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Small-Molecule Inhibitors Targeting Receptor Tyrosine Kinases in Cancer
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Mohammad Hojjat-Farsangi, Gholamreza Khamisipour
PDGFR members belong to the type 3 tyrosine kinase family Members of this family are not expressed in normal organs and tissues with the exception of smooth muscle cells and fibroblasts in lungs and pericytes of the vascular wall. Overexpression of PDGFR members leads to constitutive activation of PDGFR that has been shown in several solid tumors as gliomas and NSCLC (Heinrich et al., 2012). PDGFRs activate PI3K, MAPK, and PLC-γ signaling pathways, which are involved in various cellular and developmental processes (Andrae et al., 2008).
An insight on the different synthetic routes for the facile synthesis of O/S-donor carbamide/thiocarbamide analogs and their miscellaneous pharmacodynamic applications
Published in Journal of Sulfur Chemistry, 2023
Faiza Asghar, Bushra Shakoor, Babar Murtaza, Ian S. Butler
Sorafenib (1) given in Table 5, a bis-aryl urea multi-targeted anticancer drug, inhibits vascular endothelial growth factor receptor (VEGFR), B-Raf, and platelet-derived growth factor receptor (PDGFR) kinases concerned in tumor proliferation [119]. The inhibition of these kinases has two effects: one is tumor growth restriction and the other is neovascularization termination [120]. The Pyridyl ring of Sorafenib orients into the adenine binding site and collaborates with the three amino acid residues (Trp530, Phe582, and Phe54), the nitrogen atom of the ring accepts a hydrogen bond from the main chain nitrogen of Cys531. The lipophilic trifluoromethyl phenyl ring inserts into the hydrophobic region. Sorafenib's urea fragment forms two hydrogen bonds with B-Raf: one with the aspartate backbone and the other with the glutamate side chain [121].
Regulation of stem cell fate and function by using bioactive materials with nanoarchitectonics for regenerative medicine
Published in Science and Technology of Advanced Materials, 2022
Wei Hu, Jiaming Shi, Wenyan Lv, Xiaofang Jia, Katsuhiko Ariga
Except the biophysical cues above, the small-molecule functional moieties tethered on hydrogels are verified to alter hMSC morphology, protein and gene expression [139]. It can also control hMSC bidirectional lineage commitment. Tanaka’s group recently developed a double-network hydrogel composed of poly(2-acrylamido-2-methylpropanesulfonic acid) (PAMPS) and poly(N,N’-dimethylacrylamide) (PDMAAm) [140]. It can primely mimic niche of cancer stem cells (CSCs) with both soft and tough features and rapidly reprogram six human cancer cell lines into CSCs within 24h of seeding on the gel. More than that, the molecular machinery of cancer cell reprogramming, which clarified through double-network hydrogels, provides potential targets for reagents that specifically eradicate CSCs, such as platelet-derived growth factor receptor and osteopontin.
Advances of engineered extracellular vesicles-based therapeutics strategy
Published in Science and Technology of Advanced Materials, 2022
Hiroaki Komuro, Shakhlo Aminova, Katherine Lauro, Masako Harada
Endogenous surface engineering has been a widely used method to target the delivery of EVs to specific sites in the body. Overexpression of a targeting molecule in the producer cell would have difficulty in selectively modifying the molecule on the EV membrane. Alternatively, EV membrane-bound proteins can be used to overcