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Results for "

M1+macrophage

" in MedChemExpress (MCE) Product Catalog:

33

Inhibitors & Agonists

2

Fluorescent Dyes

2

Peptides

5

Inhibitory Antibodies

8

Natural
Products

2

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-B1218
    Sulfaphenazole
    Maximum Cited Publications
    14 Publications Verification

    		 Cytochrome P450 Antibiotic Bacterial Necroptosis Apoptosis Infection Cardiovascular Disease
    Sulfaphenazole is a selective inhibitor of human cytochrome P450 (CYP) 2C9 enzyme. Sulfaphenazole is a cytoprotective agent against light-induced death of photoreceptors. Sulfaphenazole inhibits light-induced necrosis and mitochondrial stress-initiated apoptosis. Sulfaphenazole is an off patent sulfonamide antibiotic and demonstrates bactericidal activity through enhanced M1 macrophage activity. Sulfaphenazole can significantly reduce infarct size and restore post-ischemic coronary flow following ischemia and reperfusion [1] .
    Sulfaphenazole
  • HY-N6871
    Abietic acid
    3 Publications Verification

    		 Bacterial IKK Ferroptosis Infection Metabolic Disease Inflammation/Immunology Cancer
    Abietic acid, an orally active diterpene isolated from Colophony, displays significant anti-proliferative, anti-inflammatory, anti-obesity effect, bacteriostatic, cell cycle arresting and pro-apoptotic activities. Abietic acid inhibits lipoxygenase activity for allergy. Abietic acid enhances cell migration and tube formation in HUVECs. Abietic acid induces significant angiogenic potential, which is associated with upregulation of extracellular signal-regulated kinase (ERK) and p38 expression. Abietic acid attenuates sepsis-induced lung injury by inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway to inhibit M1 macrophage polarization. Abietic acid exhibits a positive effect against liver injury by attenuating inflammation and ferroptosis. Abietic acid shows accelerated wound closure in a mouse model of cutaneous wounds. Abietic acid significantly reduces the proliferation and growth of NSCLC cells by IKKβ inhibition.Additionally, Abietic acid ameliorates psoriasis-like inflammation and modulates gut microbiota in mice. Abietic acid is promising for research in non-small-cell lung cancer (NSCLC), liver injury-related deseases and psoriasis [1] .
    Abietic acid
  • HY-143712
    Allolithocholic acid
    1 Publications Verification

    		 Drug Metabolite G protein-coupled Bile Acid Receptor 1 ROR Metabolic Disease Inflammation/Immunology Cancer
    Allolithocholic acid is an orally active metabolite of Lithocholic acid (HY-B0172). Allolithocholic acid is a dual GPBAR1 agonist (EC50 = 2.7 μM) and RORγt inverse agonist (IC50 = 3.4 μM). Allolithocholic acid modulates immune and metabolic pathways, regulates immune cell polarization, prevents M1 macrophage and Th17 CD4 cell polarization. Allolithocholic acid improves insulin sensitivity, reduces liver lipid accumulation, reverses liver immunological, inflammatory and metabolic signaling dysregulation, restores bile acid homeostasis, adipose tissue histopathology/function, and intestinal microbiota composition, modulates intestinal immunity. Allolithocholic acid can be used for the researches of cancer, inflammayion, immunology and metabolic disease [1] .
    Allolithocholic acid
  • HY-152830
    Adrixetinib

    Q702

    		 c-Fms TAM Receptor MHC Cancer
    Adrixetinib (Q702) is an orally active triple inhibitor against CSF1R, Mer, and Axl, with Kd values of 8.7 nM, 0.8 nM, and 0.3 nM, respectively. Adrixetinib acts as a potent immune modulator that remodels the tumor microenvironment. Adrixetinib increases the abundance of M1 macrophages and CD8⁺ T cells, while decreasing the levels of M2 macrophages and myeloid-derived suppressor cells (MDSCs). Adrixetinib upregulates the expression of MHC class I and E-cadherin in tumor cells. Adrixetinib shows remarkable antitumor efficacy in syngeneic mouse tumor models. Adrixetinib is suitable for the research of breast cancer, renal adenocarcinoma, colon carcinoma, and melanoma [1] .
    Adrixetinib
  • HY-P99364
    Icrucumab
    1 Publications Verification

