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Results for "

M2 mRNA

" in MedChemExpress (MCE) Product Catalog:

9

Inhibitors & Agonists

3

Natural
Products

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N3415
    Kumatakenin
    1 Publications Verification

    		 Apoptosis Autophagy Caspase Ferroptosis SARS-CoV Neurological Disease Inflammation/Immunology Cancer
    Kumatakenin is an orally active apoptosis inducer and autophagy inhibitor, with a Kd value of 2.94 μM for mouse ATG5. Kumatakenin increases the activities of caspase-3, caspase-8 and caspase-9, thereby inducing caspase-dependent apoptosis in ovarian cancer cells. Kumatakenin reduces the expression of chemokines and pro-oncogenic factors in ovarian cancer cells, and inhibits M2 macrophage polarization. Kumatakenin inactivates TRIM65 function, reduces the expression and stability of FASN, and thus inhibits the proliferation, migration, invasion and tumor progression of esophageal cancer cells. Kumatakenin interacts with ATG5 to reduce its protein level, decrease LC3 level, and reduce the number of autophagosomes in the hippocampus. Kumatakenin binds to Eno3 to upregulate its expression, reduce the stability and expression level of IRP1 mRNA, inhibit ferroptosis, alleviate intestinal inflammation, and restore epithelial barrier function. Kumatakenin enhances the efficacy of antibiotics against pathogenic bacteria, inhibits SARS-CoV-2 replication, and reduces cytokine production. Kumatakenin is applicable to research related to ovarian cancer, esophageal cancer, depression and colitis .
    Kumatakenin
  • HY-N2983
    Cajanin

    		Tyrosinase Others
    Cajanin is a potent and orally active anti-melanogenic agent. Cajanin shows antiproliferative activity in MNT1 Cells. Cajanin efficiently decreases the melanin content. Cajanin down-regulates the mRNA and protein expression levels of MITF, tyrosinase, TRP-1 and Dct (TRP-2). Cajanin induces cell cycle arrest at G2/M and S phase. Cajanin stimulates osteoblast proliferation. Cajanin has the potential for the research of human hyperpigmented disorders and menopausal osteoporosis .
    Cajanin
  • HY-N1956
    Rubiadin-1-methyl ether
    1 Publications Verification

    		 NF-κB RANKL/RANK Autophagy TGF-β Receptor Metabolic Disease Inflammation/Immunology
    Rubiadin-1-methyl ether is an orally potent NF-κB p65 inhibitor and autophagy inhibitor. Rubiadin-1-methyl ether inhibits RANKL-induced phosphorylation and nuclear translocation of p65, suppresses BECN1 transcription, blocks LC3 conversion and autophagosome formation, thereby reducing the levels of BECN1 mRNA and Beclin1 protein. Rubiadin-1-methyl ether inhibits osteoclastogenesis, cell proliferation, macrophage M2 polarization and the TGF-β1 signaling pathway, and effectively alleviates pulmonary inflammation. Rubiadin-1-methyl ether is widely used in research on osteoporosis, pulmonary fibrosis, idiopathic pulmonary fibrosis, acute lung injury and other related diseases .
    Rubiadin-1-methyl ether
  • HY-172609
    SL-176

    		Phosphatase Apoptosis MDM-2/p53 Caspase Metabolic Disease Cancer
    SL-176 is a PPM1D (Wip1) inhibitor. SL-176 inhibits lipid droplet formation, downregulates the mRNA and protein expression of PPARγ and C/EBPα, and blocks adipocyte differentiation. SL-176 induces G2/M cell cycle arrest, apoptosis and inhibits cell proliferation in breast cancer cells overexpressing PPM1D, and activates components of the p53 pathway. SL-176 suppresses tumor growth in a zebrafish model of neuroblastoma. SL-176 is applicable to research related to obesity, breast cancer and neuroblastoma .
    SL-176
  • HY-175034
    Topoisomerase I/II-IN-1

    		Topoisomerase Apoptosis MDM-2/p53 Bcl-2 Family Caspase Cancer
    Topoisomerase I/II-IN-1 is a dual inhibitor of topoisomerase I/II. Topoisomerase I/II-IN-1 induces G2/M arrest and apoptosis in cancer cells by upregulating p53, p21, and Bax mRNA levels, caspase-3 protein levels, and the Bax/Bcl-2 ratio, while downregulating Bcl-2. Topoisomerase I/II-IN-1 is useful in the study of various cancers, including melanoma, renal cancer, colorectal cancer, and breast cancer .
    Topoisomerase I/II-IN-1
  • HY-168895
    c-Fos-IN-1

    		AP-1 ERK Apoptosis Cancer
    c-Fos-IN-1 (Compound P16) is a c-Jun inhibitor, and decreases mRNA levels and protein levels of c-Fos. c-Fos-IN-1 also inhibits the phosphorylation activity of ERK and the transcriptional activity of AP-1. c-Fos-IN-1 shows anticancer activity by inhibiting ERK/c-Fos/Jun pathway. c-Fos-IN-1 inhibits the proliferation and migration of gastric cancer cells (IC50: 2.31 μM for MGC-803 cell). c-Fos-IN-1 arrests cell cycle at G2/M phase and induces cancer cell apoptosis. c-Fos-IN-1 inhibits gastric cancer tumor growth .
    c-Fos-IN-1
  • HY-184289
    KJ001-12a

    		Influenza Virus DNA/RNA Synthesis Infection
    KJ001-12a is an orally active anti-influenza agent with activity against influenza A and B strains. KJ001-12a acts as an RNA-dependent RNA polymerase inhibitor that reduces the expression levels of viral M2 mRNA and vRNA. KJ001-12a shows low sensitivity to the loss of inhibitory activity caused by the I38T mutation. KJ001-12a is applicable for influenza-related research .
    KJ001-12a
  • HY-181076
    FOXM1-IN-3

    		FOXM1 PI3K CDK Apoptosis Cancer
    FOXM1-IN-3 is a potent FOXM1 inhibitor. FOXM1-IN-3 downregulates FOXM1 expression at protein and mRNA levels, suppressing downstream effectors CCNB1 and CDC25. FOXM1-IN-3 induces G2/M cell cycle arrest and apoptosis in colorectal cancer cells. FOXM1-IN-3 inhibits colony formation and cell migration in colorectal cancer cells. FOXM1-IN-3 targets the cancer stem cell phenotype in colorectal cancer cells, reducing cancer stem cell marker expression. FOXM1-IN-3 reduces tumor growth in a zebrafish xenograft model. FOXM1-IN-3 can be used for the research of colorectal cancer .
    FOXM1-IN-3
  • HY-168895A
    (E,E)-c-Fos-IN-1

    		Drug Isomer Cancer
    (E,E)-c-Fos-IN-1 is the active stereoisomer of c-Fos-IN-1 (HY-168895) in which both double bonds are in the trans configuration. c-Fos-IN-1 (Compound P16) is a c-Jun inhibitor, and decreases mRNA levels and protein levels of c-Fos. c-Fos-IN-1 also inhibits the phosphorylation activity of ERK and the transcriptional activity of AP-1. c-Fos-IN-1 shows anticancer activity by inhibiting ERK/c-Fos/Jun pathway. c-Fos-IN-1 inhibits the proliferation and migration of gastric cancer cells (IC50: 2.31 μM for MGC-803 cell). c-Fos-IN-1 arrests cell cycle at G2/M phase and induces cancer cell apoptosis. c-Fos-IN-1 inhibits gastric cancer tumor growth .
    (E,E)-c-Fos-IN-1

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