This is a working overview of GHRH receptor, written for readers who want more than a one-paragraph summary but less than a textbook.
This page was last updated on 2026-05-26 and is reviewed periodically as new material appears.
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 backbone includes a D-alanine at position two, which resists cleavage by dipeptidyl peptidase IV, and several other substitutions that reduce degradation. Its molecular weight is roughly 3.4 kDa without the linker and about 3.6 kDa with it. The molecule is water soluble and is normally supplied as a lyophilized powder. Precise sequence and mass values depend on which variant is described, so technical documents usually state the exact form being referenced.
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 |
|---|---|---|
| Molecular weight (no linker) | ~3.37 kDa | Calculated from peptide sequence |
| Molecular weight (with linker) | ~3.65 kDa | Includes albumin-binding moiety |
| Appearance | White to off-white powder | Typically lyophilized |
| Solubility | Soluble in water | Also dissolves in aqueous buffers |
| Common synonyms | Modified GRF(1-29), DAC:GRF | Usage varies by source |
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.
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.
Research material is normally supplied as a freeze-dried powder in sealed vials. In that state the peptide is comparatively robust, but prolonged exposure to warmth, moisture, or light accelerates degradation. Storage at minus twenty degrees Celsius or lower, with desiccant and protection from light, is the commonly described practice. Vials should be allowed to reach room temperature before opening to limit condensation on the powder. Moisture uptake during handling is a recognized source of variability in later measurements.
The attached maleimide group explains the unusual duration of the DAC version. After injection it reacts with the thiol of cysteine-34 on serum albumin, forming a stable covalent bond. The resulting conjugate is too large for rapid kidney filtration and is shielded from many peptidases. Reported half-lives for this form reach several days, whereas the version without the group is cleared in roughly half an hour. That gap is the main pharmacological difference between the two.
Downstream of growth hormone, the liver and other tissues increase production of insulin-like growth factor 1, a mediator of many growth-promoting effects. Studies have documented elevated levels of both hormones after dosing, and the rise from the long-acting form persists longer than that produced by shorter-acting analogues. What remains unclear is whether sustained elevation of these markers translates into meaningful clinical benefit, and whether prolonged exposure carries risks that short trials could not detect.
On the contrary, in the septal area is largely consistent of atrial cells (88±19%) while maintains a uniform presence of all four types of sinoatrial node cells: Elongated spindle-shaped cells, Spindle cells, Spider cells and Atrial cells. Action potentials pass from one cardiac cell to the next through pores known as gap junctions. These gap junctions are made of proteins called connexins. There are fewer gap junctions within the SA node and they are smaller in size. This is again important in insulating the SA node from the surrounding atrial cells.
The tiger snake (Notechis scutatus) is highly venomous. Its venom possesses potent neurotoxins, coagulants, haemolysins and myotoxins and the venom is quick-acting with rapid onset of breathing difficulties and paralysis. The untreated mortality rate from tiger snake bites is reported to be between 40 and 60%. It is a major cause of snakebites and occasional snakebite deaths in Australia. The African tiger snake (Telescopus semiannulatus), 60–70 cm long, on the other hand, is rear-fanged and only mildly venomous and not dangerous to humans.
Resurgence of train ridership in the 21st century pushed the current Pennsylvania Station under Madison Square Garden to capacity, leading to several proposals to renovate or rebuild the station, often characterized as correcting for the 1960s demolition of the original facility. The Times noted in 2025 that a succession of elected officials over several decades—including Governors Pataki, Spitzer, Cuomo, and Hochul—had made gestures at reconstructing the station, though no such reconstruction ultimately materialized. Among the reasons, the Times cited the controlling interests of multiple transit companies—Amtrak, which owns the station, along with NJ Transit and the MTA, which operate within it—and the influence of James Dolan, whose company owns Madison Square Garden and the air rights above the station. Several of the failed plans were entangled with questions of if and how to move the Garden; in 2008, Eliot Spitzer induced the Garden to sign a memorandum of understanding to move one block west as part of a planned station reconstruction, although his plan fizzled after he was felled by a prostitution scandal only a week later. In 2013, the Regional Plan Association and Municipal Art Society formed the Alliance for a New Penn Station, advocating for limiting the extension of Madison Square Garden's operating permit to ten years and soliciting designs to move the arena.
