Protocols · Regenerative
Dosage and protocol information sourced exclusively from PeptideDosages.com.
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Dosage and protocol figures on this page are reproduced only from the matching PeptideDosages.com protocol. The 3 ml table is arithmetic based on those source amounts and the listed vial sizes. Educational research only — not instructions or medical advice.
The dosage amounts and schedules below come only from PeptideDosages.com. Syringe-unit figures are mathematical conversions of those source amounts using exactly 3 ml of bacteriostatic water. Educational reference only — not instructions or medical advice.
ARA-290 · 16 mg Vial
Ara-290 is dosed at 2 mg–4 mg daily via subcutaneous injection in educational protocols.
| Week | Daily Dose |
|---|---|
| Week 1 | 2 mg (2,000 mcg) |
| Weeks 2–8 (or up to 16) | 4 mg (4,000 mcg) |
10 mg + 3 ml = 3.33 mg/ml. Choose your vial strength to update the units below.
| Source dose | U-100 syringe |
|---|---|
| 2 mg | 60 units |
| 0 mcg | 0.0 units |
| 4 mg | 120 units |
Cibinetide, also known as ARA-290, is a non-hematopoietic erythropoietin analogue (PMID 26683514, PMID 24555851). It is an erythropoietin-derived polypeptide that possesses tissue protective and healing properties but does not stimulate red blood cell production (erythropoiesis) (PMID 24555851, PMID 26683514). It is derived from the B-subunit of erythropoietin (EPO) (PMID 35317117).
Cibinetide primarily functions by activating the innate repair receptor (IRR) (PMID 29026145, PMID 32345869, PMID 26774587). The IRR is formed by a heteromer of the erythropoietin receptor (EPOR) and the β-common receptor (CD131) in various cell types, including immune cells, to exert tissue protective effects (PMID 29026145). Activation of the IRR by cibinetide dampens innate immune cell functions, leading to anti-inflammatory effects (PMID 29026145). In LPS-activated primary macrophages (cells), cibinetide's anti-inflammatory effects were dependent on CD131 and JAK2 functionality, and mediated via inhibition of NF-κB subunit p65 activity (PMID 29026145). Cibinetide can also directly inhibit TRPV1 channel activity, a mechanism that may contribute to its analgesic effects (PMID 26774587).
In mice with experimentally induced colitis, cibinetide ameliorated the clinical course, improving weight gain and survival (PMID 29026145). This was associated with reduced infiltration of myeloid cells and diminished production of pro-inflammatory mediators (PMID 29026145). In islet transplantation models, cibinetide protected mouse pancreatic islets from cytokine-induced damage and apoptosis, inhibited pro-inflammatory cytokine secretion from murine macrophages (cells), and improved blood glucose levels after marginal islet transplantation (PMID 26683514). It also suppressed the upregulation of pro-inflammatory messenger RNA expression in the liver (PMID 26683514). In allogeneic mouse pancreatic islet transplantation, cibinetide reduced local inflammation in the liver, improved glycemic control, and delayed graft loss (PMID 32345869). It also lowered bone-marrow-derived immature dendritic cell maturation (cells) and reduced allogeneic T-cell response (PMID 32345869). Studies with human islets (cells) showed cibinetide maintained ATP levels, reduced caspase 3/7 activity in pro-inflammatory conditions, and improved insulin secreting capacity (PMID 34498509). It also reduced platelet consumption in an in vitro model mimicking the immediate blood-mediated inflammatory reaction (PMID 34498509). When human islets were transplanted into athymic mice, cibinetide treatment resulted in increased human insulin in livers and higher serum human C-peptide, with reduced CD11b+ cell infiltration around grafts (PMID 34498509). In a rat model of cardiac ischemia, a modified cibinetide derivative accumulated in the ischemic region, suggesting its potential for diagnosing cardiac ischemia (PMID 35317117).
In two Phase II clinical trials (humans), cibinetide treatment was associated with significant improvement in neuropathic pain symptoms in sarcoidosis patients (PMID 24555851). This included a decrease in pain scores on validated questionnaires, increases in corneal nerve fibers, improved sensory pain thresholds, and improved quality of life and physical functioning (PMID 24555851). The compound has an excellent safety profile (PMID 24555851).
The complexity of study design and the slow progression of conditions like diabetic neuropathy necessitate long duration trials to prove efficacy of treatments (PMID 33423557). For diabetic neuropathy, there are approved agents for pain relief, but these do not affect the underlying pathological process (PMID 33423557). The long-lasting beneficial effects of cibinetide in sarcoidosis patients prompt additional studies on its potential disease-modifying properties (PMID 24555851).
Erythropoietin (EPO): A protein that stimulates red blood cell production (PMID 29026145). Non-hematopoietic: Not involved in blood cell formation (PMID 26683514). Innate repair receptor (IRR): A receptor formed by EPOR and CD131, mediating tissue protective effects in various cells (PMID 29026145). Neurogenic inflammation: Inflammation involving nerves (PMID 26774587). Small fiber neuropathy: Damage to small nerve fibers, often causing neuropathic pain (PMID 24555851). TRP channels (Transient Receptor Potential): A family of ion channels; TRPV1 is involved in pain sensation (PMID 26774587). Myeloid cells: A type of immune cell (PMID 29026145). NF-κB: A protein complex that controls DNA transcription, cytokine production, and cell survival, often involved in inflammation (PMID 29026145). Islet transplantation: Transferring pancreatic islets, which contain insulin-producing cells, typically to treat type 1 diabetes (PMID 32345869).
Summarised from the PubMed abstracts listed above. Educational reference only — not medical advice or instructions.
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