NPI-503 would be prescribed in advance to patients ‘at risk’ of stroke. Patients that may benefit from NPI-503 are those individuals with increased risk of stroke. These include the following US populations:
- 350,000 coronary artery bypass patients (CABG)
- 2.2 Million patients with atrial fibrillation
- 4.6 million stroke survivors
- 50 million individuals with hypertension
References:
Stevens SL, Stenzel-Poore MP. Toll-like receptors and tolerance to ischaemic injury in the brain. Biochem Soc Trans. 2006 Dec;34(Pt 6):1352-5. PubMed Reference
Rosenzweig HL, Lessov NS, Henshall DC, Minami M, Simon RP, Stenzel-Poore MP. Endotoxin preconditioning prevents cellular inflammatory response during ischemic neuroprotection in mice. Stroke. 2004 Nov;35(11):2576-81. PubMed Reference
Stenzel-Poore MP, Stevens SL, Simon RP. Genomics of preconditioning. Stroke. 2004 Nov;35(11 Suppl 1):2683-6. PubMed Reference
Stevens SL, Shaw TE, Dykhuizen E, Lessov NS, Hill JK, Wurst W, Stenzel-Poore MP. Reduced cerebral injury in CRH-R1 deficient mice after focal ischemia: a potential link to microglia and atrocytes that express CRH-R1. J Cereb Blood Flow Metab. 2003 Oct;23:1151-9. PubMed Reference
Stenzel-Poore MP, Stevens SL, Xiong Z, Lessov NS, Harrington CA, Mori M, Meller R, Rosenzweig HL, Tobar E, Shaw TE, Chu X, Simon RP. Effect of ischaemic preconditioning on genomic response to cerebral ischaemia: similarity to neuroprotective strategies in hibernation and hypoxia-tolerant states. Lancet. 2003 Sep 27;362:1028-37. PubMed Reference
Treatment with NPI-503 may reduce the severity of brain injury if the patient were to suffer a stroke. In pre-clinical studies, NPI-503 protects the brain for at least one week following treatment.
In pre-clinical studies, NPI-503 given one day before a stroke resulted in 60% less brain damage. Protection lasted for at least 7 days, when there was still 40% less damage.