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Results for "

M1 macrophage

" in MedChemExpress (MCE) Product Catalog:

65

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1

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3

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1

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9

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6

Inhibitory Antibodies

11

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2

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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 .
    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 .
    Abietic acid
  • HY-125783
    1-Palmitoyl-sn-glycero-3-phosphocholine
    2 Publications Verification

    16:0 Lyso PC

    		 Endogenous Metabolite Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    1-Palmitoyl-sn-glycero-3-phosphocholine (16:0 Lyso PC) is an abundant lysophosphatidylcholine. 1-Palmitoyl-sn-glycero-3-phosphocholine exhibits proinflammatory activity. 1-Palmitoyl-sn-glycero-3-phosphocholine can be used in the study of atherosclerosis .
    1-Palmitoyl-sn-glycero-3-phosphocholine
  • HY-B1077
    Penfluridol
    5+ Cited Publications

    R-16341

    		 Calcium Channel Dopamine Receptor Autophagy Apoptosis Neurological Disease Inflammation/Immunology Cancer
    Penfluridol (R-16341) is a potent, long-acting, first-generation, oral diphenylbutylpiperidine antipsychotic agent by targeting D2-like dopamine receptor. Penfluridol effectively inhibits TNFα-induced NF-κB activation and alleviates the severity of arthritis and colitis in vivo. Penfluridol is a Ca2+-calmodulin inhibitor. Penfluridol induces apoptosis and autophagy. Penfluridol is used for chronic schizophrenia, acute psychosis, Tourette syndrome and autoimmune diseases. Penfluridol inhibites the growth of E. faecalis planktonic cells with the MIC of 7.81 μg/ml .
    Penfluridol
  • HY-P6292A
    KS-133 TFA

    		PACAP Receptor Neurological Disease Inflammation/Immunology Cancer
    KS-133 TFA is a highly selective and potent antagonist of the vascular active enteropeptide receptor 2 (VIPR2) with IC50 values for Ca influx measurement and cAMP measurement of 24.8 nM and 500 nM, respectively. KS-133 TFA reverses the tumor-promoting M2 phenotype of tumor-associated macrophages to the anti-tumor M1 phenotype, alters the tumor immune microenvironment, and inhibits tumor growth. KS-133 TFA can be used for research on schizophrenia and cancer immune regulation .
    KS-133 TFA
  • 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 .
    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 .
    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 .
    Icrucumab
  • HY-106373
    Adrenocorticotropic hormone
    1 Publications Verification

    ACTH; Adrenocorticotrophic hormone

    		 Androgen Receptor Reactive Oxygen Species (ROS) Mitochondrial Metabolism Interleukin Related TNF Receptor Metabolic Disease Inflammation/Immunology
    Adrenocorticotropic hormone (ACTH; Adrenocorticotrophic hormone) is a polypeptide tropic hormone produced by the anterior pituitary gland. Adrenocorticotropic hormone stimulates cortisol secretion from the adrenal cortex via the hypothalamic-pituitary-adrenal (HPA) axis. Adrenocorticotropic hormone regulates cortisol and androgen production. Adrenocorticotropic hormone can promote the development of spermatogenesis. Adrenocorticotropic hormone can relieve acute inflammation in gout models by inhibiting the polarization of macrophages to M1 type, inhibiting ROS and proinflammatory factor production and protecting mitochondrial function. Adrenocorticotropic hormone can be used for the researches of inflammation, endocrinology, metabolic disease, such as gout and nephrotic syndrome .
    Adrenocorticotropic hormone
  • 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 .
    2,4,5-Trimethoxybenzoic acid
  • HY-P99236
    Bexmarilimab
    1 Publications Verification

    FP-1305

    		 Transmembrane Glycoprotein Inflammation/Immunology Cancer
    Bexmarilimab (FP-1305) is a potent humanized anti-CLEVER-1 IgG4 antibody with an IC50 value of 4.51 nM. Bexmarilimab is capable of inducing a phenotypic M2 to M1 immune switch of tumor-associated macrophages. Bexmarilimab can promote antigen presentation and pro-inflammatory cytokine secretion. Bexmarilimab can induce B-cell and T-cell activation. Bexmarilimab can be used in researches of immunology and cancer, such as colorectal carcinoma .
    Bexmarilimab
  • 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 .
    KPLH1130
  • 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-P6292
    KS-133

