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Results for "

neutrophil+migration

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Akt (1) Antibiotic (1) Bacterial (1) Bombesin Receptor (1) Complement System (1) COX (2) CRFR (2) CXCR (1) Endogenous Metabolite (3) ERK (1) Fungal (1) Integrin (1) Interleukin Related (3) Isotope-Labeled Compounds (1) JNK (1) L-Selectin (1) Leukotriene Receptor (1) Macrophage migration inhibitory factor (MIF) (1) NO Synthase (2) PKA (1) PKC (1) PPAR (1) Prostaglandin Receptor (1) ROCK (1) SGK (1) TNF Receptor (1)
By Research Areas:	Cancer (2) Infection (1) Inflammation/Immunology (16) Metabolic Disease (1) Neurological Disease (2)

By Targets:

Akt (1)

Antibiotic (1)

Bacterial (1)

Bombesin Receptor (1)

Complement System (1)

COX (2)

CRFR (2)

CXCR (1)

Endogenous Metabolite (3)

ERK (1)

Fungal (1)

Integrin (1)

Interleukin Related (3)

Isotope-Labeled Compounds (1)

JNK (1)

L-Selectin (1)

Leukotriene Receptor (1)

Macrophage migration inhibitory factor (MIF) (1)

NO Synthase (2)

PKA (1)

PKC (1)

PPAR (1)

Prostaglandin Receptor (1)

ROCK (1)

SGK (1)

TNF Receptor (1)

By Research Areas:

Cancer (2)

Infection (1)

Inflammation/Immunology (16)

Metabolic Disease (1)

Neurological Disease (2)

Inhibitors & Agonists

Biochemical Assay Reagents

Peptides

Inhibitory Antibodies

Natural
Products

Isotope-Labeled Compounds

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-125527

Resolvin D1 1 Publications Verification RvD1	Endogenous Metabolite	Inflammation/Immunology
Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α–mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages .

HY-NP004

Cobra Venom Factor CVF	Complement System	Inflammation/Immunology
Cobra Venom Factor (CVF) is a selective activator targeting complement components C3, C5, and factor B in the complement system. After binding to factor B, Cobra Venom Factor is cleaved by factor D, forming a stable C3/C5 convertase resistant to regulatory proteins H and I. This continuously hydrolyzes C3 and C5, depleting serum complement while inducing neutrophil migration, vascular leakage, and increased TNF-α levels. Cobra Venom Factor can be used to deplete complement and mimic complement activation-related pathological states, and is applied in animal models of complement-mediated diseases such as acute respiratory distress syndrome (ARDS), sepsis, and shock. Cobra Venom Factor can be isolated from the venom of cobras (e.g., Naja atra, Naja melanoleuca, Naja kaouthia, etc.) .

HY-P1108

Astressin 2B 1 Publications Verification	CRFR	Neurological Disease Inflammation/Immunology
Astressin 2B is a blood-brain barrier-impermeable, highly selective CRFR2 antagonist (rCRFR2, IC₅₀=0.57 nM). Astressin 2B blocks the protective effects mediated by CRFR2, thereby exacerbating indomethacin (HY-14397)-induced hemorrhagic intestinal injury in rats. Astressin 2B reverses the protective effects of Urocortin 1 against intestinal hypermotility, bacterial invasion and upregulation of inflammatory mediators. Astressin 2B also blocks the anxiogenic effect of Urocortin 2 and attenuates stress-induced anxiety-related behaviors. In the Clostridioides difficile toxin A (C. difficile toxin A)-mediated enteritis model, Astressin 2B mimics the phenotype of CRFR2-deficient mice, significantly exacerbating intestinal epithelial damage, edema, neutrophil migration and the expression of multiple proinflammatory cytokines. Astressin 2B is an important tool molecule for investigating the intestinal protective mechanisms of CRFR2 .

