Epobis

An erythropoietin-receptor agonist peptide designed from the EPO binding Site 1, published as a DENDRIMERIC peptide by Pankratova, Bock, Berezin and Walmod in Copenhagen. Reported non-erythropoietic. NOT erythropoietin, and not the same peptide as Epotris, which came from EPO helix C

Epobis (An erythropoietin-receptor agonist peptide designed from the EPO binding Site 1, published as a DENDRIMERIC peptide by Pankratova, Bock, Berezin and Walmod in Copenhagen. Reported non-erythropoietic. NOT erythropoietin, and not the same peptide as Epotris, which came from EPO helix C) is a cognitive & mood research compound. An 18-residue peptide built from the high-affinity binding face of erythropoietin rather than from the whole cytokine. EPO engages its receptor at two unequal sites — a high-affinity Site 1 and a low-affinity Site 2 — and dimerizes it, triggering Jak2/STAT5 and the survival cascades downstream. Working from the crystal structure of the EPO:EPOR2 complex, the Copenhagen group designed a peptide whose sequence encompasses amino acids from binding Site 1, and published it as a DENDRIMER: several copies on one backbone, because a single short peptide cannot reproduce the geometry of a receptor-dimerizing cytokine. The design goal is separation of function. Erythropoiesis needs full receptor engagement on erythroid progenitors, while tissue protection appears to run through a different receptor configuration, so a partial mimic can in principle keep neurite outgrowth, neuronal survival and anti-inflammatory signaling while losing the effect on red cell production. Both peptides from this program report exactly that: receptor binding and neuroprotection with no stimulation of erythropoiesis.

How Epobis works

An 18-residue peptide built from the high-affinity binding face of erythropoietin rather than from the whole cytokine. EPO engages its receptor at two unequal sites — a high-affinity Site 1 and a low-affinity Site 2 — and dimerizes it, triggering Jak2/STAT5 and the survival cascades downstream. Working from the crystal structure of the EPO:EPOR2 complex, the Copenhagen group designed a peptide whose sequence encompasses amino acids from binding Site 1, and published it as a DENDRIMER: several copies on one backbone, because a single short peptide cannot reproduce the geometry of a receptor-dimerizing cytokine. The design goal is separation of function. Erythropoiesis needs full receptor engagement on erythroid progenitors, while tissue protection appears to run through a different receptor configuration, so a partial mimic can in principle keep neurite outgrowth, neuronal survival and anti-inflammatory signaling while losing the effect on red cell production. Both peptides from this program report exactly that: receptor binding and neuroprotection with no stimulation of erythropoiesis.

Proposed benefits

Researched as a non-erythropoietic erythropoietin-receptor agonist for neuroprotection, neurite outgrowth, anti-inflammatory signaling and memory in animal models.

Where to get Epobis

The evidence for Epobis

Graded by what exists behind each claim.

✅ Clinically validated

• No human study of Epobis exists — not a phase 1, not a single-dose safety study, not a case series. There is no human pharmacokinetic data, no human hematology data and no human dose.
• The class does have a human-dosed member, and it is a different peptide. Cibinetide (ARA 290), an 11-residue EPO-derived peptide, was self-administered at 4mg/day subcutaneously for 12 weeks by 9 patients with diabetic macular edema; 8 completed. The trial missed its primary endpoints: no improvement in best-corrected visual acuity, central retinal thickness, central retinal sensitivity or tear production. It reported an improvement in a quality-of-life questionnaire score and improvements in some individual participants, no serious adverse events or reactions, and no anti-cibinetide antibodies. That is the honest state of human evidence for non-erythropoietic EPO peptides: one small trial, safe, negative on its primary outcomes.
• Why the human EPO literature belongs on this page at all. The entire safety case for Epobis is the claim that it does NOT do what EPO does to red cells, so the consequences of being wrong are set by EPO's own human trials. In 4,038 patients with type 2 diabetes, chronic kidney disease and anemia, darbepoetin alfa targeting a hemoglobin of about 13 g/dL produced fatal or nonfatal stroke in 101 patients versus 53 on placebo, a hazard ratio of 1.92 (95% CI 1.38-2.68, p<0.001), with no reduction in either primary composite outcome. And in 1,233 hemodialysis patients with cardiac disease, targeting a hematocrit of 42% versus 30% gave 183 deaths versus 150 and 19 versus 14 nonfatal myocardial infarctions, risk ratio 1.3, and the study was halted with the conclusion that raising hematocrit to 42% is not recommended. Neither trial studied Epobis. They are here because they price the downside of the one claim this product rests on.

