See how research connects peptides to biological targets, signaling pathways, and biological processes.
This tool shows, for each peptide, which biological target the available research points to, how directly that relationship is supported, and how it connects to broader signaling pathways and biological processes. It describes what research suggests about biological mechanisms -- not proven health or treatment outcomes, and not medical advice. See each peptide's full research profile for complete detail, citations, and safety information.
Mechanism research for MitoCore's current product catalog.
Showing 37 of 37 peptides
Evidence legend
Relationship support
Directly supported
Supported indirectly
Inferred from related evidence
Uncertain
Evidence context
Human research
Preclinical research
Human + preclinical research
Review / established literature
Related compound/program context
Evidence context uncertain
Understanding mechanism evidence
This tool describes research into biological targets, signaling pathways, and biological processes -- not proven health or treatment outcomes, and not medical advice. Relationship-support and evidence-context labels describe the type and directness of research available, not proof of safety or effectiveness. See each peptide's full research profile for complete detail, citations, and safety information.
Mechanism profiles
ARA-290 / Cibinetide
1 mechanism relationship · Supported indirectly · Preclinical research
ARA-290 / Cibinetide → CD131 receptor — Supported indirectlyARA-290/cibinetide effects in multiple preclinical models depend on beta-common receptor (CD131) signaling, supported by knockout and siRNA loss-of-function evidence; this does not establish direct ARA-290-CD131 binding.
Evidence context
Preclinical research
ARA-290 was effective in wild-type mice but produced no effect in mice lacking the beta-common receptor, and in a separate model cibinetide's anti-inflammatory effect in LPS-activated macrophages depended on CD131 and JAK2 functionality; a third study found ARA-290's neuroprotective effect in a stroke model was significantly suppressed by beta-common-receptor siRNA knockdown. This genetic/functional dependence is not direct ligand-binding evidence: no clean isolated binding assay establishes ARA-290 binding to CD131, to EPOR, or to a purified EPOR/CD131 complex, and the physical EPOR/CD131 'innate repair receptor' architecture remains scientifically contested. A 2018 biophysical study (PMID 30127368) found that the extracellular regions of EPOR and the beta-common receptor did not specifically associate under tested in vitro conditions, including in the presence of ARA290; this counterevidence means the record does not treat the complex as a settled physical target, though it does NOT negate the distinct functional CD131-dependence findings from the knockout/knockdown studies above. This record does not claim canonical EPOR homodimer agonism. JAK2, Akt, NF-kB/p65, SRF, HSF1, and AP-1 are downstream/context only, not independent targets of this record. Evidence is preclinical only.
Sources
Central Citation Library reference: ara-290-08-ara290-a-peptide-derived-from-the-tertiary-st
Central Citation Library reference: ara290-nairz-2017-cibinetide-cd131-colitis-pmid29026145
Central Citation Library reference: ara290-wang-2024-beta-common-receptor-stroke-pmid38488446
Central Citation Library reference: ara290-cheung-tung-shing-2018-epor-beta-common-counterweight-pmid30127368
What is established
A target (CD131 receptor) and pathway family (Immune & Inflammatory Signaling) are documented.
What remains unclear
Specific downstream signaling steps and biological-process associations are not yet documented.
ARA-290 was effective in wild-type mice but produced no effect in mice lacking the beta-common receptor, and in a separate model cibinetide's anti-inflammatory effect in LPS-activated macrophages depended on CD131 and JAK2 functionality; a third study found ARA-290's neuroprotective effect in a stroke model was significantly suppressed by beta-common-receptor siRNA knockdown. This genetic/functional dependence is not direct ligand-binding evidence: no clean isolated binding assay establishes ARA-290 binding to CD131, to EPOR, or to a purified EPOR/CD131 complex, and the physical EPOR/CD131 'innate repair receptor' architecture remains scientifically contested. A 2018 biophysical study (PMID 30127368) found that the extracellular regions of EPOR and the beta-common receptor did not specifically associate under tested in vitro conditions, including in the presence of ARA290; this counterevidence means the record does not treat the complex as a settled physical target, though it does NOT negate the distinct functional CD131-dependence findings from the knockout/knockdown studies above. This record does not claim canonical EPOR homodimer agonism. JAK2, Akt, NF-kB/p65, SRF, HSF1, and AP-1 are downstream/context only, not independent targets of this record. Evidence is preclinical only.
Key terms
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