A: Patient’s iron status should be within normal limits i.e., patient should not be iron deficient. Also patient should not be from special population like pregnant/lactating female, children or geriatric >80 years. Patient’s liver dysfunction should not be on severe category and contraindications and warnings should be taken care of while starting Oxemia™ in a patient.
A. Oxemia™ is a molecule belonging to hypoxia inducible factor prolyl hydroxylase inhibitor class. In hypoxic conditions, it reversibly inhibit the prolyl hydroxylase domain, which in turn increases the activity of HIF-a. This HIF-a binds to HIF-ß, forming a dimer which binds to DNA sequences or hypoxia response elements (HREs) to induce expression of target genes. EPO-producing gene is one of the target gene for this. Therefore, it enhances endogenous EPO production. Besides, HIF-a also enhances the enteral iron absorption by boosting production of divalent metal transporter 1 and duodenal cytochrome B, improving iron transportation from the intestinal lumen to the enterocytes. Furthermore, it also inhibits the production of hepcidin which suppresses the iron uptake and mobilisation. In CKD patients, there is a discrepancy between oxygen supply and demand in the kidneys, disturbing the hypoxia-induced signaling in renal EPO-producing cells. Inhibition of PH will restore the HIF-2 a pathway and stimulate erythropoiesis in CKD patients, improving renal anaemia. Click here to view the MoA.
A. In both DREAM-D and DREAM-N D trials, there have not been any major safety concerns associated with Oxemia™ compared to ESAs. The safety profile was similar in both the arms.
A. Currently there’s no data of Oxemia™ with concomitant administration with ESAs. Also, it is not recommended as per APSN guidelines.
A. Oxemia™ has minimal potential to cause CYP-mediated clinical drug-drug interaction at therapeutically relevant concentrations in human. It did not interact significantly with other human drug transporters such as OATP1B1, OATP1B3, OAT1, OCT2 at 30 µM, but it showed interaction with OAT3 (IC50 of 1.7 µM).
A. When a patient misses a dose of Oxemia™, next scheduled dose will be administered to the subjects. However, missed dose will not be administered to the subject.
A. No incidence of overdose with Oxemia™ has been reported. In case of overdose with Oxemia™, general supportive care of the patient is indicated, including monitoring of vital signs and observation of clinical status.
A. Pleotropic benefits include reduction in serum Hepcidin and LDL-C in both DD and N DD population. In DD population apolipoprotein-B was also reduced significantly with Oxemia™ therapy.
A. Food delays the time to reach peak blood levels (Tmax), reduced Cmax and exposure. Oxemia™ should not be consumed with food. Nothing should be taken 1 hour before and 2 hour after taking Oxemia™ per orally.
A. Ideally, Oxemia™ should be given at the end of dialysis session.
A. In phase 3 trials, most common side effects were non serious mainly including gastrointestinal symptoms like nausea, vomiting and constipation. Apart from GI symptoms, peripheral edema was 2nd most common side effect.