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Results for "

Angiogenesis Stimulator

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Akt (6) AMPK (1) AP-1 (1) Apelin Receptor (APJ) (1) Bacterial (8) Biochemical Assay Reagents (2) CD44 (2) Drug Derivative (1) Endogenous Metabolite (8) FGFR (2) Guanylate Cyclase (1) HCV (2) HIF/HIF Prolyl-Hydroxylase (1) Integrin (1) Interleukin Related (1) MMP (1) NF-κB (1) Phosphodiesterase (PDE) (1) PI3K (5) PKA (1) Prostaglandin Receptor (1) Proteasome (2) Reference Standards (2) SDCBP (1) TRP Channel (1) TSH Receptor (1) VEGFR (6)
By Research Areas:	Cancer (13) Cardiovascular Disease (8) Infection (4) Inflammation/Immunology (14) Metabolic Disease (5) Neurological Disease (4)
Oligonucleotides:	Polymers (1)

Inhibitors & Agonists

Screening Libraries

Biochemical Assay Reagents

Peptides

Inhibitory Antibodies

Natural
Products

Oligonucleotides

Targets Recommended: STING

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-B0633A

Hyaluronic acid 15+ Cited Publications Hyaluronan; Hyaluronate	Endogenous Metabolite Bacterial Akt PI3K	Infection Neurological Disease Inflammation/Immunology Cancer
Hyaluronic acid is a biopolymer composed of repeating units of disaccharides with various applications. Hyaluronic acid is a major component of the extracellular matrix (ECM). Hyaluronic acid is synthesized at the plasma membrane. Increased hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion and angiogenesis in digestive cancers. Hyaluronic acid participates in tissue remodeling and rapid cell proliferation in some physiological processes including embryonic morphogenesis and wound-healing. Hyaluronic acid activates the PI3K-Akt signaling. Hyaluronic acid acts as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid also enhances cell invasion and angiogenesis by promoting proteolytic MMP-9 binding to cell surface or stimulating MMP-9 binding to cell surface. Hyaluronic acid can be used as drug delivery for sodium butyrate to improve the anti-proliferative activity on breast cancer cell line. Hyaluronic acid can be studied in joint diseases, wound healing and cancer .

HY-B0633

Hyaluronic acid sodium 15+ Cited Publications Sodium hyaluronate	Endogenous Metabolite Bacterial PI3K Akt	Inflammation/Immunology Cancer
Hyaluronic acid sodium (Sodium hyaluronate) is a biopolymer composed of repeating units of disaccharides with various applications. Hyaluronic acid sodium is a major component of the extracellular matrix (ECM). Hyaluronic acid sodium is synthesized at the plasma membrane. Increased hyaluronic acid sodium levels are associated with tumor cell growth, adhesion, migration, invasion and angiogenesis in digestive cancers. Hyaluronic acid sodium participates in tissue remodeling and rapid cell proliferation in some physiological processes including embryonic morphogenesis and wound-healing. Hyaluronic acid sodium activates the PI3K-Akt signaling. Hyaluronic acid sodium acts as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid sodium also enhances cell invasion and angiogenesis by promoting proteolytic MMP-9 binding to cell surface or stimulating MMP-9 binding to cell surface. Hyaluronic acid sodium can be used as drug delivery for sodium butyrate to improve the anti-proliferative activity on breast cancer cell line. Hyaluronic acid sodium can be studied in joint diseases, wound healing and cancer .

HY-P991202

Anti-TSHR Antibody (M22)	TSH Receptor PKA	Metabolic Disease Inflammation/Immunology
Anti-TSHR Antibody (M22) is a selective agonist targeting TSHR (thyroid-stimulating hormone receptor), acting through competitive binding to the extracellular domain of TSHR. Anti-TSHR Antibody (M22) can mimic the biological effects of thyroid-stimulating hormone (TSH), activating downstream cAMP-PKA and other signaling pathways. Anti-TSHR Antibody (M22) can stimulate the proliferation of thyroid follicular epithelial cells and human umbilical vein endothelial cells (HUVECs), promote angiogenesis and tube formation, cell migration, and also upregulate the expression of angiogenesis-related proteins such as PROX1. Anti-TSHR Antibody (M22) can be used in research areas such as the mechanisms of goiter formation in Graves' disease (GD), angiogenesis regulation, and TSHR antagonist screening .

