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Results for "

M1+phenotype

" in MedChemExpress (MCE) Product Catalog:

9

Inhibitors & Agonists

2

Peptides

Cat. No. Product Name Target Research Areas Chemical Structure
  • 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 [1] .
    KS-133 TFA
  • HY-W614507
    Dihydronicotinamide riboside

    		NADPH Oxidase Apoptosis Bcl-2 Family Metabolic Disease Cancer
    Dihydronicotinamide riboside is a potent NAD + concentration enhancer. Dihydronicotinamide riboside modulates targets BAX, PUMA, NQO2, and IκB kinase. Dihydronicotinamide riboside mediates apoptosis, induces pro-oxidant activity, mitochondrial dysfunction, metabolic dysregulation, redox modulation, and pro-inflammatory M1 phenotype induction. Dihydronicotinamide riboside increases intracellular and mitochondrial NAD + levels, maintains cell survival against NAD +-depleting genotoxins. Dihydronicotinamide riboside can be used for the research of hepatocellular carcinoma [1] .
    Dihydronicotinamide riboside
  • 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-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 [1] .
    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) [1] .
    RP-832c
  • 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 [1].
    CSF1R-IN-3
  • HY-155762
    Anti-neuroinflammation agent 1

    		NOD-like Receptor (NLR) Interleukin Related Neurological Disease Inflammation/Immunology
    Anti-neuroinflammation agent 1 is a potent anti-neuroinflammation agent that regulates polarization BV2 microglia cells from M1 phenotype to M2 phenotype [1].
    Anti-neuroinflammation agent 1
  • HY-169103
    Neuroprotective agent 5

    		NO Synthase COX Cholinesterase (ChE) Amyloid-β Neurological Disease Inflammation/Immunology
    Neuroprotective agent 5 (compound 28) is a brain permeabilizing agent with anti-neuritis, anti-oxidative damage and neuroprotective effects. Neuroprotective agent 5 exhibits a potent NO inhibitory effect (EC50=0.49 μM), inhibits the release of proinflammatory factors PGE2 and TNF-α, downregulates the expression of iNOS and COX-2 proteins, and promotes the polarization of BV-2 cells from the proinflammatory M1 phenotype to the anti-inflammatory M2 phenotype. In addition, Neuroprotective agent 5 can also inhibit acetylcholinesterase (AChE) activity and Aβ42 aggregation in a dose-dependent manner. Neuroprotective agent 5 can be used for the study of Alzheimer's disease [1].
    Neuroprotective agent 5
  • 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 [1].
    CSF1R-IN-22

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