    		PACAP Receptor PKA ERK PI3K Akt GSK-3 Neurological Disease Cancer
    KS-133 is a bicyclic peptide with VIPR2 antagonistic activity that can cross the blood-brain barrier. KS-133 selectively blocks VIPR2-mediated Gq/Ca, Gs/cAMP, cAMP/PKA/ERK and PI3K/AKT/GSK3β signaling pathways. KS-133 inhibits VIPR2 agonist-induced CREB phosphorylation in the prefrontal cortex of mice. KS-133 shifts the polarization direction of macrophages toward M1. KS-133 attenuates cancer cell proliferation and reduces the cell cycle distribution level at the S-M phase. KS-133 exerts antitumor effects in a mouse model of colorectal cancer. KS-133 reverses cognitive decline in mouse models of psychiatric disorders. KS-133 can be used for research related to schizophrenia, colorectal cancer and breast cancer .
    KS-133
  • HY-D1056F
    Biotin-Lipopolysaccharide, from E.coli O111:B4

    Biotin-LPS, from Escherichia coli (O111:B4)

    		 Biochemical Assay Reagents Inflammation/Immunology
    Biotin-Lipopolysaccharide, from E.coli O111:B4 (Biotin-LPS, from Escherichia coli (O111:B4)) is a biotin-conjugated Lipopolysaccharide (LPS) (HY-D1056A1) that can be coupled with streptavidin protein. Biotin-Lipopolysaccharide, from E.coli O111:B4 can be used to identify Lipopolysaccharide ligands. Lipopolysaccharides, from E. coli O111:B4 (LPS, from Escherichia coli (O111:B4)) are endotoxins and TLR4 activators extracted from Escherichia coli (E. coli O111:B4) and are classified as S (smooth) type LPS. Lipopolysaccharides, from E. coli O111:B4 possess the typical three-part structure: O-antigen, R3-type core oligosaccharide, and lipid A. Lipopolysaccharides, from E. coli O111:B4 activate TLR-4 in immune cells and can cause significant gastric diseases. Lipopolysaccharides, from E. coli O111:B4 can also induce M1-type polarization in mouse macrophages .
    It is recommended to prepare a solution with concentration ≥2 mg/mL. Vortex thoroughly for more than 10 minutes. Due to the adsorption characteristics of LPS, silanized container or low adsorption centrifuge tubes should be used for aliquoting and storage, and mix thoroughly before use.
    Biotin-Lipopolysaccharide, from E.coli O111:B4
  • HY-113481
    Prostaglandin E3

    		Transmembrane Glycoprotein COX PKA Prostaglandin Receptor Inflammation/Immunology Cancer
    Prostaglandin E3 is an eicosanoid derived from eicosapentaenoic acid. Prostaglandin E3 inhibits polarization towards M1 but promotes polarization of M2a macrophages. Prostaglandin E3 shows anti-inflammatory and anti-tumor activity .
    Prostaglandin E3
  • HY-105005
    Crisdesalazine

    AAD-2004

    		 Prostaglandin Receptor PGE synthase Reactive Oxygen Species (ROS) Apoptosis Neurological Disease Inflammation/Immunology
    Crisdesalazine (AAD-2004) is a microsomal prostaglandin E2 synthase-1 (mPGES-1) inhibitor. Crisdesalazine acts as a potent free radical scavenger that directly neutralizes reactive oxygen species (ROS) including hydrogen peroxide, exerting neuroprotective effects against apoptosis and axonal damage. Crisdesalazine inhibits PGE2 production, mediates inflammatory responses, and promotes the conversion of macrophages from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype. Crisdesalazine is applicable to neuroprotection research in multiple sclerosis and spinal cord injury .
    Crisdesalazine
  • 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) .
    RP-832c
  • HY-P4111
    Peptide R

    		CXCR Inflammation/Immunology Cancer
    Peptide R is a cyclic peptide and a specific CXCR4 antagonist. Peptide R exhibits excellent ability to effectively remodel tumor stroma. Peptide R has potential for use in tumor research .
    Peptide R
  • HY-177106
    ADT-1004

    		Drug Intermediate Ras Cancer
    ADT-1004 is an orally active prodrug of ADT-007 (HY-157887). ADT-007 is a reversible, highly potent and selective pan-RAS inhibitor that binds to the nucleotide-free conformation of RAS proteins and blocks their GTP activation, thereby inhibiting the downstream MAPK and AKT signaling pathways. ADT-1004 can be used for the research of pancreatic ductal adenocarcinoma .
    ADT-1004
  • HY-106373A
    Adrenocorticotropic hormone TFA
    1 Publications Verification

