147 Results for "

EMT

" in MedChemExpress (MCE) Product Catalog:
Products (147)

147 Results for "EMT" in MCE Product Catalog:

Cat. No.: HY-N3463
CAS No.: 5835-26-7
Isopimaric acid is a coniferous tree defense compound. Isopimaric acid binds to AKT and inhibits mTOR phosphorylation, thereby regulating the AKT/mTOR pathway. Isopimaric acid inhibits oxidative stress, inflammation, microglial migration, apoptosis, autophagic flux, ornithine decarboxylase activity, breast cancer proliferation and metastasis, and fungal spore germination. Isopimaric acid also induces M2 microglial polarization, mitochondrial damage, ROS accumulation, starvation-induced colon cancer cell apoptosis, and breast cancer cell cycle arrest. Isopimaric acid activates potassium channels, regulates sodium channels and calcium channels, reduces myocardial excitability, and improves arrhythmia. Isopimaric acid acts as an oxidative substrate for CYP6BW1/3, down-regulates PINK1/Parkin, and regulates calcium homeostasis, oxidative phosphorylation, EMT, and the Wnt pathway. Isopimaric acid exhibits activity against drug-resistant Staphylococcus aureus, repels feeding, and promotes the growth of rice seedlings. Isopimaric acid is suitable for research related to epilepsy, tumors, drug-resistant bacterial infections, atrial fibrillation, hypertension, hyperlipidemia, pulmonary tuberculosis, etc .
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Cat. No.: HY-13689G
CAS No.: 133053-19-7
Go 6983 GMP is Go 6983 (HY-13689) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Go 6983 is a dual inhibitor targeting Suv39h1/2 (KMT1A/KMT1B) and PKC, as well as a transcriptional activator capable of inducing DNA hypomethylation. Go 6983 stimulates the transcription of Prdm14 by reducing Suv39h1/2 protein levels, decreasing histone modifications in the Prdm14 promoter region, and increasing the recruitment of RNA polymerase II. Go 6983 induces genome-wide DNA hypomethylation by inhibiting de novo methyltransferase expression and increasing Tet1/Tet2 levels, thereby promoting self-renewal and pluripotency maintenance of stem cells. Meanwhile, Go 6983 can block PKC-mediated signaling pathways to reduce the expression of EMT-related genes and eliminate the upregulation of antioxidant genes downstream of NRF2. Go 6983 is mainly used in mechanism studies related to myocardial ischemia/reperfusion injury .
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Cat. No.: HY-15244G
CAS No.: 1217486-61-7
Alpelisib GMP is Alpelisib (HY-15244) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
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Cat. No.: HY-15244R
CAS No.: 1217486-61-7
Synonyms: BYL-719 (Standard)
Alpelisib (BYL-719) (Standard) is the analytical standard of Alpelisib (HY-15244). This product is intended for research and analytical applications. Alpelisib (BYL-719) is an orally active PI3Kα-selective inhibitor that blocks the conversion of PIP2 to PIP3, thereby inhibiting pathways including PI3K/AKT/mTOR, MAPK/ERK, Notch and JAK-STAT. Alpelisib also induces apoptosis, G0/G1 phase arrest and senescence; it significantly inhibits the proliferation, self-renewal, stemness and epithelial-mesenchymal transition (EMT) of tumor cells, reduces cancer stem cell populations and decreases the expression of stem cell markers. Alpelisib not only enhances the sensitivity to Eribulin (HY-13442) and exerts a synergistic effect with Paclitaxel (HY-B0015), but may also induce drug resistance by upregulating the SGK3/GSK3β/β-catenin signaling pathway. Alpelisib can be applied to research related to breast cancer, gastric cancer and lipomas associated with PTEN hamartoma tumor syndrome .
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Cat. No.: HY-179427
NSD2/H3K36me2 modulator-1 is an orally active NSD2/H3K36me2 modulator. NSD2/H3K36me2 modulator-1 competitively binds to the SAM pocket of NSD2, potently inhibits NSD2 expression and suppresses H3K36me2 methylation. NSD2/H3K36me2 modulator-1 reverses epithelial-mesenchymal transition (EMT), inhibits cell migration, and induces G0/G1 phase arrest and apoptosis. NSD2/H3K36me2 modulator-1 induces decreased Mitochondrial membrane potential (MMP) and subsequent Reactive oxygen species (ROS) generation. NSD2/H3K36me2 modulator-1 can be used to research the NSD2-targeting epigenetic anticancer strategies for hepatocellular carcinoma (HCC) .
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Cat. No.: HY-184501
CAS No.: 486440-74-8
Research Areas:  

Cancer

UE01 is an orally active, selective small-molecule modulator targeting both ULK1/ERK1/2. UE01 activates hULK1 with an EC50 of 695.30 nM and a KD of 114.3 nM for ULK1; it inhibits hERK1 with an IC50 of 179.90 nM and a KD of 114 nM for ERK1; it shows weak binding to ERK2 with a KD of 2.8 mM. UE01 induces the conformational transition of ULK1 from an inactive to an active state, enhances the phosphorylation of ULK1 Ser317 and mAtg13 Ser355, and reduces the phosphorylation of ULK1 Ser757. UE01 competitively occupies the ATP-binding pocket of ERK1, inhibits ERK1 kinase activity, and reduces the activity of the ERK1/2 signaling pathway. UE01 induces complete autophagy flux and apoptosis, upregulates Atg5, Atg7, LC3-II/LC3-I, Bax, cytochrome C (Cyt c), Cleaved-Caspase 3, Cleaved-PARP1 and E-cadherin, downregulates p62, Bcl-2, MMP-2 and MMP-9, reduces the phosphorylation of Exo70 Ser250, and promotes the proteasome-dependent degradation of Cav-1, thereby inhibiting EMT-related phenotypes and extracellular matrix degradation. UE01 can be used in studies related to triple-negative breast cancer .
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Cat. No.: HY-N2259R
CAS No.: 19431-84-6
Synonyms: (+)-Curcumenol (Standard)
Curcumenol (Standard) ((+)-Curcumenol (Standard)) is the analytical standard of Curcumenol (HY-N2259). This product is intended for research and analytical applications. Curcumenol ((+)-Curcumenol) is a natural compound with oral efficacy, exhibiting an IC50 of 12.6 μM and a Ki of 10.8 μM against human CYP3A4. Curcumenol inhibits TNFα-induced phosphorylation/degradation of IκBα, phosphorylation/nuclear translocation of NF-κB p65, as well as the upregulation of MMP3, MMP9, MMP13, TRAF3, IL1RL1, TNFα and IL-1β. Curcumenol suppresses LPS-induced phosphorylation of Akt and p38 MAPK, as well as the production of pro-inflammatory mediators/proteins, and downregulates the SLC7A11/NF-κB/TGF-β pathway. Curcumenol binds to and inhibits the activation of Fyn and Lyn, blocks the function of downstream FcεRI signaling components, and reduces the release of allergic mediators/cytokines. Curcumenol upregulates the expression of KDM6B, and promotes chondrocyte proliferation and cartilage repair. Curcumenol induces ferroptosis and apoptosis, regulates the EMT process, and inhibits tumor growth and metastasis of triple-negative breast cancer. Curcumenol possesses anti-inflammatory, neuroprotective, antioxidant, antitumor, antiviral and hepatoprotective activities. Curcumenol can be used in research related to intervertebral disc degeneration, cancer, inflammation, central nervous system neurodegenerative diseases, allergic reactions and knee osteoarthritis .
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