    Anti-VEGFR1/FLT1 Reference Antibody; IMC-18F1

    		 VEGFR Apoptosis p38 MAPK Akt Endocrinology Cancer
    Icrucumab (Anti-VEGFR1/FLT1 Reference Antibody; IMC-18F1) is an IgG1 antibody inhibitor targeting VEGFR-1/FLT1 with anti-tumor activity. By blocking ligand-dependent phosphorylation and downstream signal transduction, Icrucumab reduces the activities of MAPK and Akt in breast cancer xenograft models, inhibits the proliferation and invasion of VEGFR-1-positive tumor cells, and reverses the conversion of M1 macrophages to the pro-tumor M2-like phenotype. Icrucumab also inhibits tumor cell proliferation, promotes apoptosis, and effectively suppresses tumor growth through direct targeting of tumors and host support mechanisms. In addition, Icrucumab exhibits a synergistic effect when combined with chemotherapeutic agents, and it is used in research related to various cancers including advanced solid malignancies, thyroid cancer, melanoma, and lung cancer [1] .
    Icrucumab
  • HY-Y0586
    2,4,5-Trimethoxybenzoic acid

    Asaronic acid

    		 NF-κB STAT Metabolic Disease Inflammation/Immunology
    2,4,5-Trimethoxybenzoic acid (Asaronic acid) is a compound identified in purple perilla extracts. 2,4,5-Trimethoxybenzoic acid inhibits LPS (HY-D1056)-induced inflammatory responses, inhibits the activation of NF-κB and STAT signaling pathways. 2,4,5-Trimethoxybenzoic acid inhibits M1 macrophage phenotype-mediated inflammation in diabetes [1].
    2,4,5-Trimethoxybenzoic acid
  • HY-N7043
    Isosilybin A
    2 Publications Verification

    		 Apoptosis PPAR NF-κB p38 MAPK ERK Androgen Receptor Inflammation/Immunology Cancer
    Isosilybin A is a PPARγ agonist that can be isolated from silymarin. Isosilybin A activates extrinsic and intrinsic pathways of apoptosis through targeting of the Akt-NF-kB-AR axis. Isosilybin A can relieve the inflammatory response in the rosacea model via inhibiting Erk and p38 signaling pathways and M1 macrophage polarization, with its targets related to RELA and VEGFA. Isosilybin A has anti-prostate cancer (PCA) activity [1][2][3].
    Isosilybin A
  • HY-P990651
    PY314

    		TREM receptor Cancer
    PY314 is a humanized antibody targeting TREM2. PY314 binds TREM2 on tumor-associated macrophages, depletes TREM2-high tumor-associated macrophages, reduces pro-tumorigenic M2 macrophage infiltration, increases CD8 + T cell, NK cell, and M1 macrophage infiltration, creates a proinflammatory tumor microenvironment, and promotes antitumor immune responseS. PY314 can be used for the research of platinum-resistant ovarian cancer, advanced solid tumors, breast cancer, and advanced refractory solid tumors [1] .
    PY314
  • HY-128578
    KPLH1130
    2 Publications Verification

    		 PDHK NO Synthase Interleukin Related HIF/HIF Prolyl-Hydroxylase Metabolic Disease Inflammation/Immunology
    KPLH1130 is a pyruvate dehydrogenase kinase (PDK) inhibitor. KPLH1130 potently inhibits M1 macrophage polarization by reducing the expression of pro-inflammatory cytokines, decreasing the levels of M1 phenotype markers (HIF-1α, iNOS) and nitric oxide (NO) production. KPLH1130 prevents the reduction of mitochondrial oxygen consumption rate (OCR) induced by inflammatory stimuli (LPS ((HY-D1056) + IFN-γ) in various macrophage types. KPLH1130 improves glucose tolerance in HFD-fed mice. KPLH1130 can be used for the study of obesity-associated metabolic disorders and other inflammatory conditions [1].
    KPLH1130
  • HY-P11107
    RP-832c

