If you have been reading about Reconstitution and want a single page that covers the useful parts, this is it: definitions, context, how it is studied, and the questions that come up repeatedly.
Updated 2026-01-23. Numbers and descriptions here follow the published literature rather than marketing material.
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.
CJC-1295 is a synthetic peptide designed to mimic growth hormone-releasing hormone (GHRH), the endogenous signal that prompts the pituitary gland to release growth hormone. The compound is a modified fragment of the natural hormone, spanning the first twenty-nine amino acids of GHRH with several substitutions that slow enzymatic breakdown. Two variants circulate in research settings: one carrying a drug affinity complex (DAC) and one without it. The DAC-free form is frequently labelled Mod GRF(1-29) in catalogs and discussion forums.
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.
| Property | Value | Notes |
|---|---|---|
| Appearance | White to off-white lyophilized powder | Visual descriptor; not a measure of purity |
| Solubility class | Freely soluble in water | Aqueous dissolution may require gentle mixing |
| Typical storage (powder) | −20 °C or below, desiccated | Protect from light and ambient moisture |
| Typical storage (solution) | 2–8 °C, short term | Freeze aliquots where longer holding is needed |
| Purity assessment | Reversed-phase HPLC, area percent | Values depend on column, gradient, and detection wavelength |
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.
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 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.
== 2013 supplements controversy == Following months of rumours and investigations, on 13 August 2013, Thompson, along with the Essendon Football Club, senior coach James Hird, football manager Danny Corcoran and club doctor Bruce Reid, were charged by the AFL with bringing the game into disrepute in relation to the supplements program at the club in 2011 and 2012. The club was given 14 days to consider the charges and faced an AFL Commission hearing on 26 August 2013. On 27 August 2013, Thompson was fined $30,000 for his role in the supplements saga.
== History == Lidocaine, the first amino amide–type local anesthetic (previous were amino esters), was first synthesized under the name 'xylocaine' by the team of chemist Nils Löfgren in 1943. Inga Fischer is credited for being the first to synthesize it at large-scale in the laboratory. Bengt Lundqvist performed the first injection anesthesia experiments on himself. It was first marketed in 1948 by Astra.
For example, studies have identified TLR4 as the receptor for the LPS component of Gram-negative bacteria. TLRs are key regulators of both innate and adaptive immune responses. Unlike RelA, RelB, and c-Rel, the p50 and p52 NF-κB subunits do not contain transactivation domains in their C terminal halves. Nevertheless, the p50 and p52 NF-κB members play critical roles in modulating the specificity of NF-κB function. Although homodimers of p50 and p52 are, in general, repressors of κB site transcription, both p50 and p52 participate in target gene transactivation by forming heterodimers with RelA, RelB, or c-Rel. In addition, p50 and p52 homodimers also bind to the nuclear protein Bcl-3, and such complexes can function as transcriptional activators.
Sources: en.wikipedia.org
== Disease relevance == In humans, there has been a significant increase in disease from pathogenic fungi, so developing anti-fungal drugs is an important biochemical task. As homoserine dehydrogenase is found mainly in plants, bacteria, and yeast, but not mammals, it is a strong target for antifungal drug development. Recently, 5-hydroxy-4-oxonorvaline (HON) was discovered to target and inhibit HSD activity irreversibly. HON is structurally similar to aspartate semialdehyde, so it is postulated that it serves as a competitive inhibitor for HSD. Likewise, (S) 2-amino-4-oxo-5-hydroxypentanoic acid (RI-331), another amino acid analog, has also been shown to inhibit HSD. Both of these compounds are effective against Cryptococcus neoformans and Cladosporium fulvum, among others. In addition to amino acid analogs, several phenolic compounds have been shown to inhibit HSD activity. Like HON and RI-331, these molecules are competitive inhibitors that bind to the enzyme active site. Specifically, the phenolic hydroxyl group interacts with the amino acid binding site.
=== PE Biosystems === In 1998, PE Applied Biosystems became PE Biosystems, and the division's revenues reached US$921.8 million. In January 1998 Perkin-Elmer acquired PerSeptive Biosystems (formerly of Framingham, Massachusetts. It was a leader in the bio-instrumentation field where it made biomolecule purification systems for protein analysis. Noubar Afeyan, Ph.D., had been the founder, chairman, and CEO of PerSeptive, and with the Perkin-Elmer successor company he set up the later tracking stock for Celera. In 1998, Perkin-Elmer formed the PE Biosystems division, by consolidating Applied Biosystems, PerSeptive Biosystems, Tropix and PE Informatics. Informatics was formed from the Perkin-Elmer combination of two other acquisitions, Molecular Informatics and Nelson Analytical Systems, with existing units of Perkin-Elmer. While planning the next new generation of machines, PE Biosystems' president, Michael W. Hunkapiller, calculated that it would be possible for their own private industry to decode the human genome before the academic consortium could complete it, by using the resources of a single, industrial-scale center, even though it would require starting from scratch. It was a bold prediction, given that the consortium target date set by Dr. Watson back in 1990 had been the forward year of 2005, only seven years away, and with the consortium already half the way to the completion target date. Also, it meant that Dr.
== Applications == Research into the AMP family—particularly in regards to their mechanism of action—has been ongoing for nearly 20 years. Despite sustained interest, treatments derived or utilizing AMPs have not been widely adopted for clinical use for several reasons. One, drug candidates from AMPs have a narrow window of bioavailability, because peptides are quickly broken down by proteases. Two, peptide drugs are more expensive than small molecule drugs to produce, which is problematic since peptide drugs must be given in large doses to counter rapid enzymatic breakdown. These qualities also limit routes of administration, typically to injection, infusion, or slow release therapy. Research into new and improved variations derived from cathelicidin continues.
ketogenic amino acid Any amino acid that can be converted directly into acetyl-CoA, which can then be oxidized for energy or used as a precursor for many compounds containing ketone groups. This is in contrast to the glucogenic amino acids, which can be converted into glucose. In humans, seven of the 20 amino acids are ketogenic, though only leucine and lysine are exclusively ketogenic; the other five (phenylalanine, isoleucine, threonine, tryptophan, and tyrosine) are both ketogenic and glucogenic.
Sources: en.wikipedia.org
Cool, dark, and dry conditions are standard, with storage at minus twenty degrees Celsius or below. Desiccant and sealed vials limit moisture uptake. Repeated warming and cooling of the container is generally avoided.
There is no single agreed limit, and laboratory practice varies widely. Refrigeration slows degradation, and freezing aliquots is often described for longer holding. Any visible cloudiness or precipitate indicates the solution should be discarded.
Mass spectrometry provides the most direct confirmation through molecular mass. Reversed-phase chromatography supports purity assessment, and peptide mapping or amino acid analysis can corroborate sequence. No single method establishes both purity and identity on its own.
The synthetic peptide keeps the receptor-binding region of GHRH but carries substitutions that resist enzymatic cleavage. In the DAC version, an added group also anchors the molecule to albumin, extending its presence in the bloodstream.