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Occludin

" in MedChemExpress (MCE) Product Catalog:

By Targets:	Amyloid-β (3) Bacterial (3) Beta-secretase (2) Biochemical Assay Reagents (1) Claudin (1) Drug Derivative (2) Glucocorticoid Receptor (3) Interleukin Related (2) Natriuretic Peptide Receptor (NPR) (1) NF-κB (4) NOD-like Receptor (NLR) (2) Reference Standards (1) Toll-like Receptor (TLR) (2) Transthyretin (TTR) (1) α-synuclein (1)
By Research Areas:	Cancer (4) Cardiovascular Disease (2) Infection (2) Inflammation/Immunology (7) Metabolic Disease (5) Neurological Disease (5)
Oligonucleotides:	Pegylated Lipids (1)

10

Inhibitors & Agonists

1

Biochemical Assay Reagents

2

Peptides

1

Natural
Products

4

Antibodies

1

Oligonucleotides

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

Methylprednisolone succinate sodium 2 Publications Verification Methylprednisolone hydrogen succinate sodium	Glucocorticoid Receptor	Infection Neurological Disease Inflammation/Immunology Cancer
Methylprednisolone succinate (Methylprednisolone hydrogen succinate) sodium is a prodrug of Methylprednisolone (HY-B0260) and glucocorticoid with immunosuppressant and anti-inflammatory activity. Methylprednisolone succinate sodium binds cytosolic glucocorticoid receptors, translocates to nuclei, and modulates target gene transcription. Methylprednisolone succinate sodium alters Bax, Bcl-2, occludin, and ZO-1 expression; attenuates TLR4/NF-κB signaling; suppresses proinflammatory cytokine production and immune cell activation. Methylprednisolone succinate sodium can be used for the research of intracranial haemorrhage, rheumatoid arthritis, multiple sclerosis, preterminal cancer, inflammatory conditions, shock, immediate-type hypersensitivity, acute myocardial ischemia, hypoxic heart muscle damage, and traumatic spinal cord injury .

Homogentisic acid	Amyloid-β Natriuretic Peptide Receptor (NPR) α-synuclein Transthyretin (TTR) Claudin	Neurological Disease Metabolic Disease Cancer
Homogentisic acid is an orally active, blood-brain barrier-permeable amyloidogenic compound that functions as both an amyloid component and a pigment precursor. Accumulation of homogentisic acid downregulates tight junction proteins (such as *claudin-5, occludin, ZO-1) and impairs blood-brain barrier integrity. Homogentisic acid and its oxidation product benzoquinone acetic acid not only induce the aggregation and fibrosis of multiple proteins (such as Aβ_1-42, α-synuclein, SAA, Transthyretin (TTR), atrial natriuretic peptide), but also trigger oxidative stress, damage to the Wnt/β-catenin* pathway, and neurotoxicity, leading to ochronosis pigment deposition and synaptic dysfunction. At specific concentrations, homogentisic acid exerts no cytotoxicity or genotoxicity on human peripheral blood lymphocytes, and even counteracts the genotoxicity induced by Irinotecan (HY-16562). Homogentisic acid serves as an important tool molecule for investigating the mechanisms of diseases including ochronosis, secondary amyloidosis, Alzheimer's disease, and colorectal cancer .

Methylprednisolone succinate 2 Publications Verification Methylprednisolone hydrogen succinate	Glucocorticoid Receptor Bacterial Toll-like Receptor (TLR) NF-κB	Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
Methylprednisolone succinate (Methylprednisolone hydrogen succinate) is a prodrug of Methylprednisolone (HY-B0260) and glucocorticoid with immunosuppressant and anti-inflammatory activity. Methylprednisolone succinate binds cytosolic glucocorticoid receptors, translocates to nuclei, and modulates target gene transcription. Methylprednisolone succinate alters Bax, Bcl-2, occludin, and ZO-1 expression; attenuates TLR4/NF-κB signaling; suppresses proinflammatory cytokine production and immune cell activation. Methylprednisolone succinate can be used for the research of intracranial haemorrhage, rheumatoid arthritis, multiple sclerosis, preterminal cancer, inflammatory conditions, shock, immediate-type hypersensitivity, acute myocardial ischemia, hypoxic heart muscle damage, and traumatic spinal cord injury .

