The Compound Report is an educational resource. Nothing on this site constitutes medical advice or encourages personal use of any compound. Always consult a qualified healthcare provider.
Educational reference only. Nothing on this page constitutes medical advice or encourages personal use of this compound. Always consult a qualified healthcare provider before any decision involving your health.
SHLP2 · Small Humanin-Like Peptide 2
Effect demonstrated in multiple animal studies; human data sparse or extrapolated. Grades summarize evidence quality, not whether a compound is appropriate, legal, or risk-free.
SHLP2 is the compound in this reference that is furthest along in its research trajectory while still being the furthest from clinical application. The mechanism is becoming clearer — a receptor has been found, a hypothalamic pathway has been identified, metabolic protection has been demonstrated. The translation to humans has not begun.
The central tension resolved: of six small humanin-like peptides discovered simultaneously in the same mitochondrial genomic neighborhood, SHLP2 emerged as the most metabolically active in vivo. A 2023 paper from an independent Chinese group identified its receptor — CXCR7 — and demonstrated that it activates POMC neurons in the hypothalamus to suppress appetite and increase thermogenesis. Lower plasma SHLP2 is associated with higher prostate cancer risk in an observational study of 200 men. All of this is preclinical or observational. No human intervention trial exists. The community using SHLP2 is making an extrapolation from compelling mechanistic and animal data to human benefit — the same extrapolation that the MDP field makes broadly, with the understanding that this is a promising compound at an early stage of characterization rather than an established therapeutic.
The strongest argument for SHLP2: the receptor has been found (CXCR7) by an independent group. The mechanism is characterized (POMC neuron activation, appetite suppression, thermogenesis) and involves the same neuronal pathway as GLP-1 drugs — one of the most clinically validated pathways in obesity medicine. Metabolic improvements in animal models have been independently replicated. The prostate cancer biomarker finding is the most specific human-biology signal in any SHLP chapter. The compound is genuinely distinct from Humanin and MOTS-c — different receptor, different primary mechanism, different application.
The strongest argument for caution: the entire beneficial effect evidence base is animal models from 2016-2023. The human data is one observational biomarker study. The dose used in community protocols is likely far below what produced effects in the animal studies. The CohBar commercial relationship creates a financial interest in positive SHLP2 research that isn't present for Humanin's neuroprotection literature (which has Japanese and other independent origins). This is the youngest and least independently validated compound in the MDP section of this reference.
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Found in Surviving Brain Cells of an Alzheimer's Patient. Encoded in Mitochondrial DNA. Higher in Centenarians' Children. Inversely Correlated With IGF-1. The GH Axis the Community Raises for Anti-Aging Suppresses It.
Mitochondrial-derived peptide studied for AMPK signaling, metabolic stress resilience, and exercise-mimetic pathways.
Every Other MDP in this reference Keeps Cells Alive. SHLP6 Tells Them to Die. This May Be Exactly the Point — and the Most Underappreciated Mechanism in the Entire Mitochondrial Peptide Family.