Discovery of a First-in-Class CD38 Inhibitor for the Treatment of Mitochondrial Myopathy.

CD38 is a crucial NADase in mammalian tissues that degrades NAD and thus regulates cellular NAD levels. Abnormal CD38 expression is linked to mitochondrial dysfunction under several pathological conditions. We present a novel CD38 inhibitor, compound , with high potency for CD38 (IC of 11 nM) and minimal activity against other targets.

[Identification and preparation of a glycol-protein fraction AN from tea extracts and its and anti-hyperglycosemia activity].

The present study compared active ingredients of tea from different sources to select tea type and the fraction of tea extracts for the highest anti-hyperglycemic activity, and to verify anti-hyperglycemic activity of the selected tea extract. Tea extracts were separated and enriched by molecular weight using ultra-filtration technology. The extracts were first screened by -glucosidase inhibition assay, followed by using a rat inverted intestine sac system to measure the effect on glucose transport.

Cellular NAD replenishment confers marked neuroprotection against ischemic cell death: role of enhanced DNA repair.

Background And Purpose: NAD(+) is an essential cofactor for cellular energy production and participates in various signaling pathways that have an impact on cell survival. After cerebral ischemia, oxidative DNA lesions accumulate in neurons because of increased attacks by ROS and diminished DNA repair activity, leading to PARP-1 activation, NAD(+) depletion, and cell death. The objective of this study was to determine the neuroprotective effects of NAD(+) repletion against ischemic injury and the underlying mechanism.