TPT-260 Dihydrochloride 2 Publications Verification NSC55712; TPU-260 Dihydrochloride	Drug Derivative Amyloid-β Beta-secretase	Cardiovascular Disease Neurological Disease Inflammation/Immunology
TPT-260 Dihydrochloride (NSC55712), a thiophene thiourea derivative, is a retromer complex stabilizer against thermal denaturation (K_d = ~5 µM). TPT-260 Dihydrochloride increases the levels of retromer proteins, shifts amyloid-precursor protein (APP) away from the endosome, and decreases the pathogenic processing of APP. TPT-260 Dihydrochloride inhibits TLR4 upregulation, IKKβ phosphorylation, NF-κB p65 nuclear translocation, and NLRP3 inflammasome formation. TPT-260 Dihydrochloride improves retromer-mediated cargo trafficking, reduces brain infarct area, and decreases amyloid plaque deposition. TPT-260 Dihydrochloride exhibits minimal cytotoxicity to primary microglia at tested concentrations. TPT-260 Dihydrochloride can be used for the research of inflammatory bowel disease, ischemic stroke and Alzheimer's disease .

DSPE-PEG2000-OH 1 Publications Verification	Biochemical Assay Reagents	Inflammation/Immunology
DSPE-PEG2000-OH is an absorption enhancer. DSPE-PEG2000-OH reduces the expression levels of ZO-1 and *Occludin*. DSPE-PEG2000-OH enhances the pulmonary absorption of poorly absorbable macromolecules via the paracellular pathway without altering pulmonary membrane fluidity .

iE-DAP dihydrochloride	NOD-like Receptor (NLR) NF-κB Interleukin Related	Metabolic Disease
iE-DAP dihydrochloride is a Nod1 agonist. iE-DAP dihydrochloride activates NOD1, which in turn activates the NF-κB signaling pathway and MLCK signaling pathway, inducing cellular inflammatory responses and tight junction disruption. iE-DAP dihydrochloride downregulates the expression of ZO-1 and *Occludin* genes. iE-DAP dihydrochloride increases the secretion of IL-6, GRO-α, MCP-1, IL-8 and MIP-1β in term human trophoblast cell cultures. iE-DAP dihydrochloride triggers preterm birth in pregnant mice, reduces fetal body weight, and induces fetal inflammation. iE-DAP dihydrochloride can be used in studies related to mastitis and preterm birth .

Methylprednisolone succinate (Standard) 1 Publications Verification Methylprednisolone hydrogen succinate (Standard)	Reference Standards Glucocorticoid Receptor Bacterial Toll-like Receptor (TLR) NF-κB	Metabolic Disease Inflammation/Immunology Cancer
Methylprednisolone succinate (Standard) is the analytical standard of Methylprednisolone succinate (HY-B1900). This product is intended for research and analytical applications. Methylprednisolone succinate (Methylprednisolone hydrogen succinate) is a prodrug of Methylprednisolone (HY-B0260) and glucocorticoid with immunosuppressant and anti-inflammatory activity. Methylprednisolone succinate binds cytosolic glucocorticoid receptors, translocates to nuclei, and modulates target gene transcription. Methylprednisolone succinate alters Bax, Bcl-2, occludin, and ZO-1 expression; attenuates TLR4/NF-κB signaling; suppresses proinflammatory cytokine production and immune cell activation. Methylprednisolone succinate can be used for the research of intracranial haemorrhage, rheumatoid arthritis, multiple sclerosis, preterminal cancer, inflammatory conditions, shock, immediate-type hypersensitivity, acute myocardial ischemia, hypoxic heart muscle damage, and traumatic spinal cord injury .

