📚 Wiki Hormonal & Reproductive CRH

CRH

● Extensive clinical research; CRHR1 antagonists in trials
Corticotropin-Releasing Hormone (CRH/CRF)
Also known as: Corticotropin-Releasing Hormone, Corticorelin, CRH, CRF, Corticotropin-Releasing Factor
Brand names: Acthrel (corticorelin ovine triflutate, diagnostic)
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Quick Summary

Corticotropin-releasing hormone (CRH, also CRF) is a 41-amino acid hypothalamic peptide first isolated by Vale et al. in 1981 after 40 years of searching.

Hypothalamic Hormone Clinical
Corticotropin-releasing hormone (CRH, also CRF) is a 41-amino acid hypothalamic peptide first isolated by Vale et al. in 1981 after 40 years of searching. CRH is the apex regulator of the hypothalamic-pituitary-adrenal (HPA) axis, stimulating pituitary acth/" class="wiki-internal-link">ACTH release which drives adrenal cortisol production. Beyond pituitary control, CRH is widely expressed as a neuropeptide throughout the brain, peripheral nervous system, and immune tissues. CRH coordinates the physiological and behavioral stress response, mobilizing energy, suppressing immunity, and modulating anxiety, arousal, and gut function. Dysregulated CRH signaling is implicated in depression, anxiety disorders, PTSD, IBS, and Cushing's disease.
Storage Stability
Lyophilized
1–2 years (-20°C)
Reconstituted
~30 days (2–8°C)
Room temp
Avoid

Mechanism of Action

CRHR1 and CRHR2 Receptor Subtypes

CRH signals through two Gs-coupled GPCRs. CRHR1 (pituitary, limbic system, frontal cortex) mediates acth/" class="wiki-internal-link">ACTH release and the anxiogenic effects of stress. CRHR2 (hypothalamus, brainstem, heart, skeletal muscle) mediates the anxiolytic and cardioprotective actions of urocortins and late-phase stress adaptation. Both receptors activate adenylyl cyclase and PKA, with additional MAPK/ERK signaling. The relative activation of CRHR1 versus CRHR2 determines whether the net response is anxiogenic or anxiety-resolving.

HPA Axis Activation

CRH released from the paraventricular nucleus (PVN) into the portal circulation reaches pituitary corticotrophs, activating CRHR1 and stimulating POMC cleavage to produce ACTH. ACTH travels to the adrenal cortex, stimulating cortisol synthesis and secretion. Cortisol then provides negative feedback to the hypothalamus and pituitary, suppressing further CRH and ACTH release. Disruption of this feedback loop underlies hypercortisolism in Cushing's disease and in chronic stress.


Research Summary

Diagnostic Use

Human

The CRH stimulation test (IV ovine or human CRH) evaluates pituitary ACTH reserve and differentiates Cushing's disease (pituitary adenoma, responds to CRH) from ectopic ACTH (often does not respond). This endocrine diagnostic test is FDA-approved and widely used in endocrinology practice.

Depression and Anxiety

Human

CSF CRH levels are elevated in major depression, PTSD, and anxiety disorders. CRHR1 antagonists (antalarmin, R121919, verucerfont) produced antidepressant and anxiolytic effects in Phase II trials without the side effects of cortisol suppression drugs. Several programs demonstrated proof-of-concept but have not yet reached Phase III.

IBS and Gut-Brain Axis

Human

Peripheral CRH mediates stress-induced gut hypermotility and visceral hypersensitivity in IBS. CRH injection in healthy subjects accelerates colonic transit and triggers pain similar to IBS. CRHR1 antagonists reduced stress-induced colonic motility in IBS patients in Phase II trials, validating the gut-brain CRH axis as an IBS target.


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Research Protocols

GoalDoseFrequencyRoute
HPA axis diagnostic test1 mcg/kg (up to 100 mcg)Single IV doseIntravenous
Stress/anxiety research50-100 mcgSingle IV doseIntravenous (human challenge model)

CRH diagnostic use is well established. Research uses IV or ICV CRH to model acute stress responses. Therapeutic development targets CRHR1 antagonism rather than CRH agonism.


Interactions

Synergistic
AVP synergizes with CRH to stimulate pituitary ACTH release through V1b receptors, key stress axis co-regulators
Related
Urocortins are CRH family members that preferentially activate CRHR2, producing cardioprotection and anxiolysis
Complementary
Cortistatin and CRH both modulate hypothalamic-pituitary circuits; cortistatin acts via somatostatin receptors

Safety Profile

Diagnostic IV CRH causes transient facial flushing, mild tachycardia, and a brief sensation of warmth lasting 1-2 minutes. These effects resolve spontaneously. No serious adverse events have been identified in the decades of diagnostic CRH test use. Research-dose CRH infusions in anxiety challenge studies are well tolerated in healthy volunteers with appropriate monitoring. CRHR1 antagonists in clinical trials have shown acceptable tolerability with no significant cortisol suppression at anxiolytic doses.


References

  • [1]Vale W, et al. Characterization of a 41-residue ovine hypothalamic peptide that stimulates secretion of corticotropin and beta-endorphin. Science. 1981;213(4514):1394-1397.
  • [2]Owens MJ, Nemeroff CB. Physiology and pharmacology of corticotropin-releasing factor. Pharmacol Rev. 1991.
  • [3]Emplit A, et al. CRF-1 antagonists and treatment of depression and anxiety: current status. CNS Drugs. 2013.
Key Terms
Reconstitution is the process of dissolving lyophilized (freeze-dried) peptide powder with a sterile diluent to create a…
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Data Sources & External References
Source: peer-reviewed literature  ·  Domain: ascendpeptide.org

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