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Product Details
Pepstatin A,26305-03-3,IC-0200525
Pepstatin A is an orally active inhibitor of aspartic proteases, which is produced by actinomycetes. It exhibits inhibitory activity with IC50 values of 4.5 nM, 6.2 nM, 150 nM, 290 nM, 520 nM, and 260 nM against hemoglobin-pepsin, hemoglobin-proctase, casein-pepsin, casein-proctase, casein-acid protease, and hemoglobin-acid protease, respectively. Additionally, pepstatin has been found to inhibit HIV protease [1-3]. Pepstatin A(0-120 µM) suppressed receptor activator of NF-κB ligand (RANKL)-induced osteoclast differentiation[4]. Pepstatin A(0.1-0.3 µM) caused a reproducible, concentration-related increase in the extracellular acidification rate in two microglial cell lines, Ra2 and 6-3[5]. Pepstatin A significantly hindered influenza virus replication, probably by modulating host cell autophagic/apoptotic responses[6]. Pepstatin (0.5-50 mg/kg; p.o.) suppresses stomach ulceration of the pylorus in ligated Shay rats[1].
Pepstatin A is an orally active inhibitor of aspartic proteases, which is produced by actinomycetes. It exhibits inhibitory activity with IC50 values of 4.5 nM, 6.2 nM, 150 nM, 290 nM, 520 nM, and 260 nM against hemoglobin-pepsin, hemoglobin-proctase, casein-pepsin, casein-proctase, casein-acid protease, and hemoglobin-acid protease, respectively. Additionally, pepstatin has been found to inhibit HIV protease [1-3]. Pepstatin A(0-120 µM) suppressed receptor activator of NF-κB ligand (RANKL)-induced osteoclast differentiation[4]. Pepstatin A(0.1-0.3 µM) caused a reproducible, concentration-related increase in the extracellular acidification rate in two microglial cell lines, Ra2 and 6-3[5]. Pepstatin A significantly hindered influenza virus replication, probably by modulating host cell autophagic/apoptotic responses[6]. Pepstatin (0.5-50 mg/kg; p.o.) suppresses stomach ulceration of the pylorus in ligated Shay rats[1].