Glucuronic acid sodium 1 Publications Verification	Bacterial	Inflammation/Immunology
Glucuronic acid sodium is a polysaccharide that exhibits anti-inflammatory activity, supporting the healing of ulcerative colitis. Glucuronic acid sodium also enhances the intestinal barrier by upregulating tight junction proteins like ZO-1 and Occludin. Furthermore, Glucuronic acid sodium plays a role in modulating gut microbiota by increasing beneficial bacterial populations while suppressing harmful ones.

iE-DAP	NOD-like Receptor (NLR) NF-κB Interleukin Related	Metabolic Disease
iE-DAP is a Nod1 agonist. iE-DAP activates NOD1, which in turn activates the NF-κB signaling pathway and MLCK signaling pathway, inducing cellular inflammatory responses and tight junction disruption. iE-DAP downregulates the expression of ZO-1 and *Occludin* genes. iE-DAP increases the secretion of IL-6, GRO-α, MCP-1, IL-8 and MIP-1β in term human trophoblast cell cultures. iE-DAP triggers preterm birth in pregnant mice, reduces fetal body weight, and induces fetal inflammation. iE-DAP is applicable to research related to mastitis and preterm birth .

TPT-260 TPU260	Drug Derivative Beta-secretase Amyloid-β	Cardiovascular Disease Neurological Disease Inflammation/Immunology
TPT-260 (TPU260), a thiophene thiourea derivative, is a retromer complex stabilizer against thermal denaturation (K_d = ~5 µM). TPT-260 increases the levels of retromer proteins, shifts amyloid-precursor protein (APP) away from the endosome, and decreases the pathogenic processing of APP. TPT-260 inhibits TLR4 upregulation, IKKβ phosphorylation, NF-κB p65 nuclear translocation, and NLRP3 inflammasome formation. TPT-260 improves retromer-mediated cargo trafficking, reduces brain infarct area, and decreases amyloid plaque deposition. TPT-260 exhibits minimal cytotoxicity to primary microglia at tested concentrations. TPT-260 can be used for the research of inflammatory bowel disease, ischemic stroke and Alzheimer's disease .

Cat. No.	Product Name	Type

DSPE-PEG2000-OH 1 Publications Verification	Biochemical Assay Reagents
DSPE-PEG2000-OH is an absorption enhancer. DSPE-PEG2000-OH reduces the expression levels of ZO-1 and *Occludin*. DSPE-PEG2000-OH enhances the pulmonary absorption of poorly absorbable macromolecules via the paracellular pathway without altering pulmonary membrane fluidity .

Cat. No.	Product Name	Target	Research Area

iE-DAP dihydrochloride	NOD-like Receptor (NLR) NF-κB Interleukin Related	Metabolic Disease
iE-DAP dihydrochloride is a Nod1 agonist. iE-DAP dihydrochloride activates NOD1, which in turn activates the NF-κB signaling pathway and MLCK signaling pathway, inducing cellular inflammatory responses and tight junction disruption. iE-DAP dihydrochloride downregulates the expression of ZO-1 and *Occludin* genes. iE-DAP dihydrochloride increases the secretion of IL-6, GRO-α, MCP-1, IL-8 and MIP-1β in term human trophoblast cell cultures. iE-DAP dihydrochloride triggers preterm birth in pregnant mice, reduces fetal body weight, and induces fetal inflammation. iE-DAP dihydrochloride can be used in studies related to mastitis and preterm birth .

iE-DAP	NOD-like Receptor (NLR) NF-κB Interleukin Related	Metabolic Disease
iE-DAP is a Nod1 agonist. iE-DAP activates NOD1, which in turn activates the NF-κB signaling pathway and MLCK signaling pathway, inducing cellular inflammatory responses and tight junction disruption. iE-DAP downregulates the expression of ZO-1 and *Occludin* genes. iE-DAP increases the secretion of IL-6, GRO-α, MCP-1, IL-8 and MIP-1β in term human trophoblast cell cultures. iE-DAP triggers preterm birth in pregnant mice, reduces fetal body weight, and induces fetal inflammation. iE-DAP is applicable to research related to mastitis and preterm birth .

