men with lower baseline testosterone levels did show an increase.
=== Tumors in CUX1 transgenic mice === CUX1 transgenic mice develop tumors in multiple organs and tissues after a long latency period. Transgenic mice expressing either p75, p110 or p200 CUX1 in mammary epithelial cells develop mammary tumours with a low penetrance (~20%) and with a long latency period. Metastasis to the lung was observed in three cases of mammary tumors expressing p75 CUX1. The mechanisms of action differ widely between p110 CUX1 and p200 CUX1. Transgenic mice expressing p110 CUX1 in mammary epithelial cells develop mammary tumors that exhibit a sub-tetraploid chromosome number, suggesting passage through tetraploidy resulting from cytokinesis failure. Cells do not usually survive as tetraploid with multiple centrosomes. Overexpression of p110 CUX1 was shown to activate a transcriptional program that reinforces the spindle assembly checkpoint and delays mitosis until extranumerary centrosomes have clustered to two poles, thereby enabling bipolar mitosis and survival of tetraploid cells. Yet, passage through a multipolar intermediate enriches for merotelic chromosome attachments, leading to chromosome mis-segregation and the rapid generation of aneuploid populations from which tumorigenic cells emerge. Tumors that develop in p200 CUX1 transgenic mice reveal a different mode of action, as 44% of these tumors harboured a spontaneous mutation activating the Kras gene. The cooperation between RAS and p200 CUX1 was confirmed by lentiviral infections in the lung. RAS oncogenes do not transform primary cells, but instead cause cellular senescence.
Sources: en.wikipedia.org
No. It is a laboratory-synthesized analog built on a fragment of the natural hormone. The natural peptide is shorter-lived and lacks the stabilizing substitutions found in the synthetic version.
DAC stands for drug affinity complex, a chemical group that binds the peptide to serum albumin. The binding slows clearance and lengthens the time the molecule stays in plasma compared with the unmodified analog.
Because two distinct molecules are discussed under one informal label. The albumin-binding version clears over several days, while the form without that group clears within roughly half an hour. Mixing results from both creates inconsistent figures.
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.