HY-P1108A

Astressin 2B TFA 1 Publications Verification	CRFR	Neurological Disease Inflammation/Immunology
Astressin 2B TFA is a blood-brain barrier-impermeable, highly selective CRFR2 antagonist (rCRFR2, IC₅₀=0.57 nM). Astressin 2B TFA blocks the protective effects mediated by CRFR2, thereby exacerbating indomethacin (HY-14397)-induced hemorrhagic intestinal injury in rats. Astressin 2B TFA reverses the protective effects of Urocortin 1 against intestinal hypermotility, bacterial invasion and upregulation of inflammatory mediators. Astressin 2B TFA also blocks the anxiogenic effect of Urocortin 2 and attenuates stress-induced anxiety-related behaviors. In the Clostridioides difficile toxin A (C. difficile toxin A)-mediated enteritis model, Astressin 2B TFA mimics the phenotype of CRFR2-deficient mice, significantly exacerbating intestinal epithelial damage, edema, neutrophil migration and the expression of multiple proinflammatory cytokines. Astressin 2B TFA is an important tool molecule for investigating the intestinal protective mechanisms of CRFR2 .

HY-P10934

LXY3 LXY2	Integrin	Cancer
LXY3 (LXY2) is a VLA-3-blocking peptide that inhibits the interaction between integrin α3β1 (VLA-3) on neutrophil surfaces and laminin in the basement membrane, thereby preventing neutrophil migration across the tumor vascular basement membrane barrier. LXY3 is used to block neutrophil-mediated nanoparticle release from perivascular pools into the tumor interstitium. LXY3 is commonly employed for targeted imaging of breast cancer .

HY-168376

9(10)-Nitrooleate 9(10)-Nitrated oleic acid	PPAR ERK Akt NO Synthase	Metabolic Disease Inflammation/Immunology
9 (10)-Nitrooleate (9(10)-Nitrated oleic acid) is an endogenous lipid signaling mediator with vasoprotective effects. 9 (10)-Nitrooleate enhances enzymatic activity and improves nitric oxide bioavailability by inducing phosphorylation of Akt and ERK1/2, regulating the multi-site phosphorylation status of eNOS and optimizing its interaction with Hsp90. 9 (10)-Nitrooleate also activates PPARα, PPARδ and PPARγ receptors, thereby regulating adipogenesis, glucose uptake and inflammation-related gene expression, and exhibits immunosuppressive effects by inhibiting neutrophil migration and cytokine secretion. 9 (10)-Nitrooleate is widely used in studies of sepsis and related inflammatory diseases .

HY-103544

[D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P	JNK Interleukin Related Bombesin Receptor	Inflammation/Immunology Cancer
[D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P, a Substance P derivative, is a biased agonist toward neuropeptide and chemokine receptors. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P activates G12. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P binds to IL-8 and GRP receptors. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P inhibits ERK-2 activation, activates JNK activity. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P stimulates an increase in neutrophil migration and Ca ²⁺ mobilization. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P is also a bombesin antagonist, and inhibits the growth of small cell lung cancer

HY-125527S

Resolvin D1-d5 RvD1-d₅	Isotope-Labeled Compounds Endogenous Metabolite	Inflammation/Immunology
Resolvin D1-d₅ is the deuterium labeled Resolvin D1. Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α-mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages .

HY-120333

Antibiotic PF 1052	Antibiotic Fungal Bacterial	Infection
Antibiotic PF 1052 is an antibiotic extracted from a natural product library. Antibiotic PF 1052 has an inhibitory effect on murine neutrophil migration .

HY-122011

PF-4950834	ROCK SGK PKA PKC	Inflammation/Immunology
PF-4950834 is a potent, selective, orally bioavailable, ATP-competitive rho kinase inhibitor with IC₅₀ values of 8.35 nM and 33.12 nM against ROCK2 and ROCK1, respectively. PF-4950834 inhibits neutrophil migration .

HY-W014049

N'-Nitro-D-arginine 1 Publications Verification	NO Synthase	Others
N'-Nitro-D-arginine, a nitric oxide synthesis inhibitor, also is a vasodilator that relaxes the smooth muscles and increases blood flow to the penis, improving erections. N'-Nitro-D-arginine also inhibits neutrophil migration by blocking receptors for tumour necrosis factor alpha (TNFα) and interleukin 8 (IL8) .

HY-113434A

5(R)-HETE	Endogenous Metabolite	Inflammation/Immunology
5(R)-HETE is a lipoxygenase product of arachidonic acid. 5(R)-HETE is an inducer of neutrophil migration through endothelial and epithelial barriers. 5(R)-HETE is important in mediating lung inflammatory processes .