📊 Correlative data

• There is no human association or observational data for Epobis. What stands in its place is the design rationale, which is a published position rather than a result: EPO's neuroprotective, anti-inflammatory and antioxidative effects are well described, and the field's stated problem is that the use of EPO as a neuroprotective agent is hampered by its erythropoietic activity. That sentence is the reason this molecule exists.
• A second group, working independently on the same problem from EPO helix C, states the class liability more bluntly still: the EPO-based therapeutic approach has side effects including hyper-erythropoietic and tumorigenic effects, which is why modified forms and derivatives have been proposed. Their lead peptide showed neuroprotection without inducing cell proliferation, attributed to a differential mode of EPO-receptor activation. Tumorigenicity is named in that abstract and has never been studied for Epobis.
• The sibling peptide is the closest correlate Epobis has, and its potency number is the one to keep. Epotris, from the same Copenhagen laboratory, corresponds to the C-alpha-helix region (residues 92-111) of human erythropoietin. It bound the EPO receptor and promoted neurite outgrowth and neuronal survival with the same efficiency as erythropoietin but with 1,000-fold lower potency, penetrated the blood-brain barrier, attenuated seizures and reduced mortality and neurodegeneration in kainic-acid neurotoxicity, and did not stimulate erythropoiesis upon chronic administration. A thousand-fold potency gap is the price of replacing a glycosylated 166-residue cytokine with a peptide, and it is the number nobody selling these mentions.

🧪 Theoretical / extrapolated

• The design is structure-based and the paper says which face of the molecule it came from. EPO binds its receptor through a high-affinity Site 1 and a low-affinity Site 2, inducing conformational change and downstream signaling. From the crystal structure of the EPO:EPOR2 complex, the group designed a peptide whose sequence encompassed amino acids from binding Site 1, and named it Epobis. It is described as a synthetic, dendrimeric peptide derived from the sequence of human EPO that binds the EPO receptor and promotes neuritogenesis and neuronal cell survival.
• What has actually been shown, in order. In vitro: Epobis promotes neuritogenesis in primary motoneurons, and decreases TNF release from activated AMJ2-C8 macrophages and from rat primary microglia — two cell types, one a line and one primary. In vivo in rats: detectable in plasma and cerebrospinal fluid after systemic administration, so it crosses the blood-brain barrier; it delays the clinical signs of experimental autoimmune encephalomyelitis; and it has long-term but not short-term effects on working memory, detected as improved social memory 3 days after administration.
• The statement the whole product hangs on, quoted exactly as published: Epobis is not erythropoietic. That is asserted in the abstract of the one in vivo paper. What the abstract does NOT give is a hematocrit, a hemoglobin, a reticulocyte count, a dose, a duration or an n for that determination, and the full text could not be read here. The parallel claim for Epotris is phrased as not stimulating erythropoiesis upon chronic administration, which at least specifies the exposure. So the load-bearing safety claim for this class rests on two abstract-level assertions from one laboratory, and the underlying hematology has not been read.
• The separation-of-function hypothesis, stated as the hypothesis it is. The reason a partial mimic might keep tissue protection while dropping erythropoiesis is that the two appear to run through different receptor configurations — full EPO-receptor homodimer engagement on erythroid progenitors versus an alternative receptor arrangement in other tissues. That framing is the field's, not this page's, and the independent helix-C program invokes a differential activating mode of EPOR signaling to explain neuroprotection without cell proliferation. It is a real, testable mechanism and it is also the convenient one, which is why the markers in the prediction section matter more than the argument.