HY-B0633D

Hyaluronic acid sodium (MW 200-1560)	CD44 Endogenous Metabolite Bacterial Akt PI3K	Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Hyaluronic acid sodium (MW 200-1560) is a biopolymer composed of repeating disaccharide units, with a molecular weight of 200-1560. Hyaluronic acid sodium is a major component of the extracellular matrix (ECM). It is synthesized on the plasma membrane. Hyaluronic acid sodium exerts its effects by binding to receptors CD44 and RHAMM. Hyaluronic acid sodium activates PI3K-Akt signaling. Hyaluronic acid sodium also enhances cell invasion and angiogenesis by promoting or stimulating the binding of proteolytic MMP-9 to the cell surface. Elevated hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion, and angiogenesis in digestive system cancers. Hyaluronic acid sodium is involved in tissue remodeling and rapid cell proliferation in several physiological processes, including embryonic morphogenesis and wound healing. Hyaluronic acid sodium can be used as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid sodium can be used as a drug delivery carrier for sodium butyrate, enhancing its anti-proliferative activity against breast cancer cell lines. Hyaluronic acid sodium can lubricate the corneal endothelium. Hyaluronic acid sodium can improve tissue hydration and enhance the resistance of cells to mechanical damage. Hyaluronic acid sodium has been conjugated with antibodies to ensure that the active compound continues to exert its effects at the site of inflammation. Hyaluronic acid sodium can be used in research in the fields of osteoarthritis, ophthalmology, cosmetic dermatology, oncology, and liver diseases .

HY-B0633E

Hyaluronic acid, low endotoxin Hyaluronan, low endotoxin; Hyaluronate, low endotoxin	Endogenous Metabolite CD44 Bacterial Akt PI3K	Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Hyaluronic acid, low endotoxin (Hyaluronan, low endotoxin) is a biopolymer composed of repeating disaccharide units containing low levels of endotoxin. Hyaluronic acid is a major component of the extracellular matrix (ECM). It is synthesized on the plasma membrane. Hyaluronic acid exerts its effects by binding to receptors CD44 and RHAMM. Hyaluronic acid activates PI3K-Akt signaling. Hyaluronic acid also enhances cell invasion and angiogenesis by promoting or stimulating the binding of proteolytic MMP-9 to the cell surface. Elevated hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion, and angiogenesis in digestive system cancers. Hyaluronic acid is involved in tissue remodeling and rapid cell proliferation in several physiological processes, including embryonic morphogenesis and wound healing. Hyaluronic acid can be used as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid can be used as a drug delivery carrier for sodium butyrate, enhancing its anti-proliferative activity against breast cancer cell lines. Hyaluronic acid can lubricate the corneal endothelium. Hyaluronic acid can improve tissue hydration and enhance the resistance of cells to mechanical damage. Hyaluronic acid has been conjugated with antibodies to ensure that the active compound continues to exert its effects at the site of inflammation. Hyaluronic acid can be used in research in the fields of osteoarthritis, ophthalmology, cosmetic dermatology, oncology, and liver diseases .

HY-B0327

Irsogladine 3 Publications Verification Dicloguamine	Phosphodiesterase (PDE) NF-κB AP-1 TRP Channel Interleukin Related	Inflammation/Immunology Cancer
Irsogladine (Dicloguamine) is an orally active gastric mucosal protective agent. Irsogladine inhibits breast cancer recurrence and lung metastasis in nude mice . Irsogladine inhibits the transcriptional activities of NF-κB and AP-1, suppresses the activities of PDE and PDE4 to elevate intracellular cAMP levels, and activates TRPV1 and K_ATP channels. Irsogladine enhances iNOS expression, NO production, and the activation of cAMP-responsive elements. Irsogladine inhibits the development and progression of intestinal polyps in Apc-mutant mice. Irsogladine alleviates oxidative stress, increases gastric mucosal blood flow, and stimulates the production of endogenous prostaglandins. Irsogladine promotes insulin secretion in MIN6 cells. Irsogladine inhibits tumor angiogenesis, cancer cell proliferation, and the production of proinflammatory cytokines. Irsogladine exerts protective effects on astrocytes in ethanol/hydrochloric acid-induced gastric ulcers in mice. Irsogladine prevents colitis in IL-10 gene-deficient mice by reducing the production of IL-12 and IL-23. Irsogladine upregulates gap junction intercellular communication in pancreatic cancer cells via the PKA pathway. Irsogladine is applicable to research related to breast cancer, intestinal polyposis, gastric ulcer, spontaneous colitis, glioma, liver cancer, and pancreatic cancer ^[5][6] .

HY-13718

Oglufanide H-Glu-Trp-OH; L-Glutamyl-L-tryptophan	VEGFR HCV Endogenous Metabolite	Infection Cardiovascular Disease Inflammation/Immunology Cancer
Oglufanide (H-Glu-Trp-OH) is a dipeptide immunomodulator isolated from calf thymus. Oglufanide inhibits vascular endothelial growth factor (VEGF). Oglufanide can stimulate the immune response to hepatitic C virus (HCV) and intracellular bacterial infections. Oglufanide shows antitumor and anti-angiogenesis activities .

