epithelial-mesenchymal transition (emt)

AXL-IN-13 is a potent and orally active AXL inhibitor with an IC50 value of 1.6 nM and a Kd value of 0.26 nM.AXL-IN-13 exhibits anticancer activity, reverses TGF-β1-induced epithelial-mesenchymal transition (EMT) and inhibits cancer cell migration and invasion.

DT-6, a potent TGF-β1 inhibitor, impedes M2 macrophage-induced epithelial-to-mesenchymal transition and the invasive migration of cancer cells, thereby showing potential for cancer research applications [1].

CPF-7 (Caerulein precursor fragment), an insulinotropic peptide, promotes insulin secretion and drives epithelial-mesenchymal transition via Snai1 upregulation in PANC-1 ductal cells. Moreover, it induces exocrine plasticity through Ngn3 upregulation, with applications in type 2 diabetes research [1] [2].

CAY10736 is an anticancer compound.1 It inhibits proliferation in a panel of melanoma and breast, pancreatic, and lung cancer cell lines (IC50s = 0.827-9.89 μM). CAY10736 inhibits migration and epithelial-to-mesenchymal transition (EMT) of A375 and B16/F10 melanoma cells in vitro in a concentration-dependent manner. It reduces the viability of spheroid A375 and B16/F10 cells (IC50s = 2.4 and 1.59 μM, respectively) and increases the production of reactive oxygen species (ROS) in these cells in a concentration-dependent manner. CAY10736 (5 mg/kg) reduces tumor growth in B16/F10 melanoma and Lewis lung carcinoma mouse models and an A375 mouse xenograft model.References1. Liu, X., Li, B., Zhang, Z., et al. Synthesis and discovery novel anti-cancer stem cells compounds derived from the natural triterpenoic acids. J. Med. Chem. 61(23), 10814-10833 (2018). CAY10736 is an anticancer compound.1 It inhibits proliferation in a panel of melanoma and breast, pancreatic, and lung cancer cell lines (IC50s = 0.827-9.89 μM). CAY10736 inhibits migration and epithelial-to-mesenchymal transition (EMT) of A375 and B16/F10 melanoma cells in vitro in a concentration-dependent manner. It reduces the viability of spheroid A375 and B16/F10 cells (IC50s = 2.4 and 1.59 μM, respectively) and increases the production of reactive oxygen species (ROS) in these cells in a concentration-dependent manner. CAY10736 (5 mg/kg) reduces tumor growth in B16/F10 melanoma and Lewis lung carcinoma mouse models and an A375 mouse xenograft model. References1. Liu, X., Li, B., Zhang, Z., et al. Synthesis and discovery novel anti-cancer stem cells compounds derived from the natural triterpenoic acids. J. Med. Chem. 61(23), 10814-10833 (2018).

Anticancer agent 94, a 4-Hydroxycoumarin derivative, inhibits lung cancer cell invasion and migration by modulating the expression of epithelial-mesenchymal transition (EMT) effectors [1].

Anticancer Agent 93, a 4-Hydroxycoumarin derivative, inhibits the invasion and migration of lung cancer cells through modulation of epithelial-mesenchymal transition (EMT) effector expression [1].

PI3K/AKT-IN-2, a dual inhibitor of PI3K and AKT, prevents the epithelial-mesenchymal transition (EMT) and promotes apoptosis. Additionally, it impedes tubulin polymerization.

Antitumor agent-77 inhibits the growth and migration of cancer cells and has anticancer effects. antitumor agent-77 inhibits GPx-4 and enhances COX2-induced iron sagging. antitumor agent-77 activates the intrinsic apoptotic pathway (Bax-Bcl-2-caspase-3) in tumor cells and prevents tumor cell epithelialization. Antitumor agent-77 activates the tumour cell intrinsic apoptotic pathway (Bax-Bcl-2-caspase-3) and blocks the epithelial mesenchymal transition (EMT) process.

EMT Inhibitor-2, targeting both CYP3A4 testosteron and CYP2C9, exhibits inhibitory effects with IC50 values of 49.72 and 5.54 μM, respectively. Furthermore, it effectively impedes the epithelial-mesenchymal transition (EMT) process, induced by immunocyte-released agents like IL-1β and TGF-β.

KY-05009 is a chemical compound that effectively suppresses TGF-β1-induced epithelial-to-mesenchymal transition (EMT) in human lung adenocarcinoma cells, reduces TNIK protein expression and the transcriptional activity of Wnt target genes, and promotes apoptosis in cancer cells, displaying anti-cancer properties. Furthermore, it functions as an ATP-competitive Traf2- and Nck-interacting kinase (TNIK) inhibitor with a Ki of 100 nM.

Sulindac (Sulindac sulfoxide) is a sulfinylindene derivative prodrug with potential antineoplastic activity. Converted in vivo to an active metabolite, sulindac, a nonsteroidal anti-inflammatory drug (NSAID), blocks cyclic guanosine monophosphate-phosphodiesterase (cGMP-PDE), an enzyme that inhibits the normal apoptosis signal pathway; this inhibition permits the apoptotic signal pathway to proceed unopposed, resulting in apoptotic cell death.

Phthalazinone pyrazole is potent, selective, and orally bioavailable inhibitor of Aurora-A kinase. Aurora-A is overexpressed in a variety of tumor types and displays oncogenic activity.

CT1-3 is a potent anti-cancer agent. CT1-3 regulates the JNK/Bcl-2/Bax/XIAP pathway, which induces mitochondria-mediated apoptosis. CT1-3 regulates the E-cadherin/Snail axis to inhibit epithelial mesenchymal transition (EMT) potentials in human cancer cells (HCCs) and suppresses tumourigenesis. CT1-3 has anti-tumour effects in mouse models and does not show significant hepatotoxicity or nephrotoxicity.

Methacycline hydrochloride (Rondomycin) is a broad-spectrum semisynthetic antibiotic related to TETRACYCLINE but excreted more slowly and maintaining effective blood levels for a more extended period.

CPUL1, a TrxR inhibitor, exhibits proliferation-inhibitory and anti-metastatic effects on A549 cells by modulating epithelial-mesenchymal transition (EMT) through the induction of ROS-mediated ERK/JNK signaling, achieved by inhibiting TrxR1 enzyme activity. The efficacy of CPUL1 is enhanced when used in conjunction with α-Lipoic Acid or Dithiodipropionic acid [1].

Sulindac (sodium) (MK-231) is an orally active nonsteroidal anti-inflammatory agent. Sulindac (sodium) is used to reduce pain, swelling, and joint stiffness from arthritis. Sulindac is also used for the research of arthritis of the spine, gouty arthritis. Sulindac (sodium), as an immunomodulatory agent, can downregulate PD-L1 through the blockade of NF-κB signaling and modulates the response of pMMR colorectal cancer (CRC) to anti-PD-L1 immunotherapy, inhibits the development and progression of colorectal cancer CRC. Sulindac (sodium) also inhibits TGF-β1- induced epithelial-mesenchymal transition (EMT) and suppresses lung cancer cell migration and invasion via downregulation of SIRT1 [1] [2].

β-Carboline-1-carboxylic acid is an alkaloid that has been found in P. quassioides and has diverse biological activities. It reduces LPS-induced increases in MCP-1, TNF-α, IL-6, and IL-1β levels in RAW 264.7 cells when used at a concentration of 15 µg/ml and inhibits the epithelial-to-mesenchymal transition (EMT) induced by TGF-β1 in A549 cells. β-Carboline-1-carboxylic acid induces cytotoxicity in CT26.WT, K562, and SGC-7901 cells (IC50s = 14.96, 22.11, and 19.7 µg/ml, respectively) but not HepG2 or A549 cells (IC50s = 36.41 and 41.51 µg/ml, respectively). It also inhibits cAMP phosphodiesterase with an IC50 value of 96 µM.

EW-7195 is a selective and potent inhibitor of ALK5 (TGFβR1) with an IC50 value of 4.83 nM.EW-7195 has an affinity for ALK5 that is more than 300-fold higher than that of p38α.EW-7195 has an inhibitory effect on TGF-β1-induced Smad signaling, epithelial mesenchymal transition (EMT), and breast cancer metastasis to the lungs.

CAY10735 is an anticancer compound.1 It inhibits proliferation in a panel of melanoma and breast, pancreatic, and lung cancer cell lines (IC50s = 0.674-11.56 μM). CAY10735 inhibits migration of and the epithelial-to-mesenchymal transition (EMT) in A375 and B16/F10 melanoma cells in vitro in a concentration-dependent manner. It reduces the viability of spheroid A375 and B16/F10 cells (IC50s = 3.04 and 1.24 μM, respectively) and increases production of reactive oxygen species (ROS) in these cells in a concentration-dependent manner. CAY10735 (5 mg/kg) reduces tumor growth in B16/F10 melanoma and Lewis lung carcinoma mouse models and an A375 mouse xenograft model.References1. Liu, X., Li, B., Zhang, Z., et al. Synthesis and discovery novel anti-cancer stem cells compounds derived from the natural triterpenoic acids. J. Med. Chem. 61(23), 10814-10833 (2018). CAY10735 is an anticancer compound.1 It inhibits proliferation in a panel of melanoma and breast, pancreatic, and lung cancer cell lines (IC50s = 0.674-11.56 μM). CAY10735 inhibits migration of and the epithelial-to-mesenchymal transition (EMT) in A375 and B16/F10 melanoma cells in vitro in a concentration-dependent manner. It reduces the viability of spheroid A375 and B16/F10 cells (IC50s = 3.04 and 1.24 μM, respectively) and increases production of reactive oxygen species (ROS) in these cells in a concentration-dependent manner. CAY10735 (5 mg/kg) reduces tumor growth in B16/F10 melanoma and Lewis lung carcinoma mouse models and an A375 mouse xenograft model. References1. Liu, X., Li, B., Zhang, Z., et al. Synthesis and discovery novel anti-cancer stem cells compounds derived from the natural triterpenoic acids. J. Med. Chem. 61(23), 10814-10833 (2018).

ML327 is a MYC blocker. ML327 can also de-repress E-cadherin transcription and reverse Epithelial-to-Mesenchymal Transition (EMT).

STAT3-IN-15, a potent and orally active inhibitor targeting STAT3, effectively combats idiopathic pulmonary fibrosis (IPF) by hindering STAT3 phosphorylation. Additionally, it impedes TGF-β1-induced migration and deformation of epithelial cells and prevents epithelial-mesenchymal transition (EMT), offering a multifaceted approach against IPF.

Antitumor agent-78 inhibits GPx-4 and elevates COX2, leading to ferroptosis. antitumor agent-78 activates the tumor cell intrinsic apoptotic pathway (Bax-Bcl-2-caspase-3) and inhibits the epithelial mesenchymal transition (EMT) process in tumor cells. Antitumor agent-78 exhibits antitumor effects and inhibits the growth and migration of cancer cells.