How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →

What Epobis actually does

Establish what this is before anything else, because the vendor's own title — Epobis (EPO) — invites the one mistake that matters. Erythropoietin is a 166-residue glycosylated cytokine that dimerizes its receptor. Epobis is a peptide built from part of one binding face of it. Pankratova 2012 describes the design precisely: EPO binds its receptor through a high-affinity Site 1 and a low-affinity Site 2, inducing conformational change followed by downstream signaling, and “based on the crystal structure of the EPO:EPOR₂ complex, we designed a peptide, termed Epobis, whose sequence encompassed amino acids from binding Site 1.” Dmytriyeva 2016 calls it a synthetic, dendrimeric peptide derived from the sequence of human EPO.

The sequence, and the two things it tells you. Peptide catalogs list Epobis as the 18-mer NENITVPDTKVNFYAWKR — Asn-Glu-Asn-Ile-Thr-Val-Pro-Asp-Thr-Lys-Val-Asn-Phe-Tyr-Ala-Trp-Lys-Arg — C₁₀₀H₁₅₁N₂₇O₂₉, about 2,195 g/mol, CAS 915091-83-7, and place it at EPO residues 63–80. That stretch checks out against the UniProt human EPO record (P01588): with the 27-residue signal peptide included, residues 63–80 are exactly NENITVPDTKVNFYAWKR, which is 36–53 of the mature 166-residue protein — the region after helix A running into the AB loop, consistent with a Site 1 contact surface. That arithmetic is done here, not read off a paper, and the sequence itself is catalog data: neither published abstract prints it. Second thing: the stretch contains Asn65, one of EPO's three N-linked glycosylation sites, and a synthetic peptide carries no glycan there at all. EPO's glycans are what give the cytokine its plasma residence and much of its receptor behavior, so this is a bare backbone standing in for a decorated one.

Monomer versus dendrimer is the identity problem, and it is not a quibble. A mass of 2,195 Da is the mass of one 18-residue chain. The published Epobis is a dendrimer: several copies of the peptide displayed on a common backbone, which is how this laboratory built its other receptor-targeting peptides and is the only way a short linear fragment can imitate a receptor-dimerizing cytokine. Multivalency buys avidity, slows proteolysis, and changes the geometry presented to the receptor. A monomer and a dendrimer of the same sequence are different drugs, and a certificate reporting a single peptide mass cannot distinguish them.

What the receptor engagement is supposed to buy, and what it is supposed to leave behind. EPO-receptor binding drives Jak2/STAT5 and downstream survival signaling; knockdown of the receptor or interference with that signaling abolished the neuritogenic and pro-survival effect of the sibling peptide Pankratova 2010. The separation-of-function hypothesis is that erythropoiesis requires full receptor engagement on erythroid progenitors while tissue protection runs through a different receptor configuration. An independent program working from helix C Cho 2022 attributes its own peptide's neuroprotection-without-proliferation to a “differential activating mode of EPOR signaling”.

And the number the class does not advertise. The sibling peptide Epotris, from EPO's C-alpha-helix (residues 92–111), promoted neurite outgrowth and survival “with the same efficiency as erythropoietin, but with 10³-fold lower potency” Pankratova 2010. A thousandfold is the cost of replacing the cytokine with a fragment. No equivalent potency comparison against EPO has been published for Epobis.

Cell, rodent, human — and where it stops

The chain for this molecule is short and it is worth stating exactly where it stops: cells, then rats, then nothing.

Cells, part one — the receptor. Pankratova 2012 designed Epobis from the EPO:EPOR₂ crystal structure and showed it induces neurite outgrowth and promotes neuronal survival. For the sibling peptide the receptor dependence was demonstrated rather than assumed: knocking down the EPO receptor or interfering with downstream signaling abolished the effect Pankratova 2010. That is the correct control and it is present in this literature.

Cells, part two — the inflammation arm. Dmytriyeva 2016 reports Epobis promoting neuritogenesis in primary motoneurons and decreasing TNF release from activated AMJ2-C8 macrophages and from rat primary microglia — one immortalized line and one primary culture, which is better than either alone.