HY-B0633I

Hyaluronic acid sodium (MW 800kDa)	Endogenous Metabolite Bacterial PI3K Akt	Inflammation/Immunology Cancer
Hyaluronic acid sodium (MW 800kDa) is a biopolymer composed of repeating units of disaccharides with various applications. Hyaluronic acid sodium is a major component of the extracellular matrix (ECM). Hyaluronic acid sodium is synthesized at the plasma membrane. Increased hyaluronic acid sodium levels are associated with tumor cell growth, adhesion, migration, invasion and angiogenesis in digestive cancers. Hyaluronic acid sodium participates in tissue remodeling and rapid cell proliferation in some physiological processes including embryonic morphogenesis and wound-healing. Hyaluronic acid sodium activates the PI3K-Akt signaling. Hyaluronic acid sodium acts as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid sodium also enhances cell invasion and angiogenesis by promoting proteolytic MMP-9 binding to cell surface or stimulating MMP-9 binding to cell surface. Hyaluronic acid sodium can be used as drug delivery for sodium butyrate to improve the anti-proliferative activity on breast cancer cell line. Hyaluronic acid sodium can be studied in joint diseases, wound healing and cancer .

HY-12379

NS-2028 1 Publications Verification	Guanylate Cyclase	Inflammation/Immunology
NS-2028 is a highly selective soluble Guanylyl Cyclase (sGC) inhibitor with IC₅₀ values of 30 nM and 200 nM for basal and NO-stimulated enzyme activity . NS-2028 inhibits soluble Guanylyl Cyclase activity in homogenates of mouse cerebellum and neuronal NO synthase with IC₅₀ values of 17 nM and 20 nM . NS-2028 inhibits 3-morpholino-sydnonimine (SIN-1)-elicited formation of cyclic GMP in human cultured umbilical vein endothelial cells with an IC₅₀ of 30 nM . NS-2028 is commonly used in the research of nitric oxide signaling pathways, it inhibits NO-dependent relaxant responses in non-vascular smooth muscle completely (1 μM) . NS-2028 reduces vascular endothelial growth factor-induced angiogenesis and permeability .

HY-P2196A

ELA-32(human) TFA 1 Publications Verification	Apelin Receptor (APJ)	Cancer
ELA-32(human) TFA is a potent, high affinity apelin receptor agonist (IC₅₀=0.27 nM; K_d=0.51 nM). ELA-32(human) TFA exhibits no binding GPR15 and GPR25. ELA-32(human) TFA activates the PI3K/AKT pathway and promotes self-renewal of hESCs via cell-cycle progression and protein translation. ELA-32(human) TFA also potentiates the TGFβ pathway, priming hESCs toward the endoderm lineage. ELA-32(human) TFA stimulates angiogenesis in HUVEC cells.

HY-NP101

Highly purified Type I collagen, from bovine skin 1 Publications Verification Bovine Type I collagen, immunization grade	Biochemical Assay Reagents	Inflammation/Immunology
Highly purified Type I collagen, from bovine skin (Bovine Type I collagen, immunization grade) plays an important role in the structure and function of skin, bone, tendons, and many others. Type I collagen potently stimulates angiogenesis in vitro and in vivo. Highly purified Type I collagen, from bovine skin is an immunization grade that can be used for immunization to generate antibodies .

HY-P1259A

PR-39 TFA	Proteasome Bacterial	Inflammation/Immunology
PR-39 TFA, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 TFAreversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 TFA stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice .

HY-142019

Tanshinol borneol ester	Akt AMPK	Cardiovascular Disease
Tanshinol borneol ester, an angiogenesis stimulator, promoted multiple key steps of angiogenesis through Akt and MAPK signalling pathways. Tanshinol borneol ester has anti-ischemic and anti-atherosclerosis activities .

HY-P1259

PR-39	Proteasome Bacterial	Inflammation/Immunology
PR-39, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 reversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice .

HY-108933

JK-P3	VEGFR FGFR	Cancer
JK-P3 is a potent and pan VEGFR2 inhibitor, with IC₅₀s of 7.83 μM, 27 μM and 5.18 μM for VEGFR2, FGFR1 and FGFR3, respectively. JK-P3 can inhibit VEGF-A-stimulated VEGFR2 activation and intracellular signalling, also inhibits endothelial monolayer wound closure and angiogenesis, as well as fibroblast growth factor receptor kinase activity in vitro. JK-P3 has anti-angiogenic activity .

HY-118543

TM6089	HIF/HIF Prolyl-Hydroxylase	Cardiovascular Disease
TM6089 is a unique Prolyl Hydroxylase (PHD) inhibitor which stimulates HIF activity without iron chelation and induces angiogenesis and exerts organ protection against ischemia. Local administration of TM6089 enhances angiogenesis, and oral administration stimulates HIF activity in transgenic rats expressing a hypoxia-responsive reporter vector .

HY-W009123R

Erucamide (Standard) cis-13-Docosenamide (Standard)	Endogenous Metabolite Reference Standards	Others
Erucamide (Standard) is the analytical standard of Erucamide. This product is intended for research and analytical applications. Erucamide inhibits intestinal diarrhea.Erucamide also regulates the volume of body fluids in other organs. Erucamide has the ability to promote angiogenesis .

