65 Results for "

phase transition

" in MedChemExpress (MCE) Product Catalog:
Products (65)

65 Results for "phase transition" in MCE Product Catalog:

Cat. No.: HY-100395R
CAS No.: 36098-33-6
F16 (Standard) is the analytical standard of F16 (HY-100395). This product is intended for research and analytical applications. F16 is a mitochondrial permeability transition pore (PTP) modulator with an EC50 of 30 μM in mice. F16 promotes PTP opening, accumulates in cancer cell mitochondria, and induces mitochondrial depolarization, swelling, cristae disruption, outer membrane rupture, ATP depletion, reactive oxygen species (ROS) production, cytochrome c release and mitochondrial uncoupling. F16 induces cell cycle arrest at the G1 (occasionally G2) phase, reduces the phosphotyrosine content of Neu, as well as the levels of phosphorylated PKB/Akt and phosphorylated MAP kinase, downregulates the protein expression levels of Neu and PKB, triggers apoptosis in cells with moderate Bcl-2 expression, and induces necrosis in cells with overexpressed Bcl-2. F16 can be used in research related to breast cancer and gastric cancer .
loading...
    loading...
Cat. No.: HY-187534
Research Areas:  

Cancer

VEGFR2 AUTOTAC-1 is a VEGFR2 AUTOTAC degrader. VEGFR2 AUTOTAC-1 recruits p62, activates the autophagy-lysosome pathway through the p62-LC3 axis cascade, forms a ternary complex with VEGFR2 and p62, and drives UPS-independent post-translational degradation of VEGFR2. VEGFR2 AUTOTAC-1 induces G1 phase arrest and endogenous apoptosis in cells via the mitochondrial and caspase apoptotic pathways, thereby inhibiting cancer cell proliferation, migration and malignant phenotypes; meanwhile, it inhibits endothelial cell tube formation, migration and endothelial-mesenchymal transition by regulating E-cadherin and MMP2. VEGFR2 AUTOTAC-1 is applicable to research related to triple-negative breast cancer.(Pink: VEGFR2 target protein ligand (HY-187558); Blue: p62 ligand (HY-W014292); Black: Linker)
loading...
    loading...
Cat. No.: HY-164184
CAS No.: 1415728-94-7
Ly101-4B is an apoptosis inducer and multi-target inhibitor with antiproliferative, antitumor and cycytotoxic effects. Ly101-4B reduces HSF1 expression, inhibits microRNA-214 synthesis, downregulates HSP27, HSP70 and HSP90 expression, while suppressing E2F-dependent transcriptional activity and downregulating its target genes. Ly101-4B induces caspase 3/7-mediated apoptosis by reducing DNA synthesis, inhibiting the cell cycle and G1/S phase transition, without affecting RNA synthesis or inducing necrosis. Ly101-4B is selective for pancreatic ductal adenocarcinoma cells with different genotypes and varying degrees of E2F dependence. Ly101-4B can be used in research related to epithelial ovarian cancer and pancreatic ductal adenocarcinoma .
loading...
    loading...
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 .
loading...
    loading...
Cat. No.: HY-184378
CAS No.: 2922221-22-3
Research Areas:  

Metabolic Disease Cancer

MDB5 is a Hedgehog pathway and Smoothened inhibitor that binds to the 7-TM domain of Smo . MDB5 reduces hepatic stellate cell activation, extracellular matrix-related gene expression, collagen deposition, hydroxyproline content and epithelial-mesenchymal transition, and prevents sinusoidal endothelial cell capillarization . MDB5 induces G1 and S phase cell cycle arrest, triggers apoptosis by upregulating Bax and downregulating Bcl-2, and also decreases oxygen consumption rate, glucose uptake, transglutaminase activity and fibronectin matrix assembly . MDB5 reduces the levels of liver injury markers, hepatic triglyceride deposition and hepatic steatosis, restores the tissue structure of the kidney and spleen, and inhibits pancreatic tumor growth without causing body weight loss . MDB5 can be loaded into PEG-PCC-g-DC micelles, achieving high drug loading, sustained release, improved water solubility, enhanced cellular uptake and optimized hepatic distribution, with good tolerance in mice . MDB5 is applicable to research related to alcohol-associated liver disease, liver fibrosis and pancreatic cancer .
loading...
    loading...