    		Apoptosis TNF Receptor Inflammation/Immunology Cancer
    RP-832c is a synthetic analogue of host defense peptides (HDP), targeting the mannose receptor CD206 on the surface of M2 polarized macrophages (Kd = 3.5 μM). RP-832c binding to CD206 induces a significant conformational change in the receptor, activating signaling pathways that lead to rapid apoptosis and repolarization of CD206-positive M2 macrophages to an M1 phenotype. RP-832c treatment significantly reduces CD206 gene expression in M2 macrophages while transiently increasing expression of TNF-α, a marker for M1 macrophages. RP-832c is used for the studies of T-cell lymphoma (CTCL) and idiopathic pulmonary fibrosis (IPF) [1] .
    RP-832c
  • HY-145491
    Resolvin D5

    		ERK NF-κB CCR Inflammation/Immunology
    Resolvin D5 is an anti-inflammatory and analgesic agent produced in M2 macrophages. Resolvin D5 alleviates Paclitaxel (HY-B0015)-induced mechanical allodynia and inflammatory pain by activating the GPR32 receptor, with gender specificity (effective only in male mice) and independence from TRPV1 or TRPA1 channels. Resolvin D5 attenuates LPS-induced ERK phosphorylation and NF-κB nuclear translocation, downregulates proinflammatory mediators such as IL-6 and CCL5, inhibits Th17 cell differentiation and osteoclastogenesis, promotes regulatory T cell differentiation, and shows no cytotoxicity to human monocytes. The level of Resolvin D5 is elevated in arthritic SKG mice, but Resolvin D5 has no effect on dendritic cell differentiation or M1 macrophage polarization, nor does it prevent ZyA-induced arthritis progression. Resolvin D5 is suitable for research related to chemotherapy-induced peripheral neuropathy, inflammatory pain and rheumatoid arthritis [1] .
    Resolvin D5
  • HY-178794
    AGU661

    		PGE synthase Inflammation/Immunology
    AGU661 is a Microsomal prostaglandin E2 synthase 1 (mPGES-1) inhibitor with an IC50 of 0.22  nM. AGU661 lowers PGE2 formation in human pro-inflammatory M1 macrophages and activated monocytes without affecting other lipid mediator pathways. AGU661 has unfavorable physicochemical properties with poor metabolic stability and strong plasma protein binding tendencies. AGU661 into PLGA-based NPs significantly enhances its bioactivity. AGU661 can be used for inflammatory disorders research [1].
    AGU661
  • HY-B1218R
    Sulfaphenazole (Standard)

    		Reference Standards Cytochrome P450 Antibiotic Bacterial Necroptosis Apoptosis Infection Cardiovascular Disease
    Sulfaphenazole (Standard) is the analytical standard of Sulfaphenazole. This product is intended for research and analytical applications. Sulfaphenazole is a selective inhibitor of human cytochrome P450 (CYP) 2C9 enzyme. Sulfaphenazole is a cytoprotective agent against light-induced death of photoreceptors. Sulfaphenazole inhibits light-induced necrosis and mitochondrial stress-initiated apoptosis. Sulfaphenazole is an off patent sulfonamide antibiotic and demonstrates bactericidal activity through enhanced M1 macrophage activity. Sulfaphenazole can significantly reduce infarct size and restore post-ischemic coronary flow following ischemia and reperfusion [1] .
    Sulfaphenazole (Standard)
  • HY-P991217
    EU-103

    		Transmembrane Glycoprotein Cancer
    EU-103 is a humanized monoclonal antibody targeting V-Set And Immunoglobulin Domain Containing 4 (VSIG4) with a KD value ranging from 10 −7 and 10 −9. EU-103 blocks the interaction between VSIG4 and CD8+ T cells, promotes the conversion of M2 macrophages into M1 macrophages, induces the proliferation of CD8+ T cells and the secretion of pro-inflammatory cytokines, thereby inhibiting tumor growth. EU-103 is promising for research of cancers, such as bladder cancer, breast cancer, and colon cancer [1].
    EU-103
  • HY-152830A
    Adrixetinib TFA

