BDS-I

Non Antibodies

Proteins

Israel

Storage as Solution: The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods (up to 6 months), small aliquots should be stored at -20°C. We do not recommend storing the product in working solutions for longer than a few days. Avoid multiple freeze-thaw cycles. - Storage before Reconstitution: The product is shipped as a lyophilized powder at room temperature. Upon receipt, store the product at -20°C. Protect from moisture. - Storage after Reconstitution: The reconstituted solution can be stored at 4°C for up to 1 week. For longer periods (up to 6 months), small aliquots should be stored at -20°C. We do not recommend storing the product in working solutions for longer than a few days. Avoid multiple freeze-thaw cycles.

Lyophilized

Blood depressing substance I, Blood depressing substance 1, Delta/Kappa-actitoxin-Avd4a - A Blocker of KV3 Channels and a Modulator of NaV Channels

A Blocker of K_V3 Channels and a Modulator of Na_V Channels

12352202

Disulfide bonds between: Cys⁴-Cys³⁹, Cys⁶-Cys³², and Cys²²-Cys⁴⁰

BDS-I inhibits 60% of KV3.4 current. The blocking effect is rapid, direct and reversible1. BDS-I also modulates voltage-gated Na+ channels. It enhances TTX-sensitive Na+ channels (highly effective on NaV1.7 channels), and weakly inhibits TTX-resistant NaV channels2.

no

BDS-I is a 43 amino acid peptidyl toxin isolated from the sea anemone Anemonia sulcata venom. It is reported to be a selective blocker of KV3.4 K+ channel. BDS-I blocks 60% of the KV3.4 current in COS-transfected cells at a concentration of 2.5 µM The blocking effect is rapid, direct and reversible1. Recently it was shown that it blocks other KV3 channels with similar potencies2.BDS-I inhibits KV currents in carotid body cells3, an effect which disappears after chronic hypoxia, establishing the unique role played by KV3 channels in the response to hypoxia4. BDS-I (2.5 µM) also reduces the native transient K+ current and increases the action potential duration in hippocampal granule neurons5. In corneal epithelial cells BDS-I (400 nM) inhibits most of the detected KV current6. In magnocellular neurosecretory neurons of the hypothalamus, 100 nM BDS-I inhibits about half of the KV current and increases the action potential duration7. In fast spiking neurons from different brain areas, 2 µM BDS-I inhibits part of the KV current and broadened the action potential and reduces spike frequency8.BDS-I also produces broadening of the spike and accelerates the upstroke of the action potential by modulating voltage-gated Na+ channels. It enhances TTX-sensitive Na+ channels (highly effective on NaV1.7 channels), and weakly inhibits TTX-resistant NaV channels9.