HY-P10335

SPARC (119-122) (mouse)	Biochemical Assay Reagents	Metabolic Disease
SPARC (119-122) (mouse) stimulates endothelial cell proliferation and angiogenesis. SPARC (119-122) (mouse) can be used to enhance neovascularization in modified polypropropylene biomaterials .

HY-162346

KN-17	Bacterial	Infection
KN-17 is a modified based on the structure of cecropin B (HY-P0092), can effectively interfere with bacterial growth and induce the migration of human bone marrow stromal cells (hBMSCs). KN-17 can significantly stimulate angiogenesis in vitro and in vivo .

HY-106893

Pimilprost SM 10902	Drug Derivative Prostaglandin Receptor	Cardiovascular Disease Metabolic Disease
Pimilprost (SM 10902) is a prostaglandin I1 analogue. Pimilprost exhibits antithrombotic and increases cAMP levels. Pimilprost can promote wound healing through the stimulation of angiogenesis and the improvement of blood flow in diabetic mice. Pimilprost can be used for the research of metabolic and cardiovascular disease, such as diabetes .

HY-13718A

Oglufanide disodium H-Glu-Trp-OH disodium; L-Glutamyl-L-tryptophan disodium	VEGFR HCV Endogenous Metabolite	Infection Cardiovascular Disease Inflammation/Immunology Cancer
Oglufanide (H-Glu-Trp-OH) disodium is a dipeptide immunomodulator isolated from calf thymus. Oglufanide disodium inhibits vascular endothelial growth factor (VEGF). Oglufanide disodium can stimulate the immune response to hepatitic C virus (HCV) and intracellular bacterial infections. Oglufanide disodium shows antitumor and anti-angiogenesis activities .

HY-P11775A

Peptide HRH acetate	VEGFR	Cardiovascular Disease
Peptide HRH acetate is a polypeptide that specifically binds to VEGF receptors. Peptide HRH acetate inhibits *VEGF*-stimulated endothelial cell proliferation. Peptide HRH acetate inhibits angiogenesis and suppresses corneal neovascularization. Peptide HRH acetate can be used in anti-angiogenesis related studies .

HY-P11775

Peptide HRH	VEGFR	Cardiovascular Disease
Peptide HRH is a polypeptide that specifically binds to VEGF receptors. Peptide HRH inhibits *VEGF*-stimulated endothelial cell proliferation. Peptide HRH inhibits angiogenesis and suppresses corneal neovascularization. Peptide HRH can be used in anti-angiogenesis related studies .

HY-118273

IPS-05002	Integrin	Inflammation/Immunology Cancer
IPS-05002 is an α5β1 antagonist. IPS-05002 can inhibit VEGF-stimulated human umbilical vein endothelial cell (HUVEC) proliferation, adhesion, and migration, and also suppresses tubular network formation. IPS-05002 can upregulate IKB-β, XRCC4, and downregulate Cdc6 in VEGF-induced HUVECs. IPS-05002 can be used for the study of tumor angiogenesis .

HY-P11777

AG73	MMP SDCBP	Cardiovascular Disease Neurological Disease Cancer
AG73 is a polypeptide. AG73 is derived from the G domain of the Laminin α1 chain. AG73 binds heparin, Syndecan-1 and Syndecan-4. AG73 promotes the adhesion of various cells, induces the differentiation of salivary gland acinar cells, stimulates neurite outgrowth, secretion of matrix metalloproteinases and angiogenesis. AG73 retains its angiogenic activity when conjugated to chitosan membranes. AG73 can be used in the research of melanoma and ischemic injury .

HY-108933R

JK-P3 (Standard)	Reference Standards VEGFR FGFR	Cancer
JK-P3 (Standard) is the analytical standard of JK-P3 (HY-108933). This product is intended for research and analytical applications. JK-P3 is a potent and pan VEGFR2 inhibitor, with IC₅₀s of 7.83 μM, 27 μM and 5.18 μM for VEGFR2, FGFR1 and FGFR3, respectively. JK-P3 can inhibit VEGF-A-stimulated VEGFR2 activation and intracellular signalling, also inhibits endothelial monolayer wound closure and angiogenesis, as well as fibroblast growth factor receptor K_inase activity in vitro. JK-P3 has anti-angiogenic activity .

Cat. No.	Product Name

HY-L015

PI3K/Akt/mTOR Compound Library	1,049 compounds
The PI3K/Akt/mTOR pathway controls many cellular processes that are important for the formation and progression of cancer, including apoptosis, transcription, translation, metabolism, angiogenesis, and cell cycle progression. Every major node of this signaling network is activated in a wide range of human tumors. Mechanisms for the pathway activation include activation of receptor tyrosine kinases (RTKs) upstream of PI3K, mutation or amplification of PIK3CA encoding p110α catalytic subunit of PI3K, mutation or loss of PTEN tumor suppressor gene, and mutation or amplification of Akt1. Once the pathway is activated, signaling through Akt can stimulate a series of substrates including mTOR which is involved in protein synthesis. Thus, inhibition of this pathway is an attractive concept for cancer prevention and/or therapy. Currently some mTOR inhibitors are approved for several indications, and there are several novel PI3K/Akt/mTOR inhibitors in clinical trials. MCE owns a unique collection of 1,049 compounds that can be used for PI3K/Akt/mTOR pathway research. PI3K/Akt/mTOR Compound Library also acts as a useful tool for anti-cancer drug discovery.