    Q702 TFA

    		 c-Fms TAM Receptor MHC Cancer
    Adrixetinib (Q702) TFA is an orally active triple inhibitor against CSF1R, Mer, and Axl, with Kd values of 8.7 nM, 0.8 nM, and 0.3 nM, respectively. Adrixetinib TFA acts as a potent immune modulator that remodels the tumor microenvironment. Adrixetinib TFA increases the abundance of M1 macrophages and CD8⁺ T cells, while decreasing the levels of M2 macrophages and myeloid-derived suppressor cells (MDSCs). Adrixetinib TFA upregulates the expression of MHC class I and E-cadherin in tumor cells. Adrixetinib TFA shows remarkable antitumor efficacy in syngeneic mouse tumor models. Adrixetinib TFA is suitable for the research of breast cancer, renal adenocarcinoma, colon carcinoma, and melanoma [1] .
    Adrixetinib TFA
  • HY-172934
    FGT-4

    		Toll-like Receptor (TLR) NO Synthase PROTACs Inflammation/Immunology Cancer
    FGT-4 is a folate receptor β (FR-β) targeting chimeric molecule. FGT-4 is a TLR7 agonist. FGT-4 facilitates the secretion of iNOS and proinflammatory cytokine IL-6 associated with M1 macrophages and enhances the proliferation of cytotoxic CD8 + T cells. FGT-4 has anti-tumor activity in the 4T1 breast cancer mouse model. FGT-4 can be used for the study of cancer immunity. (Pink: target protein TLR7/8 agonist 1 ligand (HY-103698); black: linker (HY-172936); blue: FR-β ligand (HY-172935)) [1].
    FGT-4
  • HY-168954
    CSF1R-IN-26

    		c-Fms Apoptosis Akt ERK STAT Inflammation/Immunology Cancer
    CSF1R-IN-26 (Compound III-1) is the inhibitor for CSF-1R with an IC50 of 20.07 nM. CSF1R-IN-26 promotes the polarization of M2 macrophages to M1 macrophages, thereby inducing apoptosis in MC-38 cancer cell. CSF1R-IN-26 inhibits the activation of AKT/ERK/STAT3 signaling pathway. CSF1R-IN-26 reconstructs the tumor immune microenvironment and exhibits antitumor activity in mouse models. CSF1R-IN-26 exhibits pharmacokinetics characteristics in SD rats with a half-life 1.86 hours, and an oral bioavailability of 79.22% [1].
    CSF1R-IN-26
  • HY-178945
    KOR agonist 7

    		Opioid Receptor Interleukin Related TNF Receptor Sigma Receptor Neurological Disease Inflammation/Immunology
    KOR agonist 7 (Compound 29) is a highly selective κ-opioid receptor (KOR) agonist with a Ki of 138 nM. KOR agonist 7 shows no activity at μ- and δ-opioid receptors or σ1 receptor, and exhibits extremely low affinity for σ2 receptor (Ki = 2.8 μM). KOR agonist 7 significantly reduces the secretion of pro-inflammatory cytokines such as IL-6, TNF-α, and IFN-γ, while increasing the production of the anti-inflammatory cytokine IL-10. KOR agonist 7 downregulates the expression of the pro-inflammatory M1 macrophage marker CD80 and upregulates the anti-inflammatory M2 macrophage marker CD163. KOR agonist 7 holds potential for applications in analgesia and immune modulation [1].
    KOR agonist 7
  • HY-143712S1
    Allolithocholic Acid-d4