HY-173624

TE-11	Macrophage migration inhibitory factor (MIF)	Inflammation/Immunology
TE-11 is a MIF tautomerase inhibitor with an IC₅₀ of 5.63 μM. TE-11 ameliorates CD-like colitis, reduces MIF-induced eosinophil and neutrophil migration, and prevents M1 polarization and associated metabolic reprogramming .

HY-139112

Leukotriene B4 dimethyl amide	Leukotriene Receptor	Inflammation/Immunology
Leukotriene B4 dimethyl amide, an immunomodulator, stimulates contraction of isolated guinea pig lung entities. Leukotriene B4 (LTB(4)) also stimulates human neutrophil migration, and LTB(4) antagonists may have anti-inflammatory activity in inflammatory pathophysiology .

HY-P10552

pCXCL8-1aa	CXCR	Inflammation/Immunology
pCXCL8-1aa is an anti-inflammatory peptide. pCXCL8-1aa competitively inhibits the binding of CXCL8 to glycosaminoglycans such as heparin sulfate (HS) by binding with high affinity. This reduces the presentation of CXCL8 on the surface of vascular endothelial cells, thereby inhibiting neutrophil migration and inflammatory responses. pCXCL8-1aa can be used to study inflammatory diseases such as rheumatoid arthritis .

HY-105424

Florifenine	COX	Inflammation/Immunology
Florifenine is a selective cyclooxygenase (COX) inhibitor with anti-inflammatory activity. Florifenine inhibits TXB₂ in human whole blood with an IC₅₀ of 32.5 nM. Florifenine exhibits anti-inflammatory effects in ear oedema. Florifenine inhibits neutrophil migration and reduces PGE₂ levles in the inflamed ears. Florifenine inhibits leukocyte migration and PGE₂ levels in the air pouch inflammation induced by Zymosan (HY-159069). Florifenine can be used for anti-inflammatory research .

HY-182610

ISP-VT Isopropyl vanillate	COX Interleukin Related	Inflammation/Immunology
ISP-VT (Isopropyl vanillate) is a COX-2 inhibitor. ISP-VT exhibits anti-inflammatory, antipyretic and immunomodulatory activities. ISP-VT reduces neutrophil migration and the release of inflammatory factors . ISP-VT can be used for the research of inflammatory and immune diseases and other conditions .

HY-160844

CT-133	Prostaglandin Receptor TNF Receptor Interleukin Related	Inflammation/Immunology
CT-133 is a selective and potent CRTH2 Receptor antagonist, with a K_i value of 2.2 nM. The K_i value for the DP1 receptor is greater than 3800 nM. CT-133 inhibits neutrophil migration induced by PGD2 (HY-101988). CT-133 significantly alleviates lung inflammation and improves lung function impairment in a mouse model of acute lung injury (ALI) induced by cigarette smoke. CT-133 effectively inhibits the excessive expression of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and chemokines (KC), and reverses the inhibition of the anti-inflammatory factor IL-10. CT-133 can be used for the study of ALI .

HY-P992212

Anti-CD62L Antibody (DREG-200)	L-Selectin	Inflammation/Immunology
Anti-CD62L Antibody (DREG-200) is a human monoclonal antibody targeting CD62L/L-selectin. Anti-CD62L Antibody (DREG-200) binds to residues 45, 46 and 47 of L-selectin, and blocks L-selectin-mediated interactions, neutrophil rolling, adhesion, aggregation, secondary anchoring, as well as leukocyte rolling on ligands. Anti-CD62L Antibody (DREG-200) reduces myocardial necrosis, coronary endothelial dysfunction, and neutrophil migration driven by neutrophil microparticles. Anti-CD62L Antibody (DREG-200) exerts cardioprotective effects in feline models. Anti-CD62L Antibody (DREG-200) can be used in studies related to myocardial ischemia-reperfusion injury. The recommended isotype control is Mouse IgG1 kappa (HY-P99977) .