PI3K/Akt/mTOR Compound Library

1,049 compounds

The PI3K/Akt/mTOR pathway controls many cellular processes that are important for the formation and progression of cancer, including apoptosis, transcription, translation, metabolism, angiogenesis, and cell cycle progression. Every major node of this signaling network is activated in a wide range of human tumors. Mechanisms for the pathway activation include activation of receptor tyrosine kinases (RTKs) upstream of PI3K, mutation or amplification of PIK3CA encoding p110α catalytic subunit of PI3K, mutation or loss of PTEN tumor suppressor gene, and mutation or amplification of Akt1. Once the pathway is activated, signaling through Akt can stimulate a series of substrates including mTOR which is involved in protein synthesis. Thus, inhibition of this pathway is an attractive concept for cancer prevention and/or therapy. Currently some mTOR inhibitors are approved for several indications, and there are several novel PI3K/Akt/mTOR inhibitors in clinical trials.

MCE owns a unique collection of 1,049 compounds that can be used for PI3K/Akt/mTOR pathway research. PI3K/Akt/mTOR Compound Library also acts as a useful tool for anti-cancer drug discovery.

HY-L045

Oxygen Sensing Compound Library	4,029 compounds
Oxygen homeostasis regulation is the most fundamental cellular process for adjusting physiological oxygen variations, and its irregularity leads to various human diseases, including cancer. Hypoxia is closely associated with cancer development, and hypoxia/oxygen-sensing signaling plays critical roles in the modulation of cancer progression. Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that functions as a master regulator of oxygen homeostasis. A variety of HF-1 target genes have been identified thus far which encode proteins that play key roles in critical developmental and physiological processes including angiogenesis/vascular remodeling, erythropoiesis, glucose transport, glycolysis, iron transport, and cell proliferation/survival. HIF-1 is a heterodimeric transcription factor consisting of a constitutively expressed β-subunit and an oxygen-regulated α-subunit. The unique feature of HIF-1 is the regulation of HIF-1α expression and activity based upon the cellular O₂ concentration. Under normoxic conditions, hydroxylation of HIF-1α on these different proline residues is essential for HIF proteolytic degradation by promoting interaction with the von Hippel-Lindau tumor-suppressor protein (pVHL) through hydrogen bonding to the hydroxyproline-binding pocket in the pVHL β-domain. As oxygen levels decrease, hydroxylation of HIF decreases; HIF-1α then no longer binds pVHL, and becomes stabilized, allowing more of the protein to translocate to the cell’s nucleus, where it acts as a transcription factor, upregulating (often within minutes) the production of proteins that stimulate blood perfusion in tissues and thus tissue oxygenation. MCE offers a unique collection of 4,029 oxygen sensing related compounds targeting HIF/HIF Prolyl-Hydroxylase, MAPK/ERK, PI3K/AKT signaling pathways, etc. MCE Oxygen Sensing Compound Library is a useful tool to study hypoxia, oxidative stress and discover new anti-cancer drugs.

Oxygen Sensing Compound Library

4,029 compounds

Oxygen homeostasis regulation is the most fundamental cellular process for adjusting physiological oxygen variations, and its irregularity leads to various human diseases, including cancer. Hypoxia is closely associated with cancer development, and hypoxia/oxygen-sensing signaling plays critical roles in the modulation of cancer progression.

Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that functions as a master regulator of oxygen homeostasis. A variety of HF-1 target genes have been identified thus far which encode proteins that play key roles in critical developmental and physiological processes including angiogenesis/vascular remodeling, erythropoiesis, glucose transport, glycolysis, iron transport, and cell proliferation/survival.

HIF-1 is a heterodimeric transcription factor consisting of a constitutively expressed β-subunit and an oxygen-regulated α-subunit. The unique feature of HIF-1 is the regulation of HIF-1α expression and activity based upon the cellular O₂ concentration. Under normoxic conditions, hydroxylation of HIF-1α on these different proline residues is essential for HIF proteolytic degradation by promoting interaction with the von Hippel-Lindau tumor-suppressor protein (pVHL) through hydrogen bonding to the hydroxyproline-binding pocket in the pVHL β-domain. As oxygen levels decrease, hydroxylation of HIF decreases; HIF-1α then no longer binds pVHL, and becomes stabilized, allowing more of the protein to translocate to the cell’s nucleus, where it acts as a transcription factor, upregulating (often within minutes) the production of proteins that stimulate blood perfusion in tissues and thus tissue oxygenation.

MCE offers a unique collection of 4,029 oxygen sensing related compounds targeting HIF/HIF Prolyl-Hydroxylase, MAPK/ERK, PI3K/AKT signaling pathways, etc. MCE Oxygen Sensing Compound Library is a useful tool to study hypoxia, oxidative stress and discover new anti-cancer drugs.

