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microvascular blood

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By Targets:	Akt (2) Aurora Kinase (1) c-Kit (1) Cadherin (3) Claudin (2) Endogenous Metabolite (1) Exosomes (1) Glycosidase (1) Interleukin Related (1) MAGL (1) MMP (2) Phosphodiesterase (PDE) (1) PI3K (2) STING (1) Tie (2) VEGFR (2)
By Research Areas:	Cancer (3) Cardiovascular Disease (4) Endocrinology (1) Infection (2) Inflammation/Immunology (3) Metabolic Disease (2) Neurological Disease (2)

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Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-110281

Dehydroascorbic acid	Endogenous Metabolite	Cardiovascular Disease Neurological Disease
Dehydroascorbic acid is an oxidized form of vitamin C that can cross the blood-brain barrier (BBB). Dehydroascorbic acid clears cytotoxic reactive oxygen species (ROS) produced after ischemic stroke by converting to ascorbic acid (AA), thereby reducing neuronal and glial cell damage and stabilizing cerebral microvascular NO signaling to maintain perfusion in the ischemic area. Dehydroascorbic acid can be used in research on ischemic stroke .

HY-N0419

Quercimeritrin 2 Publications Verification Quercetin-7-O-β-D-glucopyranoside	Glycosidase c-Kit MMP VEGFR Aurora Kinase	Metabolic Disease Cancer
Quercimeritrin (Quercetin-7-O-β-D-glucopyranoside) is an orally active α-glucosidase inhibitor (with an IC₅₀ of 79.88 μM against the Saccharomyces cerevisiae enzyme) and a P-gp substrate, with anti-angiogenic and antioxidant activities. Quercimeritrin does not cross the blood-brain barrier and does not inhibit cytochrome P450 enzymes. Quercimeritrin precisely binds to and inhibits the active sites of c-Kit, MMP-2, Aurora-A kinases and α-glucosidase, thereby disrupting target functions. Quercimeritrin effectively regulates postprandial blood glucose and also exhibits significant anti-angiogenic activity, which inhibits endothelial cell proliferation and microvascular growth. Quercimeritrin can be used in the research of diabetes and breast cancer .

HY-125864B

Murine Fibrinogen	MMP Cadherin	Cardiovascular Disease Neurological Disease
Murine Fibrinogen is a native fibrinogen derived from mouse plasma. Murine Fibrinogen acts as a cerebrovascular permeability enhancer. Murine Fibrinogen activates matrix metalloproteinase-9 (MMP-9), downregulates the expression of vascular endothelial cadherin (VE-cadherin), and upregulates the expression of plasmalemmal vesicle-associated protein-1 (PV-1). Murine Fibrinogen increases macromolecular leakage from pial veins, thereby disrupting the microvascular integrity of cerebral blood vessels. Murine Fibrinogen can be used in studies related to cerebrovascular dysfunction .

HY-P10580

Vasculotide	Tie PI3K Akt Cadherin Claudin	Cardiovascular Disease Infection Inflammation/Immunology
Vasculotide is a blood-brain barrier (BBB)-penetrant Tie2 agonist. Vasculotide binds to a unique domain of Tie2, induces receptor clustering to drive phosphorylation, activates downstream PI3K/Akt and eNOS pathways, enhances inter-endothelial cell junctions (such as VE-cadherin and claudin-5), and inhibits inflammatory adhesion molecules, ultimately stabilizing the vascular endothelial barrier and reducing its permeability . Vasculotide alleviates pulmonary microvascular leakage and microcirculatory dysfunction caused by cardiopulmonary bypass, acts as an adjuvant radioprotective agent to reduce acute radiation dermatitis, and promotes BBB recovery after focused ultrasound (FUS). Combination of Vasculotide with antibiotics reduces lung injury .

HY-P10580A

Vasculotide TFA	Cadherin Tie Claudin PI3K Akt	Cardiovascular Disease Infection Inflammation/Immunology
Vasculotide TFA is a blood-brain barrier (BBB)-penetrant Tie2 agonist. Vasculotide TFA binds to a unique domain of Tie2, induces receptor clustering to drive phosphorylation, activates downstream PI3K/Akt and eNOS pathways, enhances inter-endothelial cell junctions (such as VE-cadherin and claudin-5), and inhibits inflammatory adhesion molecules, ultimately stabilizing the vascular endothelial barrier and reducing its permeability . Vasculotide TFA alleviates pulmonary microvascular leakage and microcirculatory dysfunction caused by cardiopulmonary bypass, acts as an adjuvant radioprotective agent to reduce acute radiation dermatitis, and promotes BBB recovery after focused ultrasound (FUS). Combination of Vasculotide TFA with antibiotics reduces lung injury .

HY-19586

Albifylline A 81-3138; HWA-138	Phosphodiesterase (PDE)	Endocrinology
Albifylline (A 81-3138; HWA-138) is a Xanthine (HY-W017389) derivate. Albifylline reduces the shock-induced leukocyte adhesions to the sinusoidal endothelium in the liver after hemorrhagic shock and improves microvascular blood flow in the liver .

HY-185379

STING antagonist-3	STING	Inflammation/Immunology
STING antagonist-3 is a potent STING antagonist with an IC₅₀ of 2.3 nM against human wild-type STING. STING antagonist-3 inhibits human wild-type STING and the gain-of-function STING mutants N154S and V155M. STING antagonist-3 suppresses IFN‑α2a production in stimulated human whole blood. STING antagonist-3 inhibits IP-10 production in activated human dermal microvascular endothelial cells (HMVEC-d). STING antagonist-3 can be used for the research of autoimmune diseases, autoinflammatory diseases, interferonopathies, and fibrotic disorders .

