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M1 macrophage polarization

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22

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1

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4

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6

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1

Isotope-Labeled Compounds

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Cat. No. Product Name Target Research Areas Chemical Structure
  • 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-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-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-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-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-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-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-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-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-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-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-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-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-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 .
    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
  • 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 .
    Fa-Au
  • HY-181059
    AMPK/mTOR modulator-1

    		Drug Derivative mTOR AMPK Metabolic Disease Inflammation/Immunology Cancer
    AMPK/mTOR modulator-1, Ginsenoside derivative, is an orally active mTOR inhibitor and AMPK activator. AMPK/mTOR modulator-1 activates AMPK signaling with a Kd of 4.759 μM. AMPK/mTOR modulator-1 promotes M1-like tumor-associated macrophage polarization while suppressing M2-like polarization. AMPK/mTOR modulator-1 can enhance glycolysis. AMPK/mTOR modulator-1 significantly inhibits tumor progression and shows anti-inflammation activity. AMPK/mTOR modulator-1 can be used for the research of colorectal cancer .
    AMPK/mTOR modulator-1
  • HY-182283
    sEH-IN-23

    		Epoxide Hydrolase Reactive Oxygen Species (ROS) Interleukin Related NF-κB Inflammation/Immunology
    sEH-IN-23 is a soluble epoxide hydrolase inhibitor with a IC50 of 0.8 nM against human sEH and 0.7 nM against murine sEH. sEH-IN-23 inhibits inflammatory factor production mediated by NF-κB activation, reactive oxygen species (ROS) generation, and the release of pro-inflammatory cytokines IL-1β, IL-6 and TNF-α. sEH-IN-23 exhibits anti-inflammatory activity in acute lung injury models. sEH-IN-23 can be used for the research of acute lung injury .
    sEH-IN-23

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