Cat. No.	Product Name	Type

HY-B0633A

Hyaluronic acid 15+ Cited Publications Hyaluronan; Hyaluronate	Biochemical Assay Reagents
Hyaluronic acid is a biopolymer composed of repeating units of disaccharides with various applications. Hyaluronic acid is a major component of the extracellular matrix (ECM). Hyaluronic acid is synthesized at the plasma membrane. Increased hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion and angiogenesis in digestive cancers. Hyaluronic acid participates in tissue remodeling and rapid cell proliferation in some physiological processes including embryonic morphogenesis and wound-healing. Hyaluronic acid activates the PI3K-Akt signaling. Hyaluronic acid acts as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid also enhances cell invasion and angiogenesis by promoting proteolytic MMP-9 binding to cell surface or stimulating MMP-9 binding to cell surface. Hyaluronic acid can be used as drug delivery for sodium butyrate to improve the anti-proliferative activity on breast cancer cell line. Hyaluronic acid can be studied in joint diseases, wound healing and cancer .

Hyaluronic acid

15+ Cited Publications

Hyaluronan; Hyaluronate

Biochemical Assay Reagents

Hyaluronic acid is a biopolymer composed of repeating units of disaccharides with various applications. Hyaluronic acid is a major component of the extracellular matrix (ECM). Hyaluronic acid is synthesized at the plasma membrane. Increased hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion and angiogenesis in digestive cancers. Hyaluronic acid participates in tissue remodeling and rapid cell proliferation in some physiological processes including embryonic morphogenesis and wound-healing. Hyaluronic acid activates the PI3K-Akt signaling. Hyaluronic acid acts as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid also enhances cell invasion and angiogenesis by promoting proteolytic MMP-9 binding to cell surface or stimulating MMP-9 binding to cell surface. Hyaluronic acid can be used as drug delivery for sodium butyrate to improve the anti-proliferative activity on breast cancer cell line. Hyaluronic acid can be studied in joint diseases, wound healing and cancer .

HY-B0633E

Hyaluronic acid, low endotoxin Hyaluronan, low endotoxin; Hyaluronate, low endotoxin	Biochemical Assay Reagents
Hyaluronic acid, low endotoxin (Hyaluronan, low endotoxin) is a biopolymer composed of repeating disaccharide units containing low levels of endotoxin. Hyaluronic acid is a major component of the extracellular matrix (ECM). It is synthesized on the plasma membrane. Hyaluronic acid exerts its effects by binding to receptors CD44 and RHAMM. Hyaluronic acid activates PI3K-Akt signaling. Hyaluronic acid also enhances cell invasion and angiogenesis by promoting or stimulating the binding of proteolytic MMP-9 to the cell surface. Elevated hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion, and angiogenesis in digestive system cancers. Hyaluronic acid is involved in tissue remodeling and rapid cell proliferation in several physiological processes, including embryonic morphogenesis and wound healing. Hyaluronic acid can be used as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid can be used as a drug delivery carrier for sodium butyrate, enhancing its anti-proliferative activity against breast cancer cell lines. Hyaluronic acid can lubricate the corneal endothelium. Hyaluronic acid can improve tissue hydration and enhance the resistance of cells to mechanical damage. Hyaluronic acid has been conjugated with antibodies to ensure that the active compound continues to exert its effects at the site of inflammation. Hyaluronic acid can be used in research in the fields of osteoarthritis, ophthalmology, cosmetic dermatology, oncology, and liver diseases .

Hyaluronic acid, low endotoxin

Hyaluronan, low endotoxin; Hyaluronate, low endotoxin

Biochemical Assay Reagents

Hyaluronic acid, low endotoxin (Hyaluronan, low endotoxin) is a biopolymer composed of repeating disaccharide units containing low levels of endotoxin. Hyaluronic acid is a major component of the extracellular matrix (ECM). It is synthesized on the plasma membrane. Hyaluronic acid exerts its effects by binding to receptors CD44 and RHAMM. Hyaluronic acid activates PI3K-Akt signaling. Hyaluronic acid also enhances cell invasion and angiogenesis by promoting or stimulating the binding of proteolytic MMP-9 to the cell surface. Elevated hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion, and angiogenesis in digestive system cancers. Hyaluronic acid is involved in tissue remodeling and rapid cell proliferation in several physiological processes, including embryonic morphogenesis and wound healing. Hyaluronic acid can be used as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid can be used as a drug delivery carrier for sodium butyrate, enhancing its anti-proliferative activity against breast cancer cell lines. Hyaluronic acid can lubricate the corneal endothelium. Hyaluronic acid can improve tissue hydration and enhance the resistance of cells to mechanical damage. Hyaluronic acid has been conjugated with antibodies to ensure that the active compound continues to exert its effects at the site of inflammation. Hyaluronic acid can be used in research in the fields of osteoarthritis, ophthalmology, cosmetic dermatology, oncology, and liver diseases .

