vda

Verteporfin (BPD-MA) is a YAP inhibitor that inhibits YAP-TEAD interactions. Verteporfin is also a photosensitizer used in photodynamic therapy. Verteporfin also induces apoptosis and inhibits autophagy.

Valecobulin hydrochloride (CKD-516 hydrochloride) is the valine prodrug and vasoblocker of S516. Valecobulin hydrochloride (CKD-516 hydrochloride) has a potent inhibitory effect on β-tubulin polymerization and has significant anti-tumor activity against solid tumors in mice and humans.

Auristatin F is an effective inhibitor of microtubule and vascular damaging agent. Auristatin F can be used in antibody-drug conjugates.

Vadimezan (DMXAA) is a vascular disrupting agent, a murine STING agonist, and an inducer of cytokines such as type I IFN. Vadimezan has antitumor activity and induces a rapid cessation of blood flow in tumors without affecting blood flow in normal tissues.

HexokinaseIIVDACbinding domain peptide (Hxk2VBD peptide) is a cell-permeable peptide derived from the hexokinase II VDAC binding domain. This peptide inhibits the mitochondrial localization of hexokinase 2 (HXK2) and also suppresses neurotrophic factor-induced axon growth.

Erastin is an iron death activator that acts on the mitochondrial VDAC in a ROS- and iron-dependent manner. Erastin has anti-tumor activity and acts selectively on tumor cells with RAS-carcinogenic mutations.

VBIT-4 is a voltage-dependent anion channel 1 (VDAC1) oligomerization inhibitor (Kd: 17 μM). VBIT-4 can be used for therapeutic purposes in apoptosis-associated disorders (such as neurodegenerative and cardiovascular diseases).

VBIT-12 is a potent inhibitor of VDAC1.

Tuvatexib is a small molecule VDAC/HK2 dual modulator.

WEHI-9625 is a tricyclic sulfone small molecule apoptosis inhibitor (EC50: 69 nM).

Ac-DEVD-AMC (AC-ASP-MET-GLN-ASP-7-AMINO-4-METHYLCOUMARIN) is the substrate of Caspase-3 .

DIDS, an anion exchange inhibitor, acts by blocking reversibly and later irreversibly, exchangers such as chloride-bicarbonate exchanger. It is also a RAD51 inhibitor.

SW016789 is a potent high-secretion inducer targeting VDAC1, which directly stimulates insulin secretion and calcium ion influx in β cells. It transiently induces endoplasmic reticulum stress (ER stress) without causing β cell death. The response it triggers is reversible and non-apoptotic, making SW016789 useful for studying β cell dysfunction in type 2 diabetes (T2DM).

NSC 15364 (1,3-Bis(4-aminophenyl)urea) can be used for screening of ALR inhibitors by detection of hydrogen peroxide production Measured in Biochemical System.

Ac-LEVD-AFC has a wide range of applications in life science related research.

Z-FA-FMK can irreversibly inhibit cysteine protease and also inhibit effector caspases.

[Deamino-4-valine, 8-D-arginine]-Vasopressin (dVDAVP) is a highly potent and specific antidiuretic agent with prolonged effects [1] [2].

Ac-DEVD-AFC, a fluorogenic substrate, undergoes cleavage by caspase-3, producing a blue fluorescent compound upon excitation at 400 nm, which can be quantified at an emission maximum of 505 nm.

BNC105P is a benzo[b]furan-based vascular disrupting agent (VDA) prodrug with potential anti-vascular and anti-tumor effects. Upon administration, BNC105P, in its disodium phosphate form, rapidly converts to BNC105. In activated endothelial cells, BNC105 binds to tubulin and inhibits its polymerization, which may block spindle formation, cause cell cycle arrest, and dismantle the tumor vasculature. This creates a hypoxic environment, depriving tumor cells of nutrients, leading to apoptosis. Apart from its VDA activity, BNC105P also exerts direct cytotoxic effects on tumor cells by inhibiting tubulin polymerization. Notably, BNC105 is not a substrate for the multidrug-resistant P-glycoprotein (Pgp) transporter.

Plinabulin (NPI-2358) (NPI-2358) is a vascular disrupting agent (VDA) against tubulin-depolymerizing tumor cells ( IC50: 9.8-18 nM). Plinabulin selectively targets and binds to the colchicine-binding site of tubulin, thereby interrupting equilibrium of microtubule dynamics. This disrupts mitotic spindle assembly leading to cell cycle arrest at M phase and blockage of cell division.

BNC105P is a benzofuran-based vascular disrupting agent (VDA) prodrug with potential anti-vascular and antineoplastic activities. Upon administration vascular disrupting agent BNC105P, the disodium phosphate ester of BNC105, is rapidly converted to BNC105; in activated endothelial cells, BNC105 binds to tubulin and inhibits its polymerization, which may result in a blockage of mitotic spindle formation, cell cycle arrest, and disruption of the tumor vasculature. Hypoxic conditions ensue, depriving tumor cells of nutrients and resulting in tumor cell apoptosis. In addition to its VDA activity, this agent has a direct cytotoxic effect on tumor cells by inhibiting tubulin polymerization. BNC105 is not a substrate for the multidrug-resistance P-glycoprotein (Pgp) transporter.