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CAYMAN CHEMICAL COMPANY Products - Page 194 of 552
| Name |
Description |
Size |
Catalog # |
| BACE (human recombinant) |
Accumulation of the beta-amyloid peptide (Abeta) in the brain is implicated as the primary cause of neurodegeneration and progression of Alzheimer s disease (AD). The beta-amyloid peptide is derived from sequential proteolytic cleavage of the amyloid precursor protein (APP) by beta- and gamma-secretases. Initial cleavage by beta-secretase (BACE), a membrane-anchored aspartic protease, generates a soluble N-terminal fragment and a membrane-associated C-terminal fragment. The C-terminal fragment then undergoes proteolysis by gamma-secretase to give the Abeta peptide. BACE has been shown to be the major beta-secretase and a promising target as it initiates the first step in Abeta production. Inhibition of BACE activity could potentially block the entire cascade of AD pathogenesis. In addition, BACE deficient mice do not generate Abeta peptide. In transgenic murine models of AD driven by Abeta overproduction, BACE deficiency rescued memory deficits and cholinergic dysfunction. Additionally, the fact that beta-secretase is an aspartic protease has also raised the hope that its therapeutic inhibitor can be as successful as that against HIV protease. |
10 µg |
10227 |
| BACE (human recombinant) |
Accumulation of the beta-amyloid peptide (Abeta) in the brain is implicated as the primary cause of neurodegeneration and progression of Alzheimer s disease (AD). The beta-amyloid peptide is derived from sequential proteolytic cleavage of the amyloid precursor protein (APP) by beta- and gamma-secretases. Initial cleavage by beta-secretase (BACE), a membrane-anchored aspartic protease, generates a soluble N-terminal fragment and a membrane-associated C-terminal fragment. The C-terminal fragment then undergoes proteolysis by gamma-secretase to give the Abeta peptide. BACE has been shown to be the major beta-secretase and a promising target as it initiates the first step in Abeta production. Inhibition of BACE activity could potentially block the entire cascade of AD pathogenesis. In addition, BACE deficient mice do not generate Abeta peptide. In transgenic murine models of AD driven by Abeta overproduction, BACE deficiency rescued memory deficits and cholinergic dysfunction. Additionally, the fact that beta-secretase is an aspartic protease has also raised the hope that its therapeutic inhibitor can be as successful as that against HIV protease. |
25 µg |
10227 |
| BACE (human recombinant) |
Accumulation of the beta-amyloid peptide (Abeta) in the brain is implicated as the primary cause of neurodegeneration and progression of Alzheimer s disease (AD). The beta-amyloid peptide is derived from sequential proteolytic cleavage of the amyloid precursor protein (APP) by beta- and gamma-secretases. Initial cleavage by beta-secretase (BACE), a membrane-anchored aspartic protease, generates a soluble N-terminal fragment and a membrane-associated C-terminal fragment. The C-terminal fragment then undergoes proteolysis by gamma-secretase to give the Abeta peptide. BACE has been shown to be the major beta-secretase and a promising target as it initiates the first step in Abeta production. Inhibition of BACE activity could potentially block the entire cascade of AD pathogenesis. In addition, BACE deficient mice do not generate Abeta peptide. In transgenic murine models of AD driven by Abeta overproduction, BACE deficiency rescued memory deficits and cholinergic dysfunction. Additionally, the fact that beta-secretase is an aspartic protease has also raised the hope that its therapeutic inhibitor can be as successful as that against HIV protease. |
50 µg |
10227 |
| BACE Inhibitor Screening Assay Kit |