HY-NP101

Highly purified Type I collagen, from bovine skin 1 Publications Verification Bovine Type I collagen, immunization grade	Biochemical Assay Reagents
Highly purified Type I collagen, from bovine skin (Bovine Type I collagen, immunization grade) plays an important role in the structure and function of skin, bone, tendons, and many others. Type I collagen potently stimulates angiogenesis in vitro and in vivo. Highly purified Type I collagen, from bovine skin is an immunization grade that can be used for immunization to generate antibodies .

Cat. No.	Product Name	Target	Research Area

HY-13718

Oglufanide H-Glu-Trp-OH; L-Glutamyl-L-tryptophan	VEGFR HCV Endogenous Metabolite	Infection Cardiovascular Disease Inflammation/Immunology Cancer
Oglufanide (H-Glu-Trp-OH) is a dipeptide immunomodulator isolated from calf thymus. Oglufanide inhibits vascular endothelial growth factor (VEGF). Oglufanide can stimulate the immune response to hepatitic C virus (HCV) and intracellular bacterial infections. Oglufanide shows antitumor and anti-angiogenesis activities .

HY-P2196A

ELA-32(human) TFA 1 Publications Verification	Apelin Receptor (APJ)	Cancer
ELA-32(human) TFA is a potent, high affinity apelin receptor agonist (IC₅₀=0.27 nM; K_d=0.51 nM). ELA-32(human) TFA exhibits no binding GPR15 and GPR25. ELA-32(human) TFA activates the PI3K/AKT pathway and promotes self-renewal of hESCs via cell-cycle progression and protein translation. ELA-32(human) TFA also potentiates the TGFβ pathway, priming hESCs toward the endoderm lineage. ELA-32(human) TFA stimulates angiogenesis in HUVEC cells.

HY-P1259A

PR-39 TFA	Proteasome Bacterial	Inflammation/Immunology
PR-39 TFA, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 TFAreversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 TFA stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice .

HY-P1259

PR-39	Proteasome Bacterial	Inflammation/Immunology
PR-39, a natural proline- and arginine-rich antibacterial peptide, is a noncompetitive, reversible and allosteric proteasome inhibitor. PR-39 reversibly binds to the α7 subunit of the proteasome and blocks degradation of NF-κB inhibitor IκBα by the ubiquitin-proteasome pathway. PR-39 stimulates angiogenesis, inhibits inflammatory responses and significant reduces myocardial infarct size in mice .

HY-P10335

SPARC (119-122) (mouse)	Biochemical Assay Reagents	Metabolic Disease
SPARC (119-122) (mouse) stimulates endothelial cell proliferation and angiogenesis. SPARC (119-122) (mouse) can be used to enhance neovascularization in modified polypropropylene biomaterials .

HY-P11775A

Peptide HRH acetate	VEGFR	Cardiovascular Disease
Peptide HRH acetate is a polypeptide that specifically binds to VEGF receptors. Peptide HRH acetate inhibits *VEGF*-stimulated endothelial cell proliferation. Peptide HRH acetate inhibits angiogenesis and suppresses corneal neovascularization. Peptide HRH acetate can be used in anti-angiogenesis related studies .

HY-P11775

Peptide HRH	VEGFR	Cardiovascular Disease
Peptide HRH is a polypeptide that specifically binds to VEGF receptors. Peptide HRH inhibits *VEGF*-stimulated endothelial cell proliferation. Peptide HRH inhibits angiogenesis and suppresses corneal neovascularization. Peptide HRH can be used in anti-angiogenesis related studies .

HY-P11777

AG73	MMP SDCBP	Cardiovascular Disease Neurological Disease Cancer
AG73 is a polypeptide. AG73 is derived from the G domain of the Laminin α1 chain. AG73 binds heparin, Syndecan-1 and Syndecan-4. AG73 promotes the adhesion of various cells, induces the differentiation of salivary gland acinar cells, stimulates neurite outgrowth, secretion of matrix metalloproteinases and angiogenesis. AG73 retains its angiogenic activity when conjugated to chitosan membranes. AG73 can be used in the research of melanoma and ischemic injury .

Cat. No.	Product Name	Target	Research Area	Image

HY-P991202

Anti-TSHR Antibody (M22)	TSH Receptor PKA	Metabolic Disease Inflammation/Immunology
Anti-TSHR Antibody (M22) is a selective agonist targeting TSHR (thyroid-stimulating hormone receptor), acting through competitive binding to the extracellular domain of TSHR. Anti-TSHR Antibody (M22) can mimic the biological effects of thyroid-stimulating hormone (TSH), activating downstream cAMP-PKA and other signaling pathways. Anti-TSHR Antibody (M22) can stimulate the proliferation of thyroid follicular epithelial cells and human umbilical vein endothelial cells (HUVECs), promote angiogenesis and tube formation, cell migration, and also upregulate the expression of angiogenesis-related proteins such as PROX1. Anti-TSHR Antibody (M22) can be used in research areas such as the mechanisms of goiter formation in Graves' disease (GD), angiogenesis regulation, and TSHR antagonist screening .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-B0633A

