6 Results for "

Endotoxin Substrate

" in MedChemExpress (MCE) Product Catalog:
Products (6)

6 Results for "Endotoxin Substrate" in MCE Product Catalog:

31
31 Publications Verification
Cat. No.: HY-13687
CAS No.: 873225-46-8
Purity:  99.88%
IKK 16 is an orally active IKK inhibitor. IKK 16 shows IC50s of 40 nM, 70 nM, 200 nM, and 50 nM for IKK2, IKK complex, IKK1, and LRRK 2, respectively. IKK 16 is also a pan-PKD inhibitor, inhibiting PKD1, PKD2, and PKD3 with IC50s of 153.9, 115, and 99.7 nM, respectively. IKK 16 is also an ABCB1 inhibitor, interfering with the binding of ABCB1 to its substrates. IKK 16 protects against LPS (HY-D1056)-induced multiple organ dysfunction by reducing the acute inflammatory response induced by endotoxin exposure. IKK 16 can restore renal function and alleviate fibrosis in acute kidney injury. IKK 16 attenuates cardiac dysfunction associated with polymicrobial sepsis in mice with type 2 diabetes mellitus (T2DM) by inhibiting the NF-κB pathway .
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31
31 Publications Verification
Cat. No.: HY-13687A
CAS No.: 1186195-62-9
Purity:  99.95%
IKK 16 hydrochloride is an orally active IKK inhibitor. IKK 16 hydrochloride shows IC50s of 40 nM, 70 nM, 200 nM, and 50 nM for IKK2, IKK complex, IKK1, and LRRK 2, respectively. IKK 16 hydrochloride is also a pan-PKD inhibitor, inhibiting PKD1, PKD2, and PKD3 with IC50s of 153.9, 115, and 99.7 nM, respectively. IKK 16 hydrochloride is also an ABCB1 inhibitor, interfering with the binding of ABCB1 to its substrates. IKK 16 hydrochloride protects against LPS (HY-D1056)-induced multiple organ dysfunction by reducing the acute inflammatory response induced by endotoxin exposure. IKK 16 hydrochloride can restore renal function and alleviate fibrosis in acute kidney injury. IKK 16 hydrochloride attenuates cardiac dysfunction associated with polymicrobial sepsis in mice with type 2 diabetes mellitus (T2DM) by inhibiting the NF-κB pathway .
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1
1 Cited Publications
Cat. No.: HY-E70005H
CAS No.: 9001-12-1
Target:  

Proteasome

Research Areas:  

Cardiovascular Disease

Collagenase, Type VIII is a mixed enzyme derived from Clostridium histolyticum that contains collagenase, a nonspecific protease, and a clostripain. Collagenase, Type VIII can hydrolyze Type VIII collagen and may be used to study the formation of atherosclerosis. Type VIII collagen is a regulator of endothelial cell differentiation and angiogenesis, a substrate for cell adhesion and migration such as smooth muscle cells, and may accumulate in atherosclerosis. After endotoxin activates the expression of Collagenase, Type VIII, it can reduce the production of Type VIII collagen and has the potential to inhibit atherosclerosis .
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Cat. No.: HY-P3936
CAS No.: 68223-96-1
Target:  

Fluorescent Dye

Research Areas:  

Others

Endotoxin Substrate (Boc-LGR-pNA) is a chromogenic substrate can be used in quantitative assays of endotoxin .
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Cat. No.: HY-P11392
CAS No.: 132567-18-1
Research Areas:  

Others

Ac-IEAR-pNA is the chromogenic substrate for quantifying endotoxin levels. Ac-IEAR-pNA is cleaved by HuBChE to produce p-nitroaniline product .
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Cat. No.: HY-13687R
CAS No.: 873225-46-8
IKK 16 (Standard) is the analytical standard of IKK 16. This product is intended for research and analytical applications. IKK 16 hydrochloride is an orally active IKK inhibitor. IKK 16 hydrochloride shows IC50s of 40 nM, 70 nM, 200 nM, and 50 nM for IKK2, IKK complex, IKK1, and LRRK 2, respectively. IKK 16 hydrochloride is also a pan-PKD inhibitor, inhibiting PKD1, PKD2, and PKD3 with IC50s of 153.9, 115, and 99.7 nM, respectively. IKK 16 hydrochloride is also an ABCB1 inhibitor, interfering with the binding of ABCB1 to its substrates. IKK 16 hydrochloride protects against LPS (HY-D1056)-induced multiple organ dysfunction by reducing the acute inflammatory response induced by endotoxin exposure. IKK 16 hydrochloride can restore renal function and alleviate fibrosis in acute kidney injury. IKK 16 hydrochloride attenuates cardiac dysfunction associated with polymicrobial sepsis in mice with type 2 diabetes mellitus (T2DM) by inhibiting the NF-κB pathway.
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