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Results for "

calcific aortic valve stenosis

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Biochemical Assay Reagents (1) Caspase (2) Isotope-Labeled Compounds (2) P2Y Receptor (1) Small Interfering RNA (siRNA) (2)
By Research Areas:	Cardiovascular Disease (5) Inflammation/Immunology (1)
Oligonucleotides:	siRNAs (2)

Inhibitors & Agonists

Isotope-Labeled Compounds

Oligonucleotides

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-112499S1

Menaquinone-7-13C6 Vitamin K2-7-¹³C₆; Vitamin K2(35)-¹³C₆; Vitamin MK-7-¹³C₆	Isotope-Labeled Compounds	Cardiovascular Disease
Menaquinone-7- ¹³C₆ is the ¹³C-labeled Menaquinone-7. Menaquinone-7 (Vitamin K2-7), belongs to a class of K2-vitamin homologs, is originally discovered as the anti-hemorrhagic factors[1]. Menaquinone-7 (Vitamin K2-7) is identified as the most bioactive cofactor for the carboxylation reaction of Gla-proteins [2]. Supplementation with Menaquinone-7 (Vitamin K2-7) is a pharmacological option for activating matrix Gla protein and intervening in the progression of calcific aortic valve stenosis (CAVS)[3].

HY-116307

2-Thio-UTP	P2Y Receptor	Cardiovascular Disease
2-Thio-UTP is a selective P2Y₂ inhibitor with an EC₅₀ value of 50 nM. 2-Thio-UTP reduces pro-fibrotic gene expression and protein α-smooth muscle actin. 2-Thio-UTP has the potential for the research of calcific aortic valve stenosis (CAVS) .

HY-158820

Cosdosiran QPI-1007	Small Interfering RNA (siRNA) Caspase	Cardiovascular Disease
Cosdosiran is a chemically modified siRNA designed to temporarily inhibit expression of the caspase 2 protein and can be used for the study of nonarteritic anterior ischemic optic neuropathy and other optic neuropathies such as glaucoma that result in the death of retinal ganglion cells.?

HY-158820A

Cosdosiran sodium QPI-1007 sodium	Small Interfering RNA (siRNA) Caspase	Cardiovascular Disease
Cosdosiran sodium is a chemically modified siRNA designed to temporarily inhibit expression of the caspase 2 protein and can be used for the study of nonarteritic anterior ischemic optic neuropathy and other optic neuropathies such as glaucoma that result in the death of retinal ganglion cells.?

HY-E70364

IgdE protease	Biochemical Assay Reagents	Inflammation/Immunology
IgdE protease is a cysteine protease, which is initially isolated from Streptococcus agalactiae. IgdE protease digests monoclonal antibodies (mAbs) of the IgG1 type specifically at their upper hinge region, produces Fc/2, hinge peptide dimers, and Fab fragment. IgdE protease can be used in disulfide bonds and free thiol analysis, as it requires no reducing agents for cleavage .

HY-112499S

Menaquinone-7-d7 Vitamin K2-7-d₇; Vitamin K2(35)-d₇; Vitamin MK-7-d₇	Isotope-Labeled Compounds	Cardiovascular Disease
Menaquinone-7-d₇ is the deuterium labeled Menaquinone-7. Menaquinone-7 (Vitamin K2-7), belongs to a class of K2-vitamin homologs, is originally discovered as the anti-hemorrhagic factors[1]. Menaquinone-7 (Vitamin K2-7) is identified as the most bioactive cofactor for the carboxylation reaction of Gla-proteins [2]. Supplementation with Menaquinone-7 (Vitamin K2-7) is a pharmacological option for activating matrix Gla protein and intervening in the progression of calcific aortic valve stenosis (CAVS)[3].

Cat. No.	Product Name	Chemical Structure

HY-112499S1

Menaquinone-7-13C6
Menaquinone-7- ¹³C₆ is the ¹³C-labeled Menaquinone-7. Menaquinone-7 (Vitamin K2-7), belongs to a class of K2-vitamin homologs, is originally discovered as the anti-hemorrhagic factors[1]. Menaquinone-7 (Vitamin K2-7) is identified as the most bioactive cofactor for the carboxylation reaction of Gla-proteins [2]. Supplementation with Menaquinone-7 (Vitamin K2-7) is a pharmacological option for activating matrix Gla protein and intervening in the progression of calcific aortic valve stenosis (CAVS)[3].

Menaquinone-7-13C6

Menaquinone-7- ¹³C₆ is the ¹³C-labeled Menaquinone-7. Menaquinone-7 (Vitamin K2-7), belongs to a class of K2-vitamin homologs, is originally discovered as the anti-hemorrhagic factors[1]. Menaquinone-7 (Vitamin K2-7) is identified as the most bioactive cofactor for the carboxylation reaction of Gla-proteins [2]. Supplementation with Menaquinone-7 (Vitamin K2-7) is a pharmacological option for activating matrix Gla protein and intervening in the progression of calcific aortic valve stenosis (CAVS)[3].

HY-112499S

Menaquinone-7-d7
Menaquinone-7-d₇ is the deuterium labeled Menaquinone-7. Menaquinone-7 (Vitamin K2-7), belongs to a class of K2-vitamin homologs, is originally discovered as the anti-hemorrhagic factors[1]. Menaquinone-7 (Vitamin K2-7) is identified as the most bioactive cofactor for the carboxylation reaction of Gla-proteins [2]. Supplementation with Menaquinone-7 (Vitamin K2-7) is a pharmacological option for activating matrix Gla protein and intervening in the progression of calcific aortic valve stenosis (CAVS)[3].

Menaquinone-7-d7

Menaquinone-7-d₇ is the deuterium labeled Menaquinone-7. Menaquinone-7 (Vitamin K2-7), belongs to a class of K2-vitamin homologs, is originally discovered as the anti-hemorrhagic factors[1]. Menaquinone-7 (Vitamin K2-7) is identified as the most bioactive cofactor for the carboxylation reaction of Gla-proteins [2]. Supplementation with Menaquinone-7 (Vitamin K2-7) is a pharmacological option for activating matrix Gla protein and intervening in the progression of calcific aortic valve stenosis (CAVS)[3].

Cat. No.	Product Name		Classification

HY-158820

Cosdosiran QPI-1007		siRNAs
Cosdosiran is a chemically modified siRNA designed to temporarily inhibit expression of the caspase 2 protein and can be used for the study of nonarteritic anterior ischemic optic neuropathy and other optic neuropathies such as glaucoma that result in the death of retinal ganglion cells.?

HY-158820A

Cosdosiran sodium QPI-1007 sodium		siRNAs
Cosdosiran sodium is a chemically modified siRNA designed to temporarily inhibit expression of the caspase 2 protein and can be used for the study of nonarteritic anterior ischemic optic neuropathy and other optic neuropathies such as glaucoma that result in the death of retinal ganglion cells.?

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