📚 Wiki Cognitive & Mood Cortistatin-14

Cortistatin-14

● Preclinical
Cortistatin-14
Also known as: CST-14, Somatostatin Homolog, Cortistatin
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Quick Summary

Cortistatin-14 (CST-14) is a cyclic neuropeptide with strong structural homology to somatostatin-14, sharing 11 of 14 residues. It activates all five somatostatin receptors (SSTR1-5) with similar affinity to somatostatin, but also binds additional receptors including the ghrelin receptor (GHS-R1a) and MrgX2.

Neuropeptide / Neuromodulator Preclinical
Cortistatin-14 (CST-14) is a cyclic neuropeptide with strong structural homology to somatostatin-14, sharing 11 of 14 residues. It activates all five somatostatin receptors (SSTR1-5) with similar affinity to somatostatin, but also binds additional receptors including the ghrelin/" class="wiki-internal-link">ghrelin receptor (GHS-R1a) and MrgX2. Unlike somatostatin, cortistatin produces slow-wave sleep promotion, reduces locomotor activity, and modulates neuroinflammation through mechanisms partly independent of somatostatin receptors.
Storage Stability
Lyophilized
1–2 years (-20°C)
Reconstituted
~30 days (2–8°C)
Room temp
Avoid

Mechanism of Action

SSTR Activation vs. Unique Targets

Cortistatin activates SSTR1-5 with comparable affinity to somatostatin, mediating inhibition of GH, insulin, glucagon, and GI secretions through Gi-coupled receptor signaling. Unique to cortistatin, it also activates GHS-R1a (the ghrelin/" class="wiki-internal-link">ghrelin receptor) and MrgX2, a mast cell receptor. These additional targets may explain the divergent CNS and immune effects not seen with somatostatin.

Neuroinflammation and Immune Modulation

Cortistatin has potent anti-inflammatory properties mediated through SSTR2 and SSTR3 on immune cells. It inhibits microglial activation, reduces pro-inflammatory cytokine production, and promotes regulatory T cell function. These immunomodulatory effects are being explored for inflammatory and autoimmune conditions.


Research Summary

Sleep Promotion

Preclinical

Unlike somatostatin (which has minimal sleep effects), cortistatin significantly increases slow-wave sleep (SWS) and reduces REM sleep when administered ICV. This distinguishing property mapped to its unique C-terminal sequence not shared with somatostatin. Cortistatin-knockout mice show impaired sleep regulation, establishing its endogenous sleep-promoting role.

Anti-Inflammatory Efficacy

Preclinical

Cortistatin treatment reduces disease severity in mouse models of rheumatoid arthritis, Crohn disease, and experimental autoimmune encephalomyelitis (EAE). In systemic inflammatory response syndrome models, cortistatin reduces mortality and cytokine storm parameters. These results have positioned cortistatin as a lead compound for anti-inflammatory drug development.


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Research Protocols

GoalDoseFrequencyRoute
Sleep induction10-100 nmol ICVSingleIntracerebroventricular
Anti-inflammatory100-300 mcg/kgDailyIV or IP injection

Preclinical only. No approved human use. Somatostatin analogs (octreotide) target the shared SSTR pathway.


Interactions

Receptor Overlap
Somatostatin
Shared SSTR1-5 activation; cortistatin has additional unique receptor targets
Competing
Ghrelin
Cortistatin binds GHS-R1a; opposes some ghrelin-mediated effects
Suppression
Cytokines
Cortistatin inhibits TNF-alpha, IL-6, and IL-1beta in immune cells

Safety Profile

Cortistatin is an endogenous neuropeptide; physiological concentrations are well tolerated. Like somatostatin, exogenous cortistatin would be expected to inhibit GH, insulin, and GI secretions, requiring monitoring for hypoglycemia and nutritional effects. No clinical safety data for cortistatin itself; somatostatin analogs provide a reference safety profile.


References

  • [1]de Lecea L et al. (1996). A cortical neuropeptide with neuronal depressant and sleep-modulating properties. Nature, 381(6579), 242-245.
  • [2]Gonzalez-Rey E et al. (2006). Cortistatin, a new anti-inflammatory peptide with therapeutic effect on lethal endotoxemia. Journal of Experimental Medicine, 203(3), 563-571.
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Data Sources & External References
Source: peer-reviewed literature  ·  Domain: ascendpeptide.org

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