parenchymal

By Targets:	Amyloid-β (3) COX (1) Cytochrome P450 (1) Endogenous Metabolite (1) Eukaryotic Initiation Factor (eIF) (1) Leukotriene Receptor (1) Liposome (1) Necroptosis (1) PPAR (1)
By Research Areas:	Cardiovascular Disease (1) Inflammation/Immunology (3) Metabolic Disease (1) Neurological Disease (4)

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-134781

CKK-E12 1 Publications Verification	Liposome	Others
CKK-E12 is a ionizable lipid in combination with other lipids make up the lipid nanoparticles which are used to deliver RNA-based research. CKK-E12 is highly selective toward liver parenchymal cell in vivo,

HY-108666

ATPγS tetralithium salt 1 Publications Verification Adenosine-5'-O-3-thiotriphosphate (tetralithium salt); Adenosine 5'-[γ-thio]triphosphate tetralithium salt	Eukaryotic Initiation Factor (eIF)	Inflammation/Immunology
ATPγS (tetralithium salt) is a substrate for the nucleotide hydrolysis and RNA unwinding activities of eukaryotic translation initiation factor eIF4A .

HY-P3858

(D-Asp1)-Amyloid β-Protein (1-42)	Amyloid-β	Neurological Disease
(D-Asp1)-Amyloid β-Protein (1-42) is a peptide fragment of amyloid β-protein (Aβ). Amyloid β-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease .

HY-P3845

(Gly22)-Amyloid β-Protein (1-42)	Amyloid-β	Neurological Disease
(Gly22)-Amyloid β-Protein (1-42) is a peptide fragment of amyloid β-protein (Aβ). Amyloid β-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease. Mutation of Glu22 to Gly22 in Aβ can increase aggregation .

HY-P3846

(Glu20)-Amyloid β-Protein (1-42)	Amyloid-β	Neurological Disease
(Glu20)-Amyloid β-Protein (1-42) is a slower fibrillizing variant of amyloid β-protein (Aβ). The Glu20 mutation reduces the aggregation propensity of Aβ42 and prevents accumulation of the slowly fibrillizing peptide. Amyloid β-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease .

HY-115381

Lipoxin A5	Endogenous Metabolite	Cardiovascular Disease
Lipoxin A5 is an eicosapentaenoic acid derived from pig white blood cells. Lipoxin A5 slowly contracted the guinea pig lung parenchymal strips with a contractile force similar to that of LXA4 and LXB4.2, but LXA5 did not have the vasodilating effect on the aortic smooth muscle shown by LXA4 and LXB4.2 .

HY-Y0698

Thioacetamide Acetothioamide; TAA; Thiacetamide	Necroptosis	Inflammation/Immunology
Thioacetamide (TAA) is an indirect hepatotoxin and causes parenchymal cell necrosis. Thioacetamide requires metabolic activation by microsomal CYP2E1 to thioacetamide-S-oxide initially and then to thioacetamide-S-dioxide, which is a highly reactive metabolite, and its reactive metabolites covalently bind to proteins and lipids thereby causing oxidative stress and centrilobular necrosis. Thioacetamide can induce chronic liver fibrosis, encephalopathy and other events model .

HY-101676

RG-12525 NID 525	Leukotriene Receptor PPAR Cytochrome P450	Metabolic Disease
RG-12525 is a a specific, competitive and orally effective antagonist of the peptidoleukotrienes, LTC4, LTD4 and LTE4, inhibiting LTC4-, LTD4- and LTE4-inducd guinea pig parenchymal strips contractions, with IC₅₀s of 2.6 nM, 2.5 nM and 7 nM, respectively; RG-12525 is also a peroxisome proliferator-activated receptor gamma (PPAR-gamma) agonist with IC₅₀ of appr 60 nM and a potent inhibitor of CYP3A4, with a K_i value of 0.5 µM.

HY-W032848

Tinoridine Y-3642	COX	Inflammation/Immunology
Tinoridine (Y-3642) is an orally active non-steroidal anti-inflammatory agent with potent antiperoxidative ability and radical scavenger activity. Tinoridine acts function by inhibiting COX enzyme, involves in hepatotoxicity inhibition. .