Accumulation of the beta-amyloid peptide (Abeta) in the brain is implicated as the primary cause of neurodegeneration and progression of Alzheimer s disease (AD). The beta-amyloid peptide is derived from sequential proteolytic cleavage of the amyloid precursor protein (APP) by beta- and gamma-secretases. Initial cleavage by beta-secretase (BACE; beta-site of APP cleaving enzyme), a membrane anchored aspartic protease, generates a soluble N-terminal fragment and a membrane-associated C-terminal fragment. The C-terminal fragment then undergoes proteolysis by gamma-secretase to give the Abeta peptide. BACE has been shown to be the major beta-secretase and a promising therapeutic target as this protease initiates the first step in Abeta production. Inhibition of BACE activity could potentially block the entire cascade of Alzheimer s disease pathogenesis. In addition, BACE deficient mice do not generate Abeta peptide. In transgenic murine models of AD driven by Abeta overproduction, BACE deficiency rescued memory deficits and cholinergic dysfunction. Additionally, the fact that beta-secretase is an aspartic protease has also raised the hope that its therapeutic inhibitor can be as successful as that against HIV protease. Cayman s BACE Inhibitor Screening Assay Kit provides a convenient method for screening human BACE inhibitors. The assay utilizes a synthetic Swedish mutant APP peptide (EVNLDAEF) that has been linked to a fluorophore (EDANS) at one end and to a quenching agent (Dabcyl) at the other. After cleavage by BACE, the product (peptide-EDANS) is brightly fluorescent and can be easily analyzed using a fluorescence plate reader or a fluorometer with excitation wavelengths of 335-345 nm and emission wavelengths of 485-510 nm. |
96 Well |
600070 |
| BADGE |
PPARgamma is a ligand-activated transcription factor involved in the regulation of lipid homeostasis and may function as a master regulator of adipogenesis. Ligands for PPARgamma include antidiabetic drugs of the thiazolidinedione structural class, 15-deoxy-delta12,14-prost aglandin J2, and NSAIDS. BADGE is a synthetic compound used in the production of polycarbonate and industrial plastics. This compound was recently identified as an antagonist of PPARgamma. BADGE binds to PPARgamma with an apparent Kd of 100 µM and interferes with the ability of 3T3-L1 and 3T3-F442A cells to undergo hormone-mediated cell differentiation. |
100 g |
70790 |
| BADGE |
PPARgamma is a ligand-activated transcription factor involved in the regulation of lipid homeostasis and may function as a master regulator of adipogenesis. Ligands for PPARgamma include antidiabetic drugs of the thiazolidinedione structural class, 15-deoxy-delta12,14-prost aglandin J2, and NSAIDS. BADGE is a synthetic compound used in the production of polycarbonate and industrial plastics. This compound was recently identified as an antagonist of PPARgamma. BADGE binds to PPARgamma with an apparent Kd of 100 µM and interferes with the ability of 3T3-L1 and 3T3-F442A cells to undergo hormone-mediated cell differentiation. |
25 g |
70790 |
| BADGE |
PPARgamma is a ligand-activated transcription factor involved in the regulation of lipid homeostasis and may function as a master regulator of adipogenesis. Ligands for PPARgamma include antidiabetic drugs of the thiazolidinedione structural class, 15-deoxy-delta12,14-prost aglandin J2, and NSAIDS. BADGE is a synthetic compound used in the production of polycarbonate and industrial plastics. This compound was recently identified as an antagonist of PPARgamma. BADGE binds to PPARgamma with an apparent Kd of 100 µM and interferes with the ability of 3T3-L1 and 3T3-F442A cells to undergo hormone-mediated cell differentiation. |
50 g |
70790 |
| BADGE |
PPARgamma is a ligand-activated transcription factor involved in the regulation of lipid homeostasis and may function as a master regulator of adipogenesis. Ligands for PPARgamma include antidiabetic drugs of the thiazolidinedione structural class, 15-deoxy-delta12,14-prost aglandin J2, and NSAIDS. BADGE is a synthetic compound used in the production of polycarbonate and industrial plastics. This compound was recently identified as an antagonist of PPARgamma. BADGE binds to PPARgamma with an apparent Kd of 100 µM and interferes with the ability of 3T3-L1 and 3T3-F442A cells to undergo hormone-mediated cell differentiation. |
500 g |
70790 |
| Bafilomycin A1 |
