Ara-290 vs KPV
Ara-290 (Synthetic erythropoietin-derived peptide (Cibinetide)) and KPV (Alpha-MSH-derived tripeptide fragment) are documented as co-studied in the PeptiDex library. This page puts the two entries side by side on class, molecular weight, half-life, origin, mechanism and studied research areas — every value taken from the entry it belongs to.
Why these two are co-studied
Cross-referenced for research context — not a usage or combination recommendation.
At a glance
| Attribute | Ara-290 | KPV |
|---|---|---|
| Compound class | Synthetic erythropoietin-derived peptide (Cibinetide) | Alpha-MSH-derived tripeptide fragment |
| Research category | Healing & Recovery | Healing & Recovery |
| Length (amino acids) | 11 amino acids | 3 amino acids |
| Molecular weight | ~1257 Da | 342.43 g/mol |
| Half-life | ~2 minutes (plasma) | Not documented |
| Origin | ARA-290, also known as Cibinetide, is a synthetic 11-amino-acid peptide derived from a region of the erythropoietin (EPO) molecule. It was designed to engage tissue-protective signaling associated with EPO while lacking EPO's erythropoietic (red-blood-cell-stimulating) activity. | KPV is a synthetic tripeptide corresponding to the C-terminal three amino acids (lysine-proline-valine) of alpha-melanocyte-stimulating hormone (alpha-MSH), a naturally occurring melanocortin peptide. It is studied as a fragment that retains some anti-inflammatory properties of the parent hormone. |
“Not documented” means the PeptiDex entry records no value for that field. Nothing on this page is estimated, and no figure is carried over from one compound to the other.
How Ara-290 works
ARA-290 is described as an agonist of the innate repair receptor, a heteroreceptor complex involving the beta-common receptor, which mediates tissue-protective and anti-inflammatory effects attributed to EPO without stimulating erythropoiesis. Through this pathway it has been studied for effects on inflammation and neuropathic processes. Mechanistic understanding derives from preclinical models and early clinical research.
How KPV works
KPV is reported in preclinical studies to exert anti-inflammatory effects, and research has explored both melanocortin-receptor-dependent signaling and intracellular actions independent of classic MSH pigmentation activity. It has been studied for downregulation of pro-inflammatory signaling such as NF-kB-associated pathways in cell and animal models of colitis. These findings derive from in-vitro and rodent research.
Mechanistic descriptions reflect published research-literature understanding and are quoted from each compound's own entry. Much peptide research is preclinical (in-vitro or animal-model); mechanism in humans may differ and is not established for many compounds.
Where each one appears in the literature
The research contexts each entry documents. Listing a research area is not a claim of efficacy or a therapeutic indication, and the two lists are not scored against each other.
Ara-290
KPV
What sets each apart
Ara-290
ARA-290 is unusual in this group for being an EPO-derived, receptor-targeted peptide that has progressed into clinical trials rather than remaining purely preclinical.
KPV
KPV is distinguished by its melanocortin-pathway anti-inflammatory focus, in contrast to the antimicrobial LL-37 or the tissue-repair emphasis of BPC-157 and TB-500.
Frequently asked questions
What is ARA-290 (cibinetide)?
ARA-290, generic name cibinetide, is a synthetic 11-amino-acid linear peptide engineered from the helix-B surface region of erythropoietin (EPO). It was designed to selectively activate the innate repair receptor (a heterodimer of the EPO receptor and the beta-common receptor/CD131) without stimulating red-blood-cell production. It is an investigational compound, not an approved drug.
What is ARA-290 studied for?
It has been investigated in clinical research for tissue protection and anti-inflammatory effects, notably in sarcoidosis-associated small-fiber neuropathy and diabetic neuropathic pain, as well as organ-protection models. The rationale is that innate-repair-receptor activation drives tissue-protective and anti-inflammatory signaling. Results are from early-phase research rather than approved indications.
Does ARA-290 raise red blood cell counts like EPO?
No. It was specifically engineered to activate the tissue-protective innate repair receptor while not engaging the classical EPO receptor homodimer that drives erythropoiesis. In principle this avoids the thrombotic and cardiovascular risks associated with erythropoiesis-stimulating agents, though it is still investigational.
What is KPV?
KPV is the C-terminal tripeptide (lysine-proline-valine) of alpha-melanocyte-stimulating hormone (alpha-MSH). It retains much of the parent hormone's anti-inflammatory activity while lacking its pigment-stimulating (melanocortin) effects. It is studied as a small anti-inflammatory peptide rather than as an approved therapeutic.
What is KPV studied for?
Preclinical research examines KPV for anti-inflammatory effects, particularly in models of intestinal inflammation and colitis, as well as skin inflammation. It is reported to enter cells and inhibit NF-kB signaling and pro-inflammatory cytokine production, and it can be transported into intestinal cells via the PepT1 transporter. No human clinical trials have confirmed these effects.
How does KPV produce anti-inflammatory effects without affecting pigmentation?
KPV corresponds only to the C-terminal tripeptide of alpha-MSH, so it preserves the anti-inflammatory activity associated with that region while omitting the sequence needed to activate melanocortin receptors that drive pigmentation. Mechanistically it is described as acting intracellularly on the NF-kB pathway, including inhibition of IkB kinase.
Answers are the ones published on each compound's own PeptiDex entry. They are educational summaries of research-literature context and are not medical advice.