HY-182639

AM9928	Exosomes MAGL Interleukin Related VEGFR	Cancer
AM9928 is a monoacylglycerol lipase (MAGL) inhibitor with IC₅₀ and K_i values of 8.9 nM and 7.3 nM, respectively. AM9928 blocks the adhesion and migration of triple-negative breast cancer (TNBC) cells, and inhibits the secretion of IL-6, IL-8 and VEGF-A by TNBC cells. AM9928 suppresses the activation of human brain microvascular endothelial cells (HBMECs) induced by TNBC-derived exosomes, and reduces the secretion of IL-8 and VEGF-A by HBMECs. AM9928 attenuates changes in blood-brain barrier permeability, inhibits tumor growth in the mammary fat pad, and reduces brain colonization of TNBC. AM9928 can be used in studies related to triple-negative breast cancer .

Cat. No.	Product Name	Target	Research Area

HY-P10580

Vasculotide	Tie PI3K Akt Cadherin Claudin	Cardiovascular Disease Infection Inflammation/Immunology
Vasculotide is a blood-brain barrier (BBB)-penetrant Tie2 agonist. Vasculotide binds to a unique domain of Tie2, induces receptor clustering to drive phosphorylation, activates downstream PI3K/Akt and eNOS pathways, enhances inter-endothelial cell junctions (such as VE-cadherin and claudin-5), and inhibits inflammatory adhesion molecules, ultimately stabilizing the vascular endothelial barrier and reducing its permeability . Vasculotide alleviates pulmonary microvascular leakage and microcirculatory dysfunction caused by cardiopulmonary bypass, acts as an adjuvant radioprotective agent to reduce acute radiation dermatitis, and promotes BBB recovery after focused ultrasound (FUS). Combination of Vasculotide with antibiotics reduces lung injury .

HY-137874

L-Glutamic γ-monohydroxamate	Peptides	Metabolic Disease Cancer
L-Glutamic γ-monohydroxamate is an antitumor agent, inhibits cell proliferation. L-Glutamic γ-monohydroxamate selectively inhibits the uptake of L-histidine into microvascular endothelial cell. L-Glutamic γ-monohydroxamate, as a vanadium ligand, activates glucose uptake and metabolism, thus decreases the blood glucose levels in vivo .

HY-P10580A

Vasculotide TFA	Cadherin Tie Claudin PI3K Akt	Cardiovascular Disease Infection Inflammation/Immunology
Vasculotide TFA is a blood-brain barrier (BBB)-penetrant Tie2 agonist. Vasculotide TFA binds to a unique domain of Tie2, induces receptor clustering to drive phosphorylation, activates downstream PI3K/Akt and eNOS pathways, enhances inter-endothelial cell junctions (such as VE-cadherin and claudin-5), and inhibits inflammatory adhesion molecules, ultimately stabilizing the vascular endothelial barrier and reducing its permeability . Vasculotide TFA alleviates pulmonary microvascular leakage and microcirculatory dysfunction caused by cardiopulmonary bypass, acts as an adjuvant radioprotective agent to reduce acute radiation dermatitis, and promotes BBB recovery after focused ultrasound (FUS). Combination of Vasculotide TFA with antibiotics reduces lung injury .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-110281

Dehydroascorbic acid	Structural Classification Ketones, Aldehydes, Acids Endogenous metabolite Source Classification	Endogenous Metabolite
Dehydroascorbic acid is an oxidized form of vitamin C that can cross the blood-brain barrier (BBB). Dehydroascorbic acid clears cytotoxic reactive oxygen species (ROS) produced after ischemic stroke by converting to ascorbic acid (AA), thereby reducing neuronal and glial cell damage and stabilizing cerebral microvascular NO signaling to maintain perfusion in the ischemic area. Dehydroascorbic acid can be used in research on ischemic stroke .

HY-N0419

Quercimeritrin 2 Publications Verification Quercetin-7-O-β-D-glucopyranoside	Flavonols Structural Classification Ginkgoaceae Classification of Application Fields Metabolic Disease Plants Compositae Endogenous metabolite Ginkgo biloba Human Gut Microbiota Metabolites Flavonoids Derris scandens Disease Research Fields Source Classification	Glycosidase c-Kit MMP VEGFR Aurora Kinase
Quercimeritrin (Quercetin-7-O-β-D-glucopyranoside) is an orally active α-glucosidase inhibitor (with an IC₅₀ of 79.88 μM against the Saccharomyces cerevisiae enzyme) and a P-gp substrate, with anti-angiogenic and antioxidant activities. Quercimeritrin does not cross the blood-brain barrier and does not inhibit cytochrome P450 enzymes. Quercimeritrin precisely binds to and inhibits the active sites of c-Kit, MMP-2, Aurora-A kinases and α-glucosidase, thereby disrupting target functions. Quercimeritrin effectively regulates postprandial blood glucose and also exhibits significant anti-angiogenic activity, which inhibits endothelial cell proliferation and microvascular growth. Quercimeritrin can be used in the research of diabetes and breast cancer .

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BODIPY 493/503 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Feb 1;16(1):1241. [Abstract]

MedchemExpress Validation 01

Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature. Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature. Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.

BODIPY 493/503 purchased from MedChemExpress. Usage Cited in: Nat Commun. 2025 Feb 1;16(1):1241. [Abstract]

MedchemExpress Validation 01

MedchemExpress Validation 03

Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred

MedchemExpress Validation 04

MedchemExpress Validation

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microvascular blood

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