Cat. No.	Product Name	Type

HY-NP004

Cobra Venom Factor CVF	Biochemical Assay Reagents
Cobra Venom Factor (CVF) is a selective activator targeting complement components C3, C5, and factor B in the complement system. After binding to factor B, Cobra Venom Factor is cleaved by factor D, forming a stable C3/C5 convertase resistant to regulatory proteins H and I. This continuously hydrolyzes C3 and C5, depleting serum complement while inducing neutrophil migration, vascular leakage, and increased TNF-α levels. Cobra Venom Factor can be used to deplete complement and mimic complement activation-related pathological states, and is applied in animal models of complement-mediated diseases such as acute respiratory distress syndrome (ARDS), sepsis, and shock. Cobra Venom Factor can be isolated from the venom of cobras (e.g., Naja atra, Naja melanoleuca, Naja kaouthia, etc.) .

Cobra Venom Factor

CVF

Biochemical Assay Reagents

Cobra Venom Factor (CVF) is a selective activator targeting complement components C3, C5, and factor B in the complement system. After binding to factor B, Cobra Venom Factor is cleaved by factor D, forming a stable C3/C5 convertase resistant to regulatory proteins H and I. This continuously hydrolyzes C3 and C5, depleting serum complement while inducing neutrophil migration, vascular leakage, and increased TNF-α levels. Cobra Venom Factor can be used to deplete complement and mimic complement activation-related pathological states, and is applied in animal models of complement-mediated diseases such as acute respiratory distress syndrome (ARDS), sepsis, and shock. Cobra Venom Factor can be isolated from the venom of cobras (e.g., Naja atra, Naja melanoleuca, Naja kaouthia, etc.) .

Cat. No.	Product Name	Target	Research Area

HY-P1108

Astressin 2B 1 Publications Verification	CRFR	Neurological Disease Inflammation/Immunology
Astressin 2B is a blood-brain barrier-impermeable, highly selective CRFR2 antagonist (rCRFR2, IC₅₀=0.57 nM). Astressin 2B blocks the protective effects mediated by CRFR2, thereby exacerbating indomethacin (HY-14397)-induced hemorrhagic intestinal injury in rats. Astressin 2B reverses the protective effects of Urocortin 1 against intestinal hypermotility, bacterial invasion and upregulation of inflammatory mediators. Astressin 2B also blocks the anxiogenic effect of Urocortin 2 and attenuates stress-induced anxiety-related behaviors. In the Clostridioides difficile toxin A (C. difficile toxin A)-mediated enteritis model, Astressin 2B mimics the phenotype of CRFR2-deficient mice, significantly exacerbating intestinal epithelial damage, edema, neutrophil migration and the expression of multiple proinflammatory cytokines. Astressin 2B is an important tool molecule for investigating the intestinal protective mechanisms of CRFR2 .

HY-P1108A

Astressin 2B TFA 1 Publications Verification	CRFR	Neurological Disease Inflammation/Immunology
Astressin 2B TFA is a blood-brain barrier-impermeable, highly selective CRFR2 antagonist (rCRFR2, IC₅₀=0.57 nM). Astressin 2B TFA blocks the protective effects mediated by CRFR2, thereby exacerbating indomethacin (HY-14397)-induced hemorrhagic intestinal injury in rats. Astressin 2B TFA reverses the protective effects of Urocortin 1 against intestinal hypermotility, bacterial invasion and upregulation of inflammatory mediators. Astressin 2B TFA also blocks the anxiogenic effect of Urocortin 2 and attenuates stress-induced anxiety-related behaviors. In the Clostridioides difficile toxin A (C. difficile toxin A)-mediated enteritis model, Astressin 2B TFA mimics the phenotype of CRFR2-deficient mice, significantly exacerbating intestinal epithelial damage, edema, neutrophil migration and the expression of multiple proinflammatory cytokines. Astressin 2B TFA is an important tool molecule for investigating the intestinal protective mechanisms of CRFR2 .

HY-P10934

LXY3 LXY2	Integrin	Cancer
LXY3 (LXY2) is a VLA-3-blocking peptide that inhibits the interaction between integrin α3β1 (VLA-3) on neutrophil surfaces and laminin in the basement membrane, thereby preventing neutrophil migration across the tumor vascular basement membrane barrier. LXY3 is used to block neutrophil-mediated nanoparticle release from perivascular pools into the tumor interstitium. LXY3 is commonly employed for targeted imaging of breast cancer .