Rats. Three findings, all from that one paper. Systemically administered Epobis was detectable in plasma and cerebrospinal fluid. It delayed the clinical signs of experimental autoimmune encephalomyelitis, a model of multiple sclerosis. And it produced long-term but not short-term effects on working memory, seen as improved social memory 3 days after administration. Note the verbs: delayed, not prevented; improved social memory, in one test, at one time point.

Humans: nothing. No phase 1, no single-dose study, no case series, no hematology, no pharmacokinetics. The chain reads cell → rat → stop.

The obstacles to it going further are specific, and there are four. (1) Potency. The sibling peptide matched EPO's efficiency at 1,000-fold lower potency Pankratova 2010; no potency ratio has been published for Epobis, and a thousandfold gap is the difference between a microgram dose and a milligram dose. (2) Identity. The published molecule is a dendrimer Dmytriyeva 2016 while the catalog mass for the name is a monomer, and no published experiment compares the two. (3) Kinetics. An unmodified 18-mer is cleared in minutes and the only published in vivo effect appeared at 3 days, so nobody knows what exposure schedule would reproduce a rodent result. (4) Replication. Every Epobis finding comes from one laboratory in Copenhagen, across two papers, and the independent work in this space is on different peptides from different regions of EPO — helix C in Pankratova 2010 and in Cho 2022, helix B for cibinetide Lois 2020.

And the translation lesson the class has already delivered once. Cibinetide is the only EPO-derived peptide anyone has put into a human trial, and it is a fair preview of what happens when this mechanism meets a clinical endpoint: 9 patients, 4mg/day subcutaneously for 12 weeks, safe, no anti-drug antibodies — and no improvement in best-corrected visual acuity, central retinal thickness, central retinal sensitivity or tear production, with the positive readout being a questionnaire score and scattered individual responses Lois 2020. That trial was run, it was reported honestly, and it missed. It is the most informative single fact about how far the non-erythropoietic EPO-peptide idea has actually traveled.

Epobis pharmacokinetics — how much of it actually gets in

There is no pharmacokinetic study of Epobis in any species — no C_max, no half-life, no bioavailability, no clearance route. What follows is the reasoning that bounds it, which is the honest substitute for a number nobody has measured.

Start from what the molecule is not wearing. The catalog form is an unmodified linear 18-mer: no glycan, no PEG, no lipid tail, no D-amino acids, no cyclization, no albumin binder. Every one of those modifications exists because short linear peptides are cleared in minutes — by serum and tissue peptidases, and by glomerular filtration, since 2.2 kDa is far below the filtration cutoff. Recombinant EPO's own long residence is a property of its three N-linked glycans, and the Epobis stretch contains one of those sites with nothing attached. The published construct's answer to this is the dendrimer: multivalent display raises avidity and hinders proteolysis, which is a structural workaround for a kinetic problem rather than a solution to it. This is the sharpest practical reason the monomer-versus-dendrimer question matters.

Two published observations constrain the picture, and they pull in interesting directions. First, Dmytriyeva 2016 reports that when administered systemically Epobis was detectable in both plasma and cerebrospinal fluid, demonstrating that it crosses the blood-brain barrier; Pankratova 2010 reports the same for Epotris. So enough intact peptide survives to be measured centrally — the abstracts give the fact, not the concentration or the time point. Second, and more revealing, the memory effect was long-term but not short-term: improved social memory 3 days after administration. A peptide with a minutes-to-hours half-life producing an effect at 72 hours is not a drug still present; it is a signaling event that outlived the molecule. That dissociation is the single most useful kinetic clue in the file, and it means plasma concentration would be a poor guide to dosing interval even if anyone had measured it.

The class's dosing habit says the same thing from the other end. The only EPO-derived peptide with human exposure is cibinetide, an 11-residue peptide given at 4mg/day subcutaneously for 12 weeks, self-administered daily Lois 2020. Daily is the tell: nobody designs a weekly schedule for a molecule of this class, because it does not persist. For scale, that is a milligram dose of a peptide roughly half the length of Epobis — which is why this page will not convert it into an Epobis number.

