caspase-12

Tauroursodeoxycholate (UR 906), also known as ursodoxicoltaurine, is a highly hydrophilic tertiary bile acid that is produced in humans at a low concentration. Tauroursodeoxycholate is the more hydrophilic form of ursodeoxycholic acid, which is the more abundant naturally produced bile acid in humans.Tauroursodeoxycholate is being investigated for use in several conditions such as Primary Biliary Cirrhosis (PBC), insulin resistance, amyloidosis, Cystic Fibrosis, Cholestasis, and Amyotrophic Lateral Sclerosis.

Tauroursodeoxycholate (TUDCA ,Taurolite) dihydrate is a water-soluble bile acid with endoplasmic reticulum stress inhibitory, mitochondrial stabilizing, and anti-apoptotic effects, which significantly reduces the expression of apoptotic molecules, such as Caspase-3 and Caspase-12, and inhibits ERK, reducing endoplasmic reticulum stress mediated cell death.

Taurochenodeoxycholic Acid (12-Deoxycholyltaurine) is one of the main bioactive substances of animals' bile acid.

Taurochenodeoxycholic acid sodium (Sodium taurochenodeoxycholate) is one of the main bioactive substances of animals' bile acid. Taurochenodeoxycholic acid sodium induces apoptosis and shows obvious anti-inflammatory and immune regulation properties. It can increase glucose-induced insulin secretion and stimulate the electrical activity of α2-cells and enhance cytosolic Ca(2+) concentration ([Ca(2+)](c)).

Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013). Nemorosone is a polycyclic polyprenylated acylphloroglucinol (PPAP) originally isolated from C. rosea that has antiproliferative properties.1 Nemorosone inhibits growth of NB69, Kelly, SK-N-AS, and LAN-1 neuroblastoma cells (IC50s = 3.1-6.3 μM), including several drug-resistant clones, but not MRC-5 human embryonic fibroblasts (IC50 = >40 μM).2 It increases DNA fragmentation in LAN-1 cells in a dose-dependent manner, and decreases N-Myc protein levels and phosphorylation of ERK1/2 by MEK1/2. Nemorosone also inhibits growth of Capan-1, AsPC-1, and MIA-PaCa-2 pancreatic cancer cells (IC50s = 4.5-5.0 μM following a 72-hour treatment) but not human dermal and foreskin fibroblasts (IC50s = >35 μM).1 It induces apoptosis, abolishes the mitochondrial membrane potential, and increases cytosolic calcium concentration in pancreatic cancer cells in a dose-dependent manner. Nemorosone activates the caspase cascade in a dose-dependent manner and inhibits cell cycle progression, increasing the proportion of cells in the G0/G1 phase, in both neuroblastoma and pancreatic cancer cells.1,2 Nemorosone (50 mg/kg, i.p., per day) also reduces tumor growth in an MIA-PaCa-2 mouse xenograft model.3 References1. Holtrup, F., Bauer, A., Fellenberg, K., et al. Microarray analysis of nemorosone-induced cytotoxic effects on pancreatic cancer cells reveals activation of the unfolded protein response (UPR). Br. J. Pharmacol. 162(5), 1045-1059 (2011).2. Díaz-Carballo, D., Malak, S., Bardenheuer, W., et al. Cytotoxic activity of nemorosone in neuroblastoma cells. J. Cell. Mol. Med. 12(6B), 2598-2608 (2008).3. Wold, R.J., Hilger, R.A., Hoheisel, J.D., et al. In vivo activity and pharmacokinetics of nemorosone on pancreatic cancer xenografts. PLoS One 8(9), e74555 (2013).

1. Bufotalin (Bufotaline)e is a kind of poisonous secretions of toads.

Taurodeoxycholic acid (Taurodeoxychloic acid) is a bile acid taurine conjugate of deoxycholic acid, a human metabolite that stabilizes mitochondrial membranes and reduces the formation of free radicals.Taurodeoxycholic acid inhibits apoptosis by blocking calcium-mediated apoptotic pathways and by activation of caspase-12. Taurodeoxycholic acid has neuroprotective activity and has been used to study 3-nitropropionic acid-induced or stabilized hereditary Huntington's chorea (HD).

Taurohyodeoxycholic acid sodium salt (Sodium taurohyodeoxycholate hydrate) prevents apoptosis by blocking a calcium-mediated apoptotic pathway as well as caspase-12 activation.

Taurodeoxycholic acid sodium hydrate (Sodium taurodeoxycholate monohydrate), a hydrophilic bile salt, influences bile salt and biliary lipid secretion in rats.

4,4′-Secalonic acid D (Compound 12) is a PARP1 inhibitor. By inhibiting PARP1, 4,4′-Secalonic acid D induces the accumulation of ROS and DNA damage, activating the caspase-3 GSDME pathway, which leads to tumor cell apoptosis (apoptosis) and pyroptosis (pyroptosis). It exhibits antitumor activity.