Bafilomycin A1 is a selective, reversible inhibitor of vacuolar H+ ATPases (V-ATPases), blocking these proton pumps in mammalian, plant, or fungal cells with an IC50 value in the 4-400 nM range. It is at least 1,000-fold less potent at most other types of ATPases. Bafilomycin A1 also inhibits autophagy by preventing vacuolar acidification necessary for autophagosome maturation. |
1 mg |
11038 |
| Bafilomycin A1 |
Bafilomycin A1 is a selective, reversible inhibitor of vacuolar H+ ATPases (V-ATPases), blocking these proton pumps in mammalian, plant, or fungal cells with an IC50 value in the 4-400 nM range. It is at least 1,000-fold less potent at most other types of ATPases. Bafilomycin A1 also inhibits autophagy by preventing vacuolar acidification necessary for autophagosome maturation. |
100 µg |
11038 |
| Bafilomycin B1 |
The bafilomycins are fungal plecomacrolide antibiotics with a 16-membered lactone ring. They inhibit the growth of Gram-positive bacteria and fungi. Bafilomycin B1 is a selective, reversible inhibitor of vacuolar H+ ATPases (V-ATPases), blocking these proton pumps in mammalian, plant, or fungal cells with an IC50 value in the 4-400 nM range. It is at least 1,000-fold less potent at most other types of ATPases. When used at 100 nM, the related macrolide bafilomycin A1 blocks V-ATPase-mediated acidification of lysosomes during autophagy, preventing protein degradation. Remarkably, at only 1 nM, both bafilomycin A1 or B1 dramatically attenuate chloroquine-induced apoptosis of neurons without altering autophagy. |
1 mg |
14005 |
| Bafilomycin B1 |
The bafilomycins are fungal plecomacrolide antibiotics with a 16-membered lactone ring. They inhibit the growth of Gram-positive bacteria and fungi. Bafilomycin B1 is a selective, reversible inhibitor of vacuolar H+ ATPases (V-ATPases), blocking these proton pumps in mammalian, plant, or fungal cells with an IC50 value in the 4-400 nM range. It is at least 1,000-fold less potent at most other types of ATPases. When used at 100 nM, the related macrolide bafilomycin A1 blocks V-ATPase-mediated acidification of lysosomes during autophagy, preventing protein degradation. Remarkably, at only 1 nM, both bafilomycin A1 or B1 dramatically attenuate chloroquine-induced apoptosis of neurons without altering autophagy. |
100 µg |
14005 |
| Bafilomycin B1 |
The bafilomycins are fungal plecomacrolide antibiotics with a 16-membered lactone ring. They inhibit the growth of Gram-positive bacteria and fungi. Bafilomycin B1 is a selective, reversible inhibitor of vacuolar H+ ATPases (V-ATPases), blocking these proton pumps in mammalian, plant, or fungal cells with an IC50 value in the 4-400 nM range. It is at least 1,000-fold less potent at most other types of ATPases. When used at 100 nM, the related macrolide bafilomycin A1 blocks V-ATPase-mediated acidification of lysosomes during autophagy, preventing protein degradation. Remarkably, at only 1 nM, both bafilomycin A1 or B1 dramatically attenuate chloroquine-induced apoptosis of neurons without altering autophagy. |
5 mg |
14005 |
| Baicalein |
Baicalein is a flavonoid originally isolated from the roots of Scutellaria baicalensis Georgi. Several different functions of baicalein have been reported. Platelet 12-lipoxygenase is inhibited by baicalein with an ID50 value of 0.12 µM, with minimal inhibition of platelet cyclooxygenase-1 (IC50 = 0.83 mM). Baicalein inhibits lipid peroxidation, as assessed by production of TBARS, with an IC50 value of 5 µM. In addition to these effects, baicalein may play a role in apoptosis, as the compound inhibits cell growth of three human hepatocellular carcinoma cell lines with IC50 values ranging from 17-70 µg/ml. |
100 mg |
70610 |
| Baicalein |
Baicalein is a flavonoid originally isolated from the roots of Scutellaria baicalensis Georgi. Several different functions of baicalein have been reported. Platelet 12-lipoxygenase is inhibited by baicalein with an ID50 value of 0.12 µM, with minimal inhibition of platelet cyclooxygenase-1 (IC50 = 0.83 mM). Baicalein inhibits lipid peroxidation, as assessed by production of TBARS, with an IC50 value of 5 µM. In addition to these effects, baicalein may play a role in apoptosis, as the compound inhibits cell growth of three human hepatocellular carcinoma cell lines with IC50 values ranging from 17-70 µg/ml. |