What the vial does and does not let you compute. Disguised Alpha sells 10MG lyophilized, stored at −20°C, avoid freeze/thaw, protect from light, and 2–8°C after reconstitution. No reconstitution volume is printed, no concentration, and no route. That is not a small omission: the same 10 mg vial is 10 mg/mL in 1 mL and 2 mg/mL in 5 mL, and there is no published human or rodent dose to anchor either choice against. A lyophilized peptide vial with no stated diluent volume and no published dose is a product whose exposure cannot be calculated by anyone, including the person selling it.

What would have to be true, and how you would know it was not

Four predictions. The first is the one that decides whether this product is what it says it is; the third is the one that cuts against buying it at all.

1. If Epobis behaves as published, hematocrit, hemoglobin and reticulocytes do not move — and that is the measurement to take. The claim in Dmytriyeva 2016 is flat: Epobis is not erythropoietic, and Pankratova 2010 says the sibling peptide did not stimulate erythropoiesis upon chronic administration. Neither abstract gives a number, so the reader has to generate it. Draw a CBC with reticulocyte count at baseline, at 1 week and at 4 weeks. The timing is not arbitrary: reticulocytes respond to an erythropoietic stimulus within roughly 3 to 7 days, while hemoglobin and hematocrit need 2 to 4 weeks to follow, so a single late draw can miss the mechanism and an unretested baseline makes the whole exercise meaningless. Add ferritin and transferrin saturation: a genuine erythropoietic drive eats iron, and a falling ferritin beside a rising reticulocyte count is the earliest unambiguous signature of one. A flat panel supports the published claim. A rising one falsifies it, and falsifying it is bad news, not good.

2. Blood pressure, weekly, with a home cuff. Raising red cell mass with an erythropoiesis-stimulating agent raises blood pressure — it is the best-characterized non-thrombotic consequence in the entire class, and it is measurable at home for the price of nothing. If hematocrit is genuinely unmoved, blood pressure should be unmoved too; a rise in both together is the class effect arriving in a product that claims not to have one.

3. THE PREDICTION THAT CUTS AGAINST THE PRODUCT, and it comes from the molecule's own design goal. Filed under Performance, an EPO-named product promises oxygen delivery. The mechanism predicts that it delivers none. Epobis was built to keep tissue protection and drop erythropoiesis Dmytriyeva 2016 Pankratova 2010; no rise in red cell mass means no rise in arterial oxygen content, which means no change in VO₂max, no change in a time trial, no change in lactate threshold. Measure it properly if you want to test it: a repeat time trial over a fixed distance plus hemoglobin, four weeks apart. The two outcomes are both informative and neither is what the shelf implies — either performance is unchanged, which is the published mechanism working, or hemoglobin rose, in which case the class's human trials are the relevant literature: darbepoetin to a hemoglobin near 13 g/dL produced stroke in 101 of 2,012 patients versus 53 of 2,026, hazard ratio 1.92 Pfeffer 2009, and targeting a hematocrit of 42% versus 30% gave 183 deaths versus 150 in a study that was halted Besarab 1998.

4. The inflammatory prediction, which is the one with the best mechanistic support and the worst instrumentation. The published in vitro effect is reduced TNF release from macrophages and microglia, with an EAE delay in vivo Dmytriyeva 2016. In a person the accessible proxy is hs-CRP at baseline and 8 weeks, which is a crude downstream readout of a cytokine the compound acts on upstream of. Expect noise; a fall in hs-CRP would be consistent with the mechanism and would prove very little on its own, and no human inflammatory marker has ever been measured on this peptide.

What nobody has tested yet

Five experiments nobody has run. The first two are cheap enough to be embarrassing.

1. A hematology panel, published, with numbers. The entire safety case for this molecule is the assertion that it is not erythropoietic Dmytriyeva 2016, and the abstract-level record contains no hematocrit, no hemoglobin, no reticulocyte count, no dose and no duration for that determination. The full text could not be read here, so the measurement may well exist in a figure — but nothing in the public abstract lets a reader check the load-bearing claim, and no independent group has repeated it. One CBC series in rats, at a stated dose, over 4 weeks, would settle the question this whole page circles.

