iNOS and nNOS inhibitor
CAS：13395-35-2
分子式：C10H17N3O2S
分子量：243.3
纯度：98%
存储：Store at -20°C

Background:

2-Iminobiotin is a novel, potent, selective inhibitor of neuronal and inducible nitric oxide synthase.

Nitric oxide synthases (NOS) are a family of enzymes catalyzing the five-electron oxidation of L-arginine to citrulline and nitric oxide. NO produced by NOS is an important cellular signaling molecule implicated in modulating vascular tone, airway tone, insulin secretion, and peristalsis, angiogenesis and neural development [2].

In vitro: 2-Iminobiotin is a reversible inhibitor of murine iNOS and rat n-cNOS with the Ki values of 21.8 and 37.5 μM, respectively. The guanidino group of 2-iminobiotin is essential for binding. 2-iminobiotin carboxy derivatives were also inhibitors of iNOS which indicates that the free carboxyl group is not required for binding.

In vivo: A dose of 30 mg/kg per day of 2-iminobiotin after hypoxia-ischemia resulted in significant long-term neuro-protection [3]. 2-iminobiotin (2-IB) reduced hypoxia-ischemia (HI)-induced brain damage in neonatal rats. In P7 rat pups, 2-Iminobiotin treatment reduced long-term brain damage in female but not male rats [4].

参考文献:
[1] Sup S J, Green B G, Grant S K.  2-Iminobiotin is an inhibitor of nitric oxide synthases[J]. Biochemical and biophysical research communications, 1994, 204(2): 962-968.
[2] Moncada S, Palmer R M L, Higgs E A.  Nitric oxide: physiology, pathophysiology, and pharmacology[J]. Pharmacological reviews, 1991, 43(2): 109-142.
[3] Tweel E R W, van Bel F, Kavelaars A, et al.  Long-term neuroprotection with 2-iminobiotin, an inhibitor of neuronal and inducible nitric oxide synthase, after cerebral hypoxia-ischemia in neonatal rats[J]. Journal of Cerebral Blood Flow & Metabolism, 2005, 25(1): 67-74.
[4] Nijboer C H A, Groenendaal F, Kavelaars A, et al.  Gender-Specific Neuroprotection by 2-Iminobiotin after Hypoxia—Ischemia in the Neonatal Rat via a Nitric Oxide Independent Pathway[J]. Journal of Cerebral Blood Flow & Metabolism, 2007, 27(2): 282-292.