1000 mg |
70610 |
| Baicalein |
Baicalein is a flavonoid originally isolated from the roots of Scutellaria baicalensis Georgi. Several different functions of baicalein have been reported. Platelet 12-lipoxygenase is inhibited by baicalein with an ID50 value of 0.12 µM, with minimal inhibition of platelet cyclooxygenase-1 (IC50 = 0.83 mM). Baicalein inhibits lipid peroxidation, as assessed by production of TBARS, with an IC50 value of 5 µM. In addition to these effects, baicalein may play a role in apoptosis, as the compound inhibits cell growth of three human hepatocellular carcinoma cell lines with IC50 values ranging from 17-70 µg/ml. |
50 mg |
70610 |
| Baicalein |
Baicalein is a flavonoid originally isolated from the roots of Scutellaria baicalensis Georgi. Several different functions of baicalein have been reported. Platelet 12-lipoxygenase is inhibited by baicalein with an ID50 value of 0.12 µM, with minimal inhibition of platelet cyclooxygenase-1 (IC50 = 0.83 mM). Baicalein inhibits lipid peroxidation, as assessed by production of TBARS, with an IC50 value of 5 µM. In addition to these effects, baicalein may play a role in apoptosis, as the compound inhibits cell growth of three human hepatocellular carcinoma cell lines with IC50 values ranging from 17-70 µg/ml. |
500 mg |
70610 |
| BAY-11-7082 |
The transcription factor NF-kappaB plays a key role in regulating over 150 target genes including the expression of inflammatory cytokines, chemokines, immunoreceptors, and cell adhesion molecules. In the cytoplasm, inactive NF-kappaB complexes are bound to an inhibitor IkappaB. However in response to certain stimuli, IkappaB is phosphorylated, ubiquitinated, and degraded, enabling the translocation of NF-kappaB to the nucleus. BAY-11-7082 selectively and irreversibly inhibits NF-kappaB activation by blocking TNF-alpha-induced phosphorylation of IkappaB-alpha without affecting constitutive IkappaB-alpha phosphorylation. This compound inhibits the TNF-alpha-induced surface expression of adhesion molecules ICAM-1, VCAM-1, and E-selectin in human endothelial cells with IC50 values of 5-10 µM. |
10 mg |
10010266 |
| BAY-11-7082 |
The transcription factor NF-kappaB plays a key role in regulating over 150 target genes including the expression of inflammatory cytokines, chemokines, immunoreceptors, and cell adhesion molecules. In the cytoplasm, inactive NF-kappaB complexes are bound to an inhibitor IkappaB. However in response to certain stimuli, IkappaB is phosphorylated, ubiquitinated, and degraded, enabling the translocation of NF-kappaB to the nucleus. BAY-11-7082 selectively and irreversibly inhibits NF-kappaB activation by blocking TNF-alpha-induced phosphorylation of IkappaB-alpha without affecting constitutive IkappaB-alpha phosphorylation. This compound inhibits the TNF-alpha-induced surface expression of adhesion molecules ICAM-1, VCAM-1, and E-selectin in human endothelial cells with IC50 values of 5-10 µM. |
25 mg |
10010266 |
| BAY-11-7082 |
The transcription factor NF-kappaB plays a key role in regulating over 150 target genes including the expression of inflammatory cytokines, chemokines, immunoreceptors, and cell adhesion molecules. In the cytoplasm, inactive NF-kappaB complexes are bound to an inhibitor IkappaB. However in response to certain stimuli, IkappaB is phosphorylated, ubiquitinated, and degraded, enabling the translocation of NF-kappaB to the nucleus. BAY-11-7082 selectively and irreversibly inhibits NF-kappaB activation by blocking TNF-alpha-induced phosphorylation of IkappaB-alpha without affecting constitutive IkappaB-alpha phosphorylation. This compound inhibits the TNF-alpha-induced surface expression of adhesion molecules ICAM-1, VCAM-1, and E-selectin in human endothelial cells with IC50 values of 5-10 µM. |
5 mg |
10010266 |
| BAY-11-7082 |