Hyaluronic acid 15+ Cited Publications Hyaluronan; Hyaluronate	Structural Classification Zea mays L. Classification of Application Fields Moisture Plants Endogenous metabolite Human Gut Microbiota Metabolites Polysaccharides Gramineae Cosmetic Research Disease Research Fields Saccharides Source Classification Cancer	Endogenous Metabolite Bacterial Akt PI3K
Hyaluronic acid is a biopolymer composed of repeating units of disaccharides with various applications. Hyaluronic acid is a major component of the extracellular matrix (ECM). Hyaluronic acid is synthesized at the plasma membrane. Increased hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion and angiogenesis in digestive cancers. Hyaluronic acid participates in tissue remodeling and rapid cell proliferation in some physiological processes including embryonic morphogenesis and wound-healing. Hyaluronic acid activates the PI3K-Akt signaling. Hyaluronic acid acts as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid also enhances cell invasion and angiogenesis by promoting proteolytic MMP-9 binding to cell surface or stimulating MMP-9 binding to cell surface. Hyaluronic acid can be used as drug delivery for sodium butyrate to improve the anti-proliferative activity on breast cancer cell line. Hyaluronic acid can be studied in joint diseases, wound healing and cancer .

HY-B0633

Hyaluronic acid sodium 15+ Cited Publications Sodium hyaluronate	Structural Classification Microorganisms Animals Classification of Application Fields Cosmetic Research Disease Research Fields Saccharides Source Classification Cancer	Endogenous Metabolite Bacterial PI3K Akt
Hyaluronic acid sodium (Sodium hyaluronate) is a biopolymer composed of repeating units of disaccharides with various applications. Hyaluronic acid sodium is a major component of the extracellular matrix (ECM). Hyaluronic acid sodium is synthesized at the plasma membrane. Increased hyaluronic acid sodium levels are associated with tumor cell growth, adhesion, migration, invasion and angiogenesis in digestive cancers. Hyaluronic acid sodium participates in tissue remodeling and rapid cell proliferation in some physiological processes including embryonic morphogenesis and wound-healing. Hyaluronic acid sodium activates the PI3K-Akt signaling. Hyaluronic acid sodium acts as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid sodium also enhances cell invasion and angiogenesis by promoting proteolytic MMP-9 binding to cell surface or stimulating MMP-9 binding to cell surface. Hyaluronic acid sodium can be used as drug delivery for sodium butyrate to improve the anti-proliferative activity on breast cancer cell line. Hyaluronic acid sodium can be studied in joint diseases, wound healing and cancer .

HY-13718

Oglufanide H-Glu-Trp-OH; L-Glutamyl-L-tryptophan	Cardiovascular Disease Classification of Application Fields Animals Ketones, Aldehydes, Acids Endogenous metabolite Inflammation/Immunology Disease Research Fields Source Classification	VEGFR HCV Endogenous Metabolite
Oglufanide (H-Glu-Trp-OH) is a dipeptide immunomodulator isolated from calf thymus. Oglufanide inhibits vascular endothelial growth factor (VEGF). Oglufanide can stimulate the immune response to hepatitic C virus (HCV) and intracellular bacterial infections. Oglufanide shows antitumor and anti-angiogenesis activities .

HY-142019

Tanshinol borneol ester	Labiatae Samanea saman (Jacq.) Merr. Phenols Polyphenols Plants Source Classification	Akt AMPK
Tanshinol borneol ester, an angiogenesis stimulator, promoted multiple key steps of angiogenesis through Akt and MAPK signalling pathways. Tanshinol borneol ester has anti-ischemic and anti-atherosclerosis activities .

Cat. No.	Product Name		Classification

HY-B0633A

Hyaluronic acid 15+ Cited Publications Hyaluronan; Hyaluronate		Polymers
Hyaluronic acid is a biopolymer composed of repeating units of disaccharides with various applications. Hyaluronic acid is a major component of the extracellular matrix (ECM). Hyaluronic acid is synthesized at the plasma membrane. Increased hyaluronic acid levels are associated with tumor cell growth, adhesion, migration, invasion and angiogenesis in digestive cancers. Hyaluronic acid participates in tissue remodeling and rapid cell proliferation in some physiological processes including embryonic morphogenesis and wound-healing. Hyaluronic acid activates the PI3K-Akt signaling. Hyaluronic acid acts as a regulator of cancer-associated lymphangiogenesis. Hyaluronic acid also enhances cell invasion and angiogenesis by promoting proteolytic MMP-9 binding to cell surface or stimulating MMP-9 binding to cell surface. Hyaluronic acid can be used as drug delivery for sodium butyrate to improve the anti-proliferative activity on breast cancer cell line. Hyaluronic acid can be studied in joint diseases, wound healing and cancer .

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