HY-103544

[D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P	JNK Interleukin Related Bombesin Receptor	Inflammation/Immunology Cancer
[D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P, a Substance P derivative, is a biased agonist toward neuropeptide and chemokine receptors. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P activates G12. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P binds to IL-8 and GRP receptors. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P inhibits ERK-2 activation, activates JNK activity. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P stimulates an increase in neutrophil migration and Ca ²⁺ mobilization. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P is also a bombesin antagonist, and inhibits the growth of small cell lung cancer

HY-W014049

N'-Nitro-D-arginine 1 Publications Verification	NO Synthase	Others
N'-Nitro-D-arginine, a nitric oxide synthesis inhibitor, also is a vasodilator that relaxes the smooth muscles and increases blood flow to the penis, improving erections. N'-Nitro-D-arginine also inhibits neutrophil migration by blocking receptors for tumour necrosis factor alpha (TNFα) and interleukin 8 (IL8) .

HY-P10552

pCXCL8-1aa	CXCR	Inflammation/Immunology
pCXCL8-1aa is an anti-inflammatory peptide. pCXCL8-1aa competitively inhibits the binding of CXCL8 to glycosaminoglycans such as heparin sulfate (HS) by binding with high affinity. This reduces the presentation of CXCL8 on the surface of vascular endothelial cells, thereby inhibiting neutrophil migration and inflammatory responses. pCXCL8-1aa can be used to study inflammatory diseases such as rheumatoid arthritis .

Cat. No.	Product Name	Target	Research Area	Image

HY-P992212

Anti-CD62L Antibody (DREG-200)	L-Selectin	Inflammation/Immunology
Anti-CD62L Antibody (DREG-200) is a human monoclonal antibody targeting CD62L/L-selectin. Anti-CD62L Antibody (DREG-200) binds to residues 45, 46 and 47 of L-selectin, and blocks L-selectin-mediated interactions, neutrophil rolling, adhesion, aggregation, secondary anchoring, as well as leukocyte rolling on ligands. Anti-CD62L Antibody (DREG-200) reduces myocardial necrosis, coronary endothelial dysfunction, and neutrophil migration driven by neutrophil microparticles. Anti-CD62L Antibody (DREG-200) exerts cardioprotective effects in feline models. Anti-CD62L Antibody (DREG-200) can be used in studies related to myocardial ischemia-reperfusion injury. The recommended isotype control is Mouse IgG1 kappa (HY-P99977) .

Cat. No.	Product Name	Category	Target	Chemical Structure

HY-125527

Resolvin D1 1 Publications Verification RvD1	Classification of Application Fields Ketones, Aldehydes, Acids Endogenous metabolite Disease Research Fields Inflammation/Immunology Source Classification	Endogenous Metabolite
Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α–mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages .

HY-120333

Antibiotic PF 1052	Infection Microorganisms Anti-inflammation/Immunoregulatory Classification of Application Fields Antibiotics Disease Research Disease Research Fields Other Antibiotics Source Classification	Antibiotic Fungal Bacterial
Antibiotic PF 1052 is an antibiotic extracted from a natural product library. Antibiotic PF 1052 has an inhibitory effect on murine neutrophil migration .

Cat. No.	Product Name	Chemical Structure

HY-125527S

Resolvin D1-d5
Resolvin D1-d₅ is the deuterium labeled Resolvin D1. Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α-mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages .

Resolvin D1-d5

Resolvin D1-d₅ is the deuterium labeled Resolvin D1. Resolvin D1 (RvD1), an endogenous pro-resolving mediator of inflammation, is derived from omega-3 docosahexaenoic acid during the resolution phase of acute inflammation. Resolvin D1 blocks proinflammatory neutrophil migration by regulating actin polymerization, reduces TNF-α-mediated inflammation in macrophages, and enhances phagocytosis of apoptotic cells by macrophages .

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neutrophil+migration

Inhibitors & Agonists

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Peptides

Inhibitory Antibodies

NaturalProducts

Isotope-Labeled Compounds

Natural
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