The transcription factor NF-kappaB plays a key role in regulating over 150 target genes including the expression of inflammatory cytokines, chemokines, immunoreceptors, and cell adhesion molecules. In the cytoplasm, inactive NF-kappaB complexes are bound to an inhibitor IkappaB. However in response to certain stimuli, IkappaB is phosphorylated, ubiquitinated, and degraded, enabling the translocation of NF-kappaB to the nucleus. BAY-11-7082 selectively and irreversibly inhibits NF-kappaB activation by blocking TNF-alpha-induced phosphorylation of IkappaB-alpha without affecting constitutive IkappaB-alpha phosphorylation. This compound inhibits the TNF-alpha-induced surface expression of adhesion molecules ICAM-1, VCAM-1, and E-selectin in human endothelial cells with IC50 values of 5-10 µM. |
50 mg |
10010266 |
| BAY-41-8543 |
Soluble guanylate cyclase (sGC) is the primary cellular receptor for nitric oxide (NO). NO binds and activates a heme group in sGC, initiating the conversion of GTP to the second messenger cyclic GMP (cGMP). BAY-41-8543 is a heme-dependent stimulator of sGC, increasing the activity of recombinant sGC dose-dependently, from 0.1 nM to 100 ?M, up to 92-fold. Surprisingly, NO donors synergize with BAY-41-8543 in stimulating recombinant sGC. BAY-41-8543 relaxes vessels and inhibits platelet aggregation in vitro at nM concentrations. In vivo, BAY-41-8543 decreases blood pressure dose-dependently, prolongs bleeding time, and reduces thrombosis. Inhalation of microparticles containing BAY-41-8543 increases pulmonary vasodilation without changing mean arterial pressure, suggesting that agonists of sGC may be efficacious in treating pulmonary hypertension. |
1 mg |
10011131 |
| BAY-41-8543 |
Soluble guanylate cyclase (sGC) is the primary cellular receptor for nitric oxide (NO). NO binds and activates a heme group in sGC, initiating the conversion of GTP to the second messenger cyclic GMP (cGMP). BAY-41-8543 is a heme-dependent stimulator of sGC, increasing the activity of recombinant sGC dose-dependently, from 0.1 nM to 100 ?M, up to 92-fold. Surprisingly, NO donors synergize with BAY-41-8543 in stimulating recombinant sGC. BAY-41-8543 relaxes vessels and inhibits platelet aggregation in vitro at nM concentrations. In vivo, BAY-41-8543 decreases blood pressure dose-dependently, prolongs bleeding time, and reduces thrombosis. Inhalation of microparticles containing BAY-41-8543 increases pulmonary vasodilation without changing mean arterial pressure, suggesting that agonists of sGC may be efficacious in treating pulmonary hypertension. |
10 mg |
10011131 |
| BAY-41-8543 |
Soluble guanylate cyclase (sGC) is the primary cellular receptor for nitric oxide (NO). NO binds and activates a heme group in sGC, initiating the conversion of GTP to the second messenger cyclic GMP (cGMP). BAY-41-8543 is a heme-dependent stimulator of sGC, increasing the activity of recombinant sGC dose-dependently, from 0.1 nM to 100 ?M, up to 92-fold. Surprisingly, NO donors synergize with BAY-41-8543 in stimulating recombinant sGC. BAY-41-8543 relaxes vessels and inhibits platelet aggregation in vitro at nM concentrations. In vivo, BAY-41-8543 decreases blood pressure dose-dependently, prolongs bleeding time, and reduces thrombosis. Inhalation of microparticles containing BAY-41-8543 increases pulmonary vasodilation without changing mean arterial pressure, suggesting that agonists of sGC may be efficacious in treating pulmonary hypertension. |
25 mg |
10011131 |
| BAY-41-8543 |
Soluble guanylate cyclase (sGC) is the primary cellular receptor for nitric oxide (NO). NO binds and activates a heme group in sGC, initiating the conversion of GTP to the second messenger cyclic GMP (cGMP). BAY-41-8543 is a heme-dependent stimulator of sGC, increasing the activity of recombinant sGC dose-dependently, from 0.1 nM to 100 ?M, up to 92-fold. Surprisingly, NO donors synergize with BAY-41-8543 in stimulating recombinant sGC. BAY-41-8543 relaxes vessels and inhibits platelet aggregation in vitro at nM concentrations. In vivo, BAY-41-8543 decreases blood pressure dose-dependently, prolongs bleeding time, and reduces thrombosis. Inhalation of microparticles containing BAY-41-8543 increases pulmonary vasodilation without changing mean arterial pressure, suggesting that agonists of sGC may be efficacious in treating pulmonary hypertension. |
5 mg |
10011131 |
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