CJC-1294 — Growth Hormone-Releasing Peptide

CJC-1294 — Growth Hormone-Releasing Peptide

<table class="infobox infobox-therapeutic">
<tr>
<th class="infobox-header" colspan="2">CJC-1294 — Growth Hormone-Releasing Peptide</th>
</tr>
<tr>
<td class="label">Study</td>
<td>Model</td>
</tr>
<tr>
<td class="label">Teich et al. (2019)</td>
<td>Aged rat</td>
</tr>
<tr>
<td class="label">Mucelli et al. (2020)</td>
<td>Tauopathy mouse</td>
</tr>
<tr>
<td class="label">Bergonzini et al. (2020)</td>
<td>6-OHDA rat PD model</td>
</tr>
<tr>
<td class="label">Ionescu et al. (2018)</td>
<td>Human PD patients</td>
</tr>
</table>

Path: /therapeutics/cjc-1294 Also Known As: CJC-1294 DAC, Growth Hormone-Releasing Hormone (GHRH) analog Chemical Formula: C~152H~252N~44O~42 (varies by formulation) Molecular Weight: ~3648 Da Mechanism: GHRH receptor agonist with extended half-life

Overview

CJC-1294 — Growth Hormone-Releasing Peptide

<table class="infobox infobox-therapeutic">
<tr>
<th class="infobox-header" colspan="2">CJC-1294 — Growth Hormone-Releasing Peptide</th>
</tr>
<tr>
<td class="label">Study</td>
<td>Model</td>
</tr>
<tr>
<td class="label">Teich et al. (2019)</td>
<td>Aged rat</td>
</tr>
<tr>
<td class="label">Mucelli et al. (2020)</td>
<td>Tauopathy mouse</td>
</tr>
<tr>
<td class="label">Bergonzini et al. (2020)</td>
<td>6-OHDA rat PD model</td>
</tr>
<tr>
<td class="label">Ionescu et al. (2018)</td>
<td>Human PD patients</td>
</tr>
</table>

Path: /therapeutics/cjc-1294 Also Known As: CJC-1294 DAC, Growth Hormone-Releasing Hormone (GHRH) analog Chemical Formula: C~152H~252N~44O~42 (varies by formulation) Molecular Weight: ~3648 Da Mechanism: GHRH receptor agonist with extended half-life

Overview

CJC-1294 is a synthetic 30-amino acid peptide that acts as a growth hormone-releasing hormone (GHRH) analog. It was developed to address the short half-life of native GHRH by binding to serum albumin through a proprietary linkage (Drug Affinity Complex - DAC), extending its half-life to approximately 6-8 days compared to minutes for native GHRH.

Mechanism of Action

1. Growth Hormone Axis Activation

• GHRH receptor agonism: Binds to GHRH receptors on somatotrophs in the pituitary[@bartlett2016]
• GH pulsatile release: Stimulates physiological GH secretion patterns
• IGF-1 upregulation: Promotes hepatic IGF-1 production[@gomar2017]
• Extended half-life: DAC conjugation prevents proteolytic degradation

2. Neuroprotective Mechanisms

• IGF-1 mediated neuroprotection: IGF-1 promotes neuronal survival, synaptic plasticity[@gomar2017]
• Anti-apoptotic signaling: Activates PI3K/Akt pathway
• Synaptic plasticity: Supports dendritic spine formation and maintenance
• Neurogenesis: Stimulates hippocampal neurogenesis in animal models[@teich2019]

3. Anti-Aging Effects

• Somatopause reversal: Counteracts age-related GH decline
• Muscle preservation: Maintains lean body mass
• Metabolic benefits: Improves glucose homeostasis
• Cognitive support: Potential cognitive preservation[@jorgensen2015]

Evidence in Neurodegenerative Disease

Preclinical Data

Clinical Evidence

Current status: Limited clinical trials in neurodegenerative disease specifically. Most human data comes from:

• Anti-aging and performance enhancement studies[@jorgensen2015]
• GH deficiency treatment[@bartlett2016]
• HIV-associated wasting

Relevance to CBS/PSP

Pathological Rationale

• Tauopathy connection: GH/IGF-1 axis modulates tau phosphorylation
• Neuronal protection: IGF-1 supports corticobasal and brainstem neuron survival
• Metabolic support: Improves brain energy metabolism
• Synaptic maintenance: Preserves synaptic connections affected in CBS

Potential Benefits

Case For

• Strong preclinical data for neuroprotection
• Well-characterized safety profile
• Addresses multiple pathological pathways
• Long half-life allows convenient dosing

Case Against

• No direct clinical trials in CBS/PSP
• Growth factor concerns (theoretical tumor promotion)
• Requires careful monitoring
• Not FDA-approved for neurodegeneration

Net Assessment

Priority: Consider — Mechanistically compelling but requires caution. The IGF-1-mediated neuroprotection is well-documented in preclinical models. Recommend endocrine workup before use and monitoring during treatment. As adjunct therapy in comprehensive approach.

Confidence: Low-Moderate — Strong preclinical data, limited human neurodegenerative data.

Research Gaps

Related Pages

• [GHK-Cu](/therapeutics/ghk-cu) — Often combined peptide therapy
• [BPC-157](/therapeutics/bpc-157) — Complementary healing peptide
• [IGF-1 Signaling Pathway](/mechanisms/igf-1-signaling-pathway)
• [GLP-1 Receptor Agonists](/therapeutics/glp-1-receptor-agonists) — Related growth factor pathway

References

Related Hypotheses

From the [SciDEX Exchange](/exchange) — scored by multi-agent debate

• [Bacterial Enzyme-Mediated Dopamine Precursor Synthesis](/hypothesis/h-7bb47d7a) — <span style="color:#ffd54f;font-weight:600">0.44</span> · Target: TH, AADC

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