    ACTH TFA; Adrenocorticotrophic hormone TFA

    		 Androgen Receptor Reactive Oxygen Species (ROS) Mitochondrial Metabolism Interleukin Related TNF Receptor Metabolic Disease Inflammation/Immunology
    Adrenocorticotropic hormone (ACTH; Adrenocorticotrophic hormone) TFA is a polypeptide tropic hormone produced by the anterior pituitary gland. Adrenocorticotropic hormone TFA stimulates cortisol secretion from the adrenal cortex via the hypothalamic-pituitary-adrenal (HPA) axis. Adrenocorticotropic hormone TFA regulates cortisol and androgen production. Adrenocorticotropic hormone TFA can promote the development of spermatogenesis. Adrenocorticotropic hormone TFA can relieve acute inflammation in gout models by inhibiting the polarization of macrophages to M1 type, inhibiting ROS and proinflammatory factor production and protecting mitochondrial function. Adrenocorticotropic hormone TFA can be used for the researches of inflammation, endocrinology, metabolic disease, such as gout and nephrotic syndrome .
    Adrenocorticotropic hormone TFA
  • 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 .
    Resolvin D5
  • HY-139990
    CSF1R-IN-3
    1 Publications Verification

    		 c-Fms Cancer
    CSF1R-IN-3 (compound 21) is a potent and orally active CSF-1R inhibitor (IC50=2.1 nM). CSF1R-IN-3 is a potent antiproliferative activity against colorectal cancer cells. CSF1R-IN-3 inhibits the progression of colorectal cancer by suppressing the migration of macrophages, reprograming M2-like macrophages to the M1 phenotype, and enhancing the antitumor immunity .
    CSF1R-IN-3
  • 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 .
    AGU661
  • HY-163642
    TNF-α agonistic 1

    		Others Cancer
    TNF-α agonistic 1 (compound 22a) can repolarize tumor-associated macrophages (TAMs) in the tumor microenvironment (TME) from the M2 phenotype to the M1 anti-tumor phenotype .
    TNF-α agonistic 1
  • HY-149365
    SIKs-IN-1

    		Salt-inducible Kinase (SIK) Inflammation/Immunology
    SIKs-IN-1 (compound 8h), a pyrimidine-5-carboxamide derivative, is a Salt-inducible kinases (SIKs) inhibitor. SIKs regulates the transformation of M1/M2 macrophages, involving in inflammation process. SIKs-IN-1 inhibits SIK activity, up-regulates anti-inflammatory cytokine IL-10, but down-regulates pro-inflammatory cytokine IL-12. SIKs-IN-1 shows excellent anti-inflammatory effects in a DSS-induced colitis model .
    SIKs-IN-1
  • HY-179047
    SMU-L11-R

    		Toll-like Receptor (TLR) MyD88 IKK p38 MAPK ERK TNF Receptor Interleukin Related Inflammation/Immunology Cancer
    SMU-L11-R is a selective TLR7 agonist with an EC50 of 0.012 μM for human TLR7. SMU-L11-R specifically activates TLR7, recruits  MyD88, and triggers MAPK/NF-κB pathways, leading to TNF-α/IL-1β/IL-6 secretion in both mouse and human peripheral blood mononuclear cells. SMU-L11-R promotes M1-like macrophage polarization. SMU-L11-R exhibits excellent synergistic anti-tumor effects with PD-L1 inhibitors by upregulating CD8 +T cells. SMU-L11-R shows potential in colorectal cancer studies .
    SMU-L11-R
  • 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 .
    Sulfaphenazole (Standard)
  • 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)) .
    FGT-4
  • HY-N3248
    Momordicoside G

    Momordicacoside G

    		 Endogenous Metabolite Reactive Oxygen Species (ROS) Apoptosis Inflammation/Immunology Cancer
    Momordicoside G (Momordicacoside G) is an orally active cucurbitane-type triterpene glycoside. Momordicoside G selectively induces apoptosis of M1-like macrophages, without affecting M2-like macrophages. Momordicoside G reduces intracellular ROS levels and promotes autophagy. Momordicoside G also has anticancer activity, inhibiting the growth of cancer cell lines. Momordicoside G stimulates M2-associated lung injury repair and prevents inflammatory lung cancer injury .
    Momordicoside G
  • 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 .
    EU-103
  • HY-178983
    SHP2-IN-45

