Research guides
ARA-290 (cibinetide): what the research says
An erythropoietin fragment engineered to keep the tissue protection and drop the red-cell activity, with a published randomised trial in type 2 diabetes.
Available in the catalogue
Supplied as research material. Sizes and pricing are on the product page. Availability is not a statement about what a compound does.
ARA-290 exists because erythropoietin does two unrelated things and only one of them was wanted. The way that problem was solved is the most instructive thing about the molecule.
What the molecule is
An eleven-amino-acid peptide taken from the tissue-protective region of erythropoietin — the hormone that drives red blood cell production. It is published as cibinetide and as pHBSP.
Two activities, two receptors
Erythropoietin makes red blood cells, and it protects injured tissue. Those activities run through different receptors: the classical erythropoietin receptor for the first, and the innate repair receptor for the second. This fragment engages only the second.
That separation is the entire reason the molecule exists. Raising red cell mass is a serious problem when you only want the tissue-protective effect — it thickens blood and carries cardiovascular risk, which is what limited erythropoietin itself as a tissue-protective agent. A fragment that keeps the protection without the haematology is a genuine piece of drug design rather than a rebranding.
The trial
A randomised controlled trial published in 2015 examined participants with type 2 diabetes, reporting changes in metabolic control and in neuropathic symptoms. Small-fibre neuropathy is the context this compound is generally studied in, and the trial measured symptom and metabolic endpoints in that population.
It is a real randomised human trial with a published result, which places this compound well above most of the catalogue on evidence. It is one trial in one population, which places it well below an established medicine.
What studies reported
Each entry states what a study examined and the model it used. Nothing below describes an outcome for a person.
Everything below is drawn from published research, and each entry names the model the study used. Approval status varies by compound and by country, and nothing described here is supplied as a medicine or for use in a person.
- Brines et al. (2015)Molecular Medicine · 20(1):658–66
Reported changes in metabolic control and in neuropathic symptoms in participants with type 2 diabetes, in a peptide engineered from erythropoietin to be non-erythropoietic.
human, randomised controlled Source
Adverse and null findings reported
No dedicated safety study has been published for this compound. That is not a finding that none exists — it means the question has not been asked in print, and the gaps below say so.
What the research does not establish
An absence cannot be cited, so these are stated plainly. They are the part of the picture that silence would otherwise hide.
- The `adverse` list is empty because no dedicated safety publication was found. The trial cited above reports on tolerability within its own population; that is not the same as a characterised safety profile.
- One randomised trial in one population is the extent of the human evidence. No phase 3 programme has been published and the compound holds no marketing authorisation anywhere.
- The design premise — that the fragment engages the innate repair receptor and not the erythropoietin receptor — is the compound's central claim. It is well argued in the literature, and long-term confirmation that red cell parameters are genuinely unaffected over extended use has not been published.
- The innate repair receptor itself is less thoroughly characterised than the classical erythropoietin receptor, so the target this molecule was built around is less well understood than the one it avoids.
- Nothing published addresses use beyond the trial durations, or in populations without diabetes.
Common questions
- What is ARA-290 designed to do?
- Engage the tissue-protective activity of erythropoietin without the red-cell-producing activity. The two run through different receptors, and this eleven-residue fragment engages only the second.
- Why not just use erythropoietin?
- Because raising red cell mass thickens blood and carries cardiovascular risk. That is what limited erythropoietin as a tissue-protective agent, and separating the two activities is the whole reason this fragment was engineered.
- Has ARA-290 been tested in humans?
- Yes. A randomised controlled trial published in 2015 in participants with type 2 diabetes reported changes in metabolic control and neuropathic symptoms.
- Does ARA-290 raise red blood cell count?
- It was engineered specifically not to, by targeting the innate repair receptor rather than the erythropoietin receptor. Long-term published confirmation over extended use is not available.
- Is ARA-290 an approved medicine?
- No. It has a published randomised trial but no marketing authorisation in any jurisdiction, and it is supplied here as a laboratory reagent for research use only.
Compounds covered
The reference page for each compound this article discusses.
Related articles
- SS-31 (elamipretide): what the research says
One of very few compounds here to reach phase 3. The MMPOWER-3 trial missed its primary endpoints, and that result is the most useful thing it has.
- LL-37 cathelicidin: what the research says
The only cathelicidin humans make, with a physical antimicrobial mechanism and a published randomised trial in venous leg ulcers. Also genuinely double-edged.
- How to store research peptides
Lyophilised peptides at -20°C, reconstituted at 2–8°C, ambient in transit. Why the dry cake tolerates shipping, and what actually degrades a vial.