    3α-hydoxy-5α-Cholaoic Acid-d4, allo-LCA-d4

    		 Isotope-Labeled Compounds Drug Metabolite G protein-coupled Bile Acid Receptor 1 ROR Metabolic Disease Inflammation/Immunology Cancer
    Allolithocholic Acid-d4 (3α-hydoxy-5α-Cholaoic Acid-d4, allo-LCA-d4) is deuterium labeled Allolithocholic acid (HY-143712). Allolithocholic acid is an orally active metabolite of Lithocholic acid (HY-B0172). Allolithocholic acid is a dual GPBAR1 agonist (EC50 = 2.7 μM) and RORγt inverse agonist (IC50 = 3.4 μM). Allolithocholic acid modulates immune and metabolic pathways, regulates immune cell polarization, prevents M1 macrophage and Th17 CD4 cell polarization. Allolithocholic acid improves insulin sensitivity, reduces liver lipid accumulation, reverses liver immunological, inflammatory and metabolic signaling dysregulation, restores bile acid homeostasis, adipose tissue histopathology/function, and intestinal microbiota composition, modulates intestinal immunity. Allolithocholic acid can be used for the researches of cancer, inflammayion, immunology and metabolic disease [1] .
    Allolithocholic Acid-d4
  • HY-162494
    PAD4-IN-4

    		Protein Arginine Deiminase Cancer
    PAD4-IN-4 (compound 28) is a potent PAD4 inhibitor (IC50=0.79±0.09 μM). PAD4-IN-4 improves the tumor immune microenvironment by reshaping neutrophil phenotype, upregulating the proportions of dendritic cells and M1 macrophages, and reducing the amount of myeloid-derived suppressor cells. PAD4-IN-4 can be used for Triple-negative breast cancer research [1].
    PAD4-IN-4
  • HY-161954
    HDAC8-IN-12

    		HDAC Cancer
    HDAC8-IN-12 (compound 5k) is a non-hydroxamic acid, selective inhibitor of HDAC8 (IC50: 0.12 nM) and a potent inhibitor of breast cancer. HDAC8-IN-12 triggers anti-tumor immunity by activating T cells, increasing the proportion of M1 macrophages and decreasing the proportion of M2 macrophages. HDAC8-IN-12 (50 mg/kg) exerts tumor suppressive effects in an orthotopic mouse model of breast cancer [1].
    HDAC8-IN-12
  • HY-N7043R
    Isosilybin A (Standard)

    		Reference Standards Apoptosis PPAR NF-κB p38 MAPK ERK Androgen Receptor Inflammation/Immunology Cancer
    Isosilybin A (Standard) is the analytical standard of Isosilybin A (HY-N7043). Isosilybin A is a PPARγ agonist that can be isolated from silymarin. Isosilybin A activates extrinsic and intrinsic pathways of apoptosis through targeting of the Akt-NF-kB-AR axis. Isosilybin A can relieve the inflammatory response in the rosacea model via inhibiting Erk and p38 signaling pathways and M1 macrophage polarization, with its targets related to RELA and VEGFA. Isosilybin A has anti-prostate cancer (PCA) activity [1][2][3].
    Isosilybin A (Standard)
  • HY-143712R
    Allolithocholic acid (Standard)

    		Reference Standards Drug Metabolite G protein-coupled Bile Acid Receptor 1 ROR Metabolic Disease Inflammation/Immunology Cancer
    Allolithocholic acid (Standard) is the analytical standard of Allolithocholic acid (HY-143712). This product is intended for research and analytical applications. Allolithocholic acid is an orally active metabolite of Lithocholic acid (HY-B0172). Allolithocholic acid is a dual GPBAR1 agonist (EC50 = 2.7 μM) and RORγt inverse agonist (IC50 = 3.4 μM). Allolithocholic acid modulates immune and metabolic pathways, regulates immune cell polarization, prevents M1 macrophage and Th17 CD4 cell polarization. Allolithocholic acid improves insulin sensitivity, reduces liver lipid accumulation, reverses liver immunological, inflammatory and metabolic signaling dysregulation, restores bile acid homeostasis, adipose tissue histopathology/function, and intestinal microbiota composition, modulates intestinal immunity. Allolithocholic acid can be used for the researches of cancer, inflammayion, immunology and metabolic disease [1] .
    Allolithocholic acid (Standard)
  • HY-P11298
    d-T101 peptide