2. Monomer against dendrimer, same assay. The published Epobis is a dendrimer; the mass that peptide catalogs attach to the name is a monomer. Nobody has published receptor binding, neuritogenesis or erythropoietic activity for the linear 18-mer alone. This is the experiment that decides whether what is in the vial is the molecule in the papers, and it is one afternoon of work for anyone with the assay.

3. Any pharmacokinetic measurement in any species. No C_max, no half-life, no bioavailability, no brain-to-plasma ratio — despite the central effect being demonstrated by cerebrospinal fluid detection, which means somebody had a measurable assay in hand. The 3-day memory effect makes the missing time course more interesting than usual, not less.

4. The tumor question, which the field itself raised. Cho 2022 names hyper-erythropoietic and tumorigenic effects as the reasons EPO derivatives are being pursued at all. EPO receptors are expressed on some tumor tissue, and this molecule is a receptor agonist. No carcinogenicity study, no proliferation screen and no repeat-dose toxicology has been published for Epobis in any species, and the one thing the independent program reports about its own peptide — neuroprotection “without additional induction of cell-proliferation” — is exactly the measurement missing here.

5. Immunogenicity, which is answerable and has been answered for a cousin. An 18-residue synthetic fragment of a human cytokine, injected repeatedly, can raise antibodies — and antibodies against an EPO-mimetic are not a neutral outcome, because cross-reaction with endogenous erythropoietin is the mechanism behind antibody-mediated anemia seen historically with erythropoiesis-stimulating agents. Lois 2020 looked for anti-drug antibodies against cibinetide over 12 weeks and found none, which proves the assay is straightforward. Nobody has run it for Epobis.

Epobis — its own safety story, not its class's

This compound's safety story is one question with a number attached, and the number belongs to its parent cytokine. Everything favorable about Epobis rests on the claim that it does not do what erythropoietin does to red cells Dmytriyeva 2016. So the first job of a safety section is to price the downside if that claim is wrong, and the human literature prices it precisely: in 4,038 patients, darbepoetin alfa targeting a hemoglobin near 13 g/dL produced fatal or nonfatal stroke in 101 versus 53 on placebo — hazard ratio 1.92 (95% CI 1.38–2.68, p<0.001) — with no reduction in either primary composite endpoint Pfeffer 2009; and in 1,233 hemodialysis patients with cardiac disease, a hematocrit target of 42% versus 30% gave 183 deaths versus 150 and the trial was halted, concluding that raising hematocrit to 42% is not recommended Besarab 1998. Neither trial used Epobis. Both describe what happens when red cell mass is driven up in people.

The markers, then, are not optional and they are cheap: hematocrit, hemoglobin, reticulocyte count and blood pressure. Reticulocytes move first, in roughly 3 to 7 days; hemoglobin and hematocrit follow over 2 to 4 weeks; ferritin and transferrin saturation fall if erythropoiesis is genuinely being driven. Mitigation is the measurement. If hematocrit climbs above the upper reference limit, the mechanism being claimed is not the mechanism operating, and the intervention is to stop — blood viscosity, platelet-vessel interaction and the stroke arithmetic above are the reason, and none of them care what the label says.

The second risk is the one the field names for itself: proliferation. Cho 2022 states the class liabilities as hyper-erythropoietic and tumorigenic effects, and reports its own peptide's neuroprotection occurring “without additional induction of cell-proliferation”. Epobis is an agonist at a receptor expressed beyond erythroid tissue. No proliferation screen, no carcinogenicity study and no repeat-dose toxicology has been published for it, which makes anyone with an active or recent malignancy the clearest group who should not be experimenting here — not because harm is demonstrated, but because the question was raised by the field and never answered for this molecule.

Third, immunogenicity, and it has a specific shape for this class. A short synthetic fragment of a human cytokine, injected repeatedly, is a plausible immunogen, and antibodies raised against an EPO-mimetic can in principle cross-react with endogenous erythropoietin — the mechanism behind the antibody-mediated anemia that has been described historically for erythropoiesis-stimulating agents. The cibinetide trial looked for anti-drug antibodies over 12 weeks and found none Lois 2020, which shows the test is routine. For Epobis, nobody has looked, in any species.