    		SHP2 Interleukin Related NO Synthase NF-κB TNF Receptor Inflammation/Immunology
    SHP2-IN-45 (Compound 6) is a potent, highly selective, and orally active SHP2 allosteric inhibitor. SHP2-IN-45 significantly reduces the expressions of IL-6, TNF-α, IL-1β, and iNOS. SHP2-IN-45 inhibits the polarization of M1-type macrophages. SHP2-IN-45 can inhibit the NF-κB pathway. SHP2-IN-45 can be used in the research of sepsis and acute lung injury .
    SHP2-IN-45
  • 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 .
    Adrixetinib TFA
  • 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% .
    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 .
    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 .
    Allolithocholic Acid-d4
  • HY-125783R
    1-Palmitoyl-sn-glycero-3-phosphocholine (Standard)

    16:0 Lyso PC (Standard)

    		 Endogenous Metabolite Reference Standards Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    1-Palmitoyl-sn-glycero-3-phosphocholine (Standard) (16:0 Lyso PC (Standard)) is the analytical standard of 1-Palmitoyl-sn-glycero-3-phosphocholine (HY-125783). This product is intended for research and analytical applications. 1-Palmitoyl-sn-glycero-3-phosphocholine is an abundant lysophosphatidylcholine. 1-Palmitoyl-sn-glycero-3-phosphocholine exhibits proinflammatory activity. 1-Palmitoyl-sn-glycero-3-phosphocholine can be used in the study of atherosclerosis .
    1-Palmitoyl-sn-glycero-3-phosphocholine (Standard)
  • HY-151188
    DHU-Se1

    		NO Synthase TNF Receptor Inflammation/Immunology
    DHU-Se1 is a potent anti-inflammatory agent. DHU-Se1 can stimulate macrophages to release the reactive selenium compound and reduce the expression of cellular inflammatory factors (eg: iNOS and TNF-α). DHU-Se1 alleviate the process of inflammation by blocking the polarization of macrophages from M0 to M1 .
    DHU-Se1
  • 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 .
    BODIPY−DOX
  • 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 .
    d-T101 peptide
  • 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 .
    HDAC8-IN-12
  • HY-155408
    ALR-27

    		FLAP Inflammation/Immunology
    ALR-27 is an antagonist of the 5-lipoxygenase (5-LOX) activating protein FLAP and has anti-inflammatory activity. ALR-27 potently inhibits 5-LOX product formation (>80%) in pro-inflammatory M1-MDM, with no significant direct inhibition of 5-LOX. ALR-27 not only reduces prostaglandin and leukotriene (LT) production in neutrophils but also increases the production of specialized prolytic mediators in specific human macrophage phenotypes .
    ALR-27
  • HY-E70390
    C1s Enzyme

    masp-2, c1 esterase, c1-esterase

    		 Wnt Cardiovascular Disease Inflammation/Immunology
    C1s Enzyme is a subunit of the complement C1 complex, which activates the complement as a serine protease. C1s Enzyme cleaves LRP5 and LRP6, and thus activates the Wnt/β-Catenin signaling pathway. C1s Enzyme promotes the macrophage M2 polarization and inhibits M1 polarization. C1s Enzyme enhances efferocytosis, exhibits anti-inflammatory activity .
    C1s Enzyme
  • 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 .
    PAD4-IN-4
  • 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-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) .
    CDr17
  • 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 .
    PLD-IN-1
  • HY-162415
    CSF1R-IN-22

    		c-Fms Apoptosis Cancer
    CSF1R-IN-22 (Compound C19) is an orally effective CSF-1R selective inhibitor (IC50<6 nM). CSF1R-IN-22 enhances the secretion of CXCL9 from M2 macrophages, increases CD8 + T cell infiltration. CSF1R-IN-22 boosts anti-tumor immune responses of anti-PD-1, and induces apoptosis in tumor cells. CSF1R-IN-22 can effectively reprogram M2-like TAMs (tumor-associated macrophages) to the M1 phenotype and reshape the TME by inducing the recruitment of CD8 + T cells into tumors and reducing the infiltration of immunosuppressive Tregs and MDSCs .
    CSF1R-IN-22
  • 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 .
    Allolithocholic acid (Standard)
  • 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 .
    SIN 14

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