    		Caspase Apoptosis JNK p38 MAPK Interleukin Related IFNAR Inflammation/Immunology Cancer
    d-T101 peptide, a human hormone-peptide, is a T1/ST2 receptor ligand. d-T101 peptide binds to the T1/ST2 receptor and activates caspases 8, 9 and 3 mediated apoptosis, together with activation of JNKinase and p38 MAPKinase. d-T101 peptide also changes Golgi structural with function loss and downregulation of the endoplasmic reticulum (ER) stress repair mechanism. d-T101 peptide has immunostimulatory and anticancer activity, selectively induces apoptosis in proliferating cancer cells and increases IL-2 and IFN-γ expression as well as the recruitment of NK cells and M1 macrophages to the tumor site [1] .
    d-T101 peptide
  • HY-169262
    PLD-IN-1

    		Phospholipase Apoptosis Cancer
    PLD-IN-1 (Compound 3r) is an orally active inhibitor for phospholipase D with an IC50 of 1.97 μM. PLD-IN-1 reduces the expression of CD24, CD47 and PD-L1, enhances the calreticulin expression, and thus modulates the immune evasion mechanism in lung cancer cells by promoting the phagocytosis of cancer cells by macrophages. PLD-IN-1 inhibits the cell viability of lung cancer cell A549, HCC44, H460 and HCC15 with IC50 of 18.44, 22.31, 24.85 and 21.45 μM, respectively. PLD-IN-1 can induce apoptosis and inhibits migration in cell A549. PLD-IN-1 enhances the level of pro-inflammatory M1 macrophages and decreases the level of anti-inflammatory M2 macrophages, exhibits antitumor efficacy in mouse model [1].
    PLD-IN-1
  • HY-173518
    SIN 14

    		Heme Oxygenase (HO) Reactive Oxygen Species (ROS) NO Synthase COX Interleukin Related Inflammation/Immunology
    SIN 14, a derivative of Sinomenine (HY-15122), is an orally active HO-1 activator (KD = 17.2 μM). SIN 14 binds to the catalytic core domain of HO-1 and induces HO-1 activation in catalysis. SIN 14 significantly increases HO-1 stability. SIN 14 has anti-inflammatory effects and inhibits M1 macrophage polarization while promoting M2 polarization in LPS (Lipopolysaccharides)(HY-D1056)-induced RAW264.7 cells. SIN 14 inhibits inflammatory mediator production (eg: NO, IL-6, IL-1β and CCL2, inhibits production of ROS and down-regulates the expression of COX-2 and iNOS. SIN 14 can inhibit RA-related inflammatory edema in collagen-induced arthritis (ClA) mice [1].
    SIN 14
  • HY-D3190
    BODIPY−DOX

    		Fluorescent Dye Apoptosis Inflammation/Immunology
    BODIPY-DOX is a conjugate composed of BODIPY and Doxorubicin (HY-15142A), as well as a pH-activated fluorescent probe for M1 macrophages and an apoptosis inducer. BODIPY-DOX undergoes pH-induced hydrazone bond cleavage in acidic M1 macrophage phagosomes, thereby releasing cytotoxic Doxorubicin (Dox) and inhibiting the function of pro-inflammatory M1 macrophages. BODIPY-DOX highly selectively inhibits the production of relevant pro-inflammatory cytokines by mouse and human monocyte-derived M1 macrophages, while exerting minimal effects on M2 or unactivated macrophages. Therefore, BODIPY-DOX enables simultaneous fluorescent tracing, differentiation and elimination of specific macrophage subsets, and exhibits the potential to regulate tissue regeneration in zebrafish models [1].
    BODIPY−DOX
  • HY-D3410
    CDr17

    		Fluorescent Dye GLUT Others
    CDr17 is a GLUT1 substrate and selective fluorescent dye staining M1 microphages. CDr17 utilizes the Gating-Oriented Live-cell Distinction (GOLD) mechanism to enter M1 macrophages (Ex/Em = 646/662 nm) [1].
    CDr17
  • HY-B1218S
    Sulfaphenazole-d4