Cat. No.	Product Name	Category	Target	Chemical Structure

Homogentisic acid	Structural Classification Other disease Classification of Application Fields Ketones, Aldehydes, Acids Disease markers Phenols Polyphenols Metabolic Disease Endogenous metabolite Disease Research Fields	Amyloid-β Natriuretic Peptide Receptor (NPR) α-synuclein Transthyretin (TTR) Claudin
Homogentisic acid is an orally active, blood-brain barrier-permeable amyloidogenic compound that functions as both an amyloid component and a pigment precursor. Accumulation of homogentisic acid downregulates tight junction proteins (such as *claudin-5, occludin, ZO-1) and impairs blood-brain barrier integrity. Homogentisic acid and its oxidation product benzoquinone acetic acid not only induce the aggregation and fibrosis of multiple proteins (such as Aβ_1-42, α-synuclein, SAA, Transthyretin (TTR), atrial natriuretic peptide), but also trigger oxidative stress, damage to the Wnt/β-catenin* pathway, and neurotoxicity, leading to ochronosis pigment deposition and synaptic dysfunction. At specific concentrations, homogentisic acid exerts no cytotoxicity or genotoxicity on human peripheral blood lymphocytes, and even counteracts the genotoxicity induced by Irinotecan (HY-16562). Homogentisic acid serves as an important tool molecule for investigating the mechanisms of diseases including ochronosis, secondary amyloidosis, Alzheimer's disease, and colorectal cancer .

Host:	Mouse (1) Rabbit (3)
Reactivity:	Human (4) Rat (4) Mouse (4)
Application:	IHC-P (3) ICC/IF (4) IP (1) WB (3) IHC-F (1) FC (1) ELISA (3)
Isotype:	IgG (2) IgG1 (1) IgG/Kappa (1)
Conjugation:	Non-conjugated (4)
Clonality:	Polyclonal (2) Monoclonal (2)
Modification:	Unmodified (4)

Cat. No.	Compare	Product Name	Application	Reactivity	Image

	Occludin Antibody 2 Publications Verification Occludin, Occludin-1; Occludin1; Occludin 1; FLJ08163; BLCPMG; FLJ18079; FLJ77961; FLJ94056; MGC34277; Occludin; OCLN; OCLN_HUMAN; Tight junction protein Occludin.	IHC-P, IHC-F, ICC/IF, FC, ELISA	Human, Mouse, Rat
	Occludin Antibody is a Rabbit-derived and non-conjugated IgG polyclonal antibody, targeting to Occludin.

	Occludin/OCLN Antibody OCLN_HUMAN; Occludin; Ocl; BLCPMG; PPP1R115; PTORCH1; Tight junction protein Occludin;	WB, IHC-P, ICC/IF	Human, Mouse, Rat
	Occludin/OCLN Antibody is a Rabbit-derived and non-conjugated IgG polyclonal antibody, targeting to Occludin/OCLN.

	Occludin Antibody (YA6112)	WB, IHC-P, ICC/IF, IP, ELISA	Human, Mouse, Rat
	Occludin Antibody (YA6112) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Occludin.

	Occludin Antibody (YA5499)	WB, ICC/IF, ELISA	Human, Mouse, Rat
	Occludin Antibody (YA5499) is a Mouse-derived and non-conjugated IgG1 monoclonal antibody, targeting to Occludin.

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DSPE-PEG2000-OH 1 Publications Verification		Pegylated Lipids
DSPE-PEG2000-OH is an absorption enhancer. DSPE-PEG2000-OH reduces the expression levels of ZO-1 and *Occludin*. DSPE-PEG2000-OH enhances the pulmonary absorption of poorly absorbable macromolecules via the paracellular pathway without altering pulmonary membrane fluidity .

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