Fourth, you cannot verify what you bought, and here the gap is wider than usual. The published molecule is a dendrimer; the mass the catalogs attach to the name (about 2,195 g/mol) is a single 18-residue chain. Disguised Alpha prints 10MG, a lyophilized format and storage instructions, and no sequence, no CAS, no formula, no molecular weight, no purity figure and no reconstitution volume. A mass spectrum showing 2,195 would confirm the monomer and tell you nothing about the construct in the papers. There is no dose to get right because there is no published dose in any species, and no concentration to compute because no diluent volume is stated.

Finally, the part that is not a medical risk but is a real one. WADA's prohibited list is written around erythropoietin-receptor agonists as a category — the 2019 edition reads “Erythropoietin-Receptor Agonists, e.g. Darbepoetins (dEPO); Erythropoietins (EPO); EPO based constructs…; EPO-mimetic agents”, and the 2026 list adds pegmolesatide, an EPO-mimetic peptide, as a further example of a substance already prohibited. The category is defined by what a substance binds, not by whether it raises hematocrit. A tested athlete using a peptide designed as an EPO-receptor agonist is in S2 on the plain wording, regardless of what their CBC says — and the fact that the vendor files it under Performance is the single most misleading thing about this product.

Sources read for this page

• Pankratova S, Gu B, Kiryushko D, Korshunova I, Kohler LB, Rathje M, Bock E, Berezin V. A new agonist of the erythropoietin receptor, Epobis, induces neurite outgrowth and promotes neuronal survival. Journal of Neurochemistry 2012;121(6):915-23 · PMID 22469063
• Dmytriyeva O, Pankratova S, Korshunova I, Walmod PS. Epobis is a Nonerythropoietic and Neuroprotective Agonist of the Erythropoietin Receptor with Anti-Inflammatory and Memory Enhancing Effects. Mediators of Inflammation 2016;2016:1346390 · PMID 27990061
• Pankratova S, Kiryushko D, Sonn K, Soroka V, Kohler LB, Rathje M, Gu B, Gotfryd K, Clausen O, Zharkovsky A, Bock E, Berezin V. Neuroprotective properties of a novel, non-haematopoietic agonist of the erythropoietin receptor. Brain 2010;133(Pt 8):2281-94 · PMID 20435631
• Cho B, Yoo SJ, Kim SY, Lee CH, Lee YI, Lee SR, Moon C. Second-generation non-hematopoietic erythropoietin-derived peptide for neuroprotection. Redox Biology 2022;49:102223 · PMID 34953452
• Lois N, Gardner E, McFarland M, Armstrong D, McNally C, Lavery NJ, Campbell C, Kirk RI, Bajorunas D, Dunne A, Cerami A, Brines M. A Phase 2 Clinical Trial on the Use of Cibinetide for the Treatment of Diabetic Macular Edema. Journal of Clinical Medicine 2020;9(7):2225 · PMID 32674280
• Pfeffer MA, Burdmann EA, Chen CY, Cooper ME, de Zeeuw D, Eckardt KU, Feyzi JM, Ivanovich P, Kewalramani R, Levey AS, et al. A trial of darbepoetin alfa in type 2 diabetes and chronic kidney disease. New England Journal of Medicine 2009;361(21):2019-32 · PMID 19880844
• Besarab A, Bolton WK, Browne JK, Egrie JC, Nissenson AR, Okamoto DM, Schwab SJ, Goodkin DA. The effects of normal as compared with low hematocrit values in patients with cardiac disease who are receiving hemodialysis and epoetin. New England Journal of Medicine 1998;339(9):584-90 · PMID 9718377

Epobis — interference & stacking

Bloodwork to run alongside Epobis

Baseline first, then again at 8–12 weeks.

The Brain Fog & Cognition panel covers these in one order — 12 markers, $233.06 with the discount applied.

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Epobis — frequently asked questions

What Epobis is used for

Epobis appears under 3 goals in the goal router.

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