Sources: en.wikipedia.org
=== Copper toxicity === The classic copper-catalyzed azide-alkyne cycloaddition has been an extremely fast and effective click reaction for bioconjugation, but it is not suitable for use in live cells due to the toxicity of Cu(I) ions. Toxicity is due to oxidative damage from reactive oxygen species formed by the copper catalysts. Copper complexes have also been found to induce changes in cellular metabolism and are taken up by cells. There has been some development of ligands to prevent biomolecule damage and facilitate removal in in vitro applications. However, it has been found that different ligand environments of complexes can still affect metabolism and uptake, introducing an unwelcome perturbation in cellular function.
== Vaccination Campaign == On 13 November, the government of Sudan requested help from the International Coordinating Group on Yellow Fever Vaccine Provision (YF-ICG) in starting a mass vaccination campaign. Besides the WHO, the YF-ICG consists of representatives of the United Nations Children's Fund (UNICEF), Médecins sans Frontières (MSF) and the International Federation of Red Cross and Red Crescent Societies (IFRC). The United Nations–African Union Mission in Darfur (UNAMID) airlifted the first batches of vaccines from Khartoum to Darfur on 18 November. Mass vaccination began on 20 November. Efforts were also undertaken to eliminate mosquitoes. A team from the Naval Medical Research Unit Three (NAMRU-3) and the WHO Collaborating Center was deployed from Cairo to help collect and test samples and train local personnel. The vaccination campaign, from late November 2012 through early January 2013, covered more than 3 million people and halted the outbreak. A new phase of the campaign beginning in January covered more than 2 million more people at risk. One of the difficulties was maintaining a cold chain for vaccine viability while transporting vaccine by donkey into remote areas. A situation report released on 10 January 2013 reported that 171 people had died of the disease as of 9 January 2013. The number of suspected cases since 2 September 2012 was 847. The Minister of Health had announced on 5 January that no additional cases had appeared in the previous 3 weeks.
== Regulation by the photoperiod == The levels of proopiomelanocortin (pomc) are regulated indirectly in some animals by the photoperiod. It is referred to the hours of light during a day and it changes across the seasons. Its regulation depends on the pathway of thyroid hormones that is regulated directly by the photoperiod. An example are the siberian hamsters who experience physiological seasonal changes dependent on the photoperiod. During spring in this species, when there is more than 13 hours of light per day, iodothyronine deiodinase 2 (DIO2) promotes the conversion of the prohormone thyroxine (T4) to the active hormone triiodothyronine (T3) through the removal of an iodine atom on the outer ring. It allows T3 to bind to the thyroid hormone receptor (TR), which then binds to thyroid hormone response elements (TREs) in the DNA sequence. The pomc proximal promoter sequence contains two thyroid-receptor 1b (Thrb) half-sites: TCC-TGG-TGA and TCA-CCT-GGA indicating that T3 may be capable of directly regulating pomc transcription. For this reason during spring and early summer, the level of pomc increases due to the increased level of T3. However, during autumn and winter, when there is less than 13 hours of light per day, iodothyronine desiodinase 3 removes an iodine atom which converts thyroxine to the inactive reverse triiodothyronine (rT3), or which converts the active triiodothyronine to diiodothyronine (T2). Consequently, there is less T3 and it blocks the transcription of pomc, which reduces its levels during these seasons.
Sources: en.wikipedia.org
No. It is a synthetic analogue modeled on the first 29 residues of human GHRH. The substitutions and any linker are laboratory modifications rather than features of the endogenous peptide.
Early development used the albumin-binding form, and a shorter variant was later discussed under the same label. Because the two differ in half-life and handling, ambiguity arises whenever a source omits the variant designation.
The compound derives from that fragment but is not identical to it. The parent fragment lacks the stabilizing substitutions, so its degradation rate and duration of action differ noticeably.
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.