    		Isotope-Labeled Compounds Cytochrome P450 Antibiotic Bacterial Necroptosis Apoptosis Infection
    Sulfaphenazole-d4 is the deuterium labeled Sulfaphenazole (HY-B1218). Sulfaphenazole is a selective inhibitor of human cytochrome P450 (CYP) 2C9 enzyme. Sulfaphenazole is a cytoprotective agent against light-induced death of photoreceptors. Sulfaphenazole inhibits light-induced necrosis and mitochondrial stress-initiated apoptosis. Sulfaphenazole is an off patent sulfonamide antibiotic and demonstrates bactericidal activity through enhanced M1 macrophage activity. Sulfaphenazole can significantly reduce infarct size and restore post-ischemic coronary flow following ischemia and reperfusion [1] .
    Sulfaphenazole-d4
  • HY-Y0586R
    2,4,5-Trimethoxybenzoic acid (Standard)

    		NF-κB Reference Standards STAT Metabolic Disease Inflammation/Immunology
    2,4,5-Trimethoxybenzoic acid (Standard) is the analytical standard of 2,4,5-Trimethoxybenzoic acid (HY-Y0586). This product is intended for research and analytical applications. 2,4,5-Trimethoxybenzoic acid (Asaronic acid) is a compound identified in purple perilla extracts. 2,4,5-Trimethoxybenzoic acid inhibits LPS (HY-D1056)-induced inflammatory responses, inhibits the activation of NF-κB and STAT signaling pathways. 2,4,5-Trimethoxybenzoic acid inhibits M1 macrophage phenotype-mediated inflammation in diabetes [1].
    2,4,5-Trimethoxybenzoic acid (Standard)
  • HY-P992338
    CT-1119

    		Mesothelin Constitutive Androstane Receptor Inflammation/Immunology Cancer
    CT-1119 is an autologous human anti-Mesothelin chimeric antigen receptor macrophage (CAR-M). CT-1119 mediates CAR-dependent, antigen-dependent functional activities. CT-1119 acts as a phagocytosis inducer, tumor cell killer, pro-inflammatory cytokine inducer, and M1 macrophage polarizer. CT-1119 exhibits stronger resistance to M2 repolarization and reduces tumor burden in a mouse lung cancer xenograft model. CT-1119 can be used for the research of mesothelin-expressing solid tumors [1].
    CT-1119
  • HY-183554
    Fa-Au

    		TrxR Glutathione Peroxidase Ferroptosis Reactive Oxygen Species (ROS) IFNAR STAT Cancer
    Fa-Au is a TrxR inhibitor. Fa-Au downregulates GPX4, induces oxidative stress, mitochondria-associated ferroptosis (ferroptosis) and immunogenic cell death. Fa-Au induces ROS production in hepatoma cells. Fa-Au remodels the tumor immune microenvironment via M1 macrophage polarization, dendritic cell maturation, CD8+ T cell activation and reduction of regulatory T cells. Fa-Au induces an anti-tumor immune feedback loop through the IFNγ/STAT1/SLC7A11 axis. Fa-Au inhibits tumor growth. Fa-Au is applicable to hepatocellular carcinoma-related research [1].
    Fa-Au
  • HY-P991927
    ZL-1201

    		CD47 Cancer
    ZL-1201 is a recombinant humanized monoclonal anti-CD47 IgG4 antibody. ZL-1201 disrupt the CD47-SIRPα interaction. ZL-1201 modulates the tumor microenvironment. ZL-1201 promotes tumor-associated macrophage phagocytic activity. ZL-1201 substantially enhances phagocytosis by M2 macrophages, but not by M1 macrophages. ZL-1201 in combination with both mAb and chemotherapy achieves the maximal antitumor effects in a variety of solid tumor models. ZL-1201 can be used in the study of lymphoma, breast cancer, ovarian cancer, head and neck squamous cell carcinoma, and gastric cancer [1].
    ZL-1201

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