Cat. No.	Product Name

HY-L073

Anti-Hepatitis C Virus Compound Library	283 compounds
Hepatitis C virus (HCV) is a hepatotropic enveloped positive- strand RNA virus (family Flaviviridae) that infects the parenchymal cells of the liver. HCV infection is a significant public health burden. Globally, an estimated 71 million people have chronic hepatitis C virus infection. A significant number of those who are chronically infected will develop cirrhosis or liver cancer. To date, there is no vaccine against HCV, and combination pegylated alpha interferon (pIFN-) and ribavirin, the main standard-of-care treatment for HCV, is effective in only a subset of patients and is associated with a wide spectrum of toxic side effects and complications. More recently, new therapeutic approaches that target essential components of the HCV life cycle have been developed, including direct-acting antiviral (DAA) that specifically block a viral enzyme or functional protein and host-targeted agents (HTA) that block interactions between host proteins and viral components that are essential to the viral life cycle. However, the genetic diversity of HCV viruses and the stage of liver disease (i.e., cirrhosis) are revealing themselves as obstacles for effective, pan-genotypic treatments. There still exists a need for the discovery and development of new HCV inhibitors. In particular, since the future of HCV therapy will likely consist of a cocktail approach using multiple inhibitors that target different steps of infection, new antivirals targeting all steps of the viral infection cycle. MCE offers a unique collection of 283 compounds with identified and potential anti-HCV activity. MCE Anti- Hepatitis C Virus Compound Library is a useful tool for discovery new anti-HCV drugs and other anti-infection research.

Anti-Hepatitis C Virus Compound Library

283 compounds

Hepatitis C virus (HCV) is a hepatotropic enveloped positive- strand RNA virus (family Flaviviridae) that infects the parenchymal cells of the liver. HCV infection is a significant public health burden. Globally, an estimated 71 million people have chronic hepatitis C virus infection. A significant number of those who are chronically infected will develop cirrhosis or liver cancer. To date, there is no vaccine against HCV, and combination pegylated alpha interferon (pIFN-) and ribavirin, the main standard-of-care treatment for HCV, is effective in only a subset of patients and is associated with a wide spectrum of toxic side effects and complications. More recently, new therapeutic approaches that target essential components of the HCV life cycle have been developed, including direct-acting antiviral (DAA) that specifically block a viral enzyme or functional protein and host-targeted agents (HTA) that block interactions between host proteins and viral components that are essential to the viral life cycle. However, the genetic diversity of HCV viruses and the stage of liver disease (i.e., cirrhosis) are revealing themselves as obstacles for effective, pan-genotypic treatments. There still exists a need for the discovery and development of new HCV inhibitors. In particular, since the future of HCV therapy will likely consist of a cocktail approach using multiple inhibitors that target different steps of infection, new antivirals targeting all steps of the viral infection cycle.

MCE offers a unique collection of 283 compounds with identified and potential anti-HCV activity. MCE Anti- Hepatitis C Virus Compound Library is a useful tool for discovery new anti-HCV drugs and other anti-infection research.

Cat. No.	Product Name	Type

HY-134781

CKK-E12 1 Publications Verification	Drug Delivery
CKK-E12 is a ionizable lipid in combination with other lipids make up the lipid nanoparticles which are used to deliver RNA-based research. CKK-E12 is highly selective toward liver parenchymal cell in vivo,

Cat. No.	Product Name	Target	Research Area

HY-P3858

(D-Asp1)-Amyloid β-Protein (1-42)	Amyloid-β	Neurological Disease
(D-Asp1)-Amyloid β-Protein (1-42) is a peptide fragment of amyloid β-protein (Aβ). Amyloid β-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease .

HY-P3845

(Gly22)-Amyloid β-Protein (1-42)	Amyloid-β	Neurological Disease
(Gly22)-Amyloid β-Protein (1-42) is a peptide fragment of amyloid β-protein (Aβ). Amyloid β-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease. Mutation of Glu22 to Gly22 in Aβ can increase aggregation .

HY-P3846

(Glu20)-Amyloid β-Protein (1-42)	Amyloid-β	Neurological Disease
(Glu20)-Amyloid β-Protein (1-42) is a slower fibrillizing variant of amyloid β-protein (Aβ). The Glu20 mutation reduces the aggregation propensity of Aβ42 and prevents accumulation of the slowly fibrillizing peptide. Amyloid β-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer's disease .

HY-P3803

[D-Pro4,D-Trp7,9] Substance P (4-11)	Peptides	Neurological Disease
[D-Pro4,D-Trp7,9] Substance P (4-11) is a potent antagonist of Substance P (HY-P0201). [D-Pro4,D-Trp7,9] Substance P (4-11) decreases plasma aldosterone (ALDO) concentration .

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