epithelial-mesenchymal transition (emt)

(R)-MMP-408 is an isomer of MMP-408, which is an effective MMP-12 inhibitor with an IC₅₀ of 2 nM against human MMP-12. (R)-MMP 408 can influence the epithelial-mesenchymal transition (EMT) process in nasal epithelial cells and is suitable for use in research on chronic obstructive pulmonary disease (COPD) and chronic sinusitis.

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

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.

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.

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.

BPU17 interacts with PHB1 and disrupts the PHB1-PHB2 interaction, causing slight mitochondrial dysfunction. This damage hinders transcription dependent on SRF/CArG-box, thereby inhibiting epithelial-mesenchymal transition (EMT) in retinal pigment epithelial cells (RPEs). BPU17 has demonstrated anti-fibrotic activity in vivo. It holds potential as a research agent for anti-angiogenic age-related macular degeneration (nAMD).

Methacycline, a tetracycline antibiotic, inhibits bacterial protein synthesis and effectively suppresses epithelial-mesenchymal transition (EMT). It blocks EMT in vitro and inhibits fibrogenesis in vivo without directly affecting the TGF-β1Smad signaling pathway. As an antimicrobial agent, Methacycline holds potential for research in pulmonary fibrosis.

HJ445A is a highly efficient and selective MYOF inhibitor with excellent water solubility, utilized for the treatment of gastric cancer. In gastric cancer cells MGC803 and MKN45, HJ445A exhibits significant antiproliferative properties with IC50 values of 0.16 μM and 0.14 μM, respectively. The compound binds to the MYOF-C2D domain with a KD value of 0.17 μM and hinders the migration of gastric cancer cells by reversing the epithelial-mesenchymal transition (EMT) process. It also inhibits colony formation in MKN45 cells in a concentration-dependent manner. Remarkably, compared to compound 6y, HJ445A's water solubility is improved by approximately 170 times. Moreover, HJ445A demonstrates superior antitumor effects in vivo.

EMT inhibitor-3 (compound 11i) is an epithelial-mesenchymal transition (EMT) inhibitor that effectively suppresses the proliferation, migration, and invasion of SK-N-SH neuroblastoma cells, with an IC50 value of 2.5 μM. It induces mitochondrial-mediated intrinsic apoptosis in tumor cells by enhancing the Bax/Bcl-2 protein expression ratio, promoting the release of cytochrome C from mitochondria, and activating caspase 9 and caspase 3. EMT inhibitor-3 is applicable for cancer research.

AXL/Angiokinase-IN-1 (compound 11b) is an inhibitor of AXL/triple angiokinase, with an IC50 of 3.75 nM for AXL expression. This compound suppresses epithelial-mesenchymal transition (EMT) in Bxpc-3 cells and prevents metastasis in lung cancer cells. Additionally, AXL/Angiokinase-IN-1 impairs the functions of vascular and fibroblast cells and induces apoptosis in both cancer and fibroblast cells. It is characterized by low toxicity and favorable metabolic stability.

FGFRs-IN-1 (Compound A16) is an orally active inhibitor targeting FGFR1/2/3/4, with IC50 values of 2.3, 7, 11, and 163 nM respectively. It also inhibits VEGFR1/2/3, Abl, and Flt3, with IC50 values of 61, 176, 112, 26, and 353 nM. The compound shows weak inhibition of CYP enzymes. FGFRs-IN-1 reduces the expression of α-SMA and collagen I, and it inhibits epithelial-mesenchymal transition (EMT) in A549 cells stimulated by TGF-β1. Additionally, FGFRs-IN-1 demonstrates anti-inflammatory activity in mouse models of lung fibrosis induced by Bleomycin and liver fibrosis induced by CCl4.

HPH-15 is an anti-cell migration compound that inhibits cell movement by binding to hnRNP U or suppressing TGF-β. Additionally, it prevents epithelial-to-mesenchymal transition (EMT). HPH-15 holds potential for research in areas such as anti-tumor metastasis and anti-fibrosis.

S118 is an orally active inhibitor of the sphingosine-1-phosphate receptor 2 (S1P2 receptor). It prevents the binding of the S1P2 receptor to dapper1 (Dpr1), reduces the accumulation of β-catenin, and blocks the nuclear translocation of the S1P2 receptor. This process inhibits inflammation, fibrosis, and epithelial-mesenchymal transition (EMT), thereby exhibiting anti-idiopathic pulmonary fibrosis (IPF) activity. S118 is considered promising for research in idiopathic pulmonary fibrosis.

Antifibrotic agent 1 is an orally active medication designed to treat idiopathic pulmonary fibrosis (IPF). It effectively mitigates IPF-related processes, including TGF-β-induced epithelial-mesenchymal transition (EMT) and fibroblast-to-myofibroblast transition (FMT), as well as profibrotic M2 polarization. Antifibrotic agent 1 selectively inhibits CSF-1R, PDGFR-α, and Src family kinases (SFKs), while sparing VEGFR, FGFR, and Abl to minimize off-target toxicity. In a bleomycin (BLM)-induced pulmonary fibrosis mouse model, it demonstrates strong antifibrotic activity.

HDAC/PSMD14-IN-1 is a derivative of gambogic acid. It serves as an orally active dual inhibitor targeting PSMD14 and HDAC1, with IC50 values of 238.7 nM and 141.2 nM, respectively. The compound exhibits significant cytotoxicity against ESCC cell lines (IC50: 30-250 nM) and effectively reverses epithelial-mesenchymal transition (EMT). Additionally, HDAC/PSMD14-IN-1 can induce apoptosis. In KYSE30 cell xenograft models in mice, it displays antitumor activity. HDAC/PSMD14-IN-1 is useful for researching esophageal cancer treatment.

MRC-G-001 is a Genipin derivative with an IC50 value of 117 μM against A549 cancer cells. It inhibits the phosphorylation of EGFR, JAK1, and STAT3, and modulates the expression of proteins related to epithelial-mesenchymal transition (EMT), thereby suppressing cell migration and invasion. MRC-G-001 induces cell cycle arrest and apoptosis (apoptosis) and is applicable in studies of cancers, including non-small cell lung cancer.

Hakin-1 is an inhibitor of the E3 ubiquitin ligase Hakai. It effectively blocks both overall ubiquitination mediated by Hakai and the specific ubiquitination of E-cadherin, thereby inhibiting the process of epithelial-mesenchymal transition (EMT). Hakin-1 can impede tumor progression and cancer metastasis and is utilized for research in colorectal cancer and other cancers.

NSD2/H3K36me2 modulator-1 is an orally active modulator targeting NSD2/H3K36me2. It competitively binds to the SAM pocket of NSD2, effectively inhibiting NSD2 expression and H3K36me2 methylation. This compound can also reverse epithelial-mesenchymal transition (EMT), inhibit cell migration, and induce G0/G1 phase arrest and apoptosis (apoptosis). Additionally, NSD2/H3K36me2 modulator-1 reduces mitochondrial membrane potential (MMP) and promotes reactive oxygen species (ROS) generation. It is used in research for developing epigenetic anticancer strategies targeting NSD2 in hepatocellular carcinoma (HCC).

β-catenin-IN-9 is a β-catenin inhibitor that induces apoptosis, causes cell cycle arrest, and suppresses the migration, invasion, and epithelial-mesenchymal transition (EMT) of colorectal cancer cells. It inhibits the transcription of β-catenin and vimentin and significantly reduces β-catenin at the protein level. β-catenin-IN-9 is applicable for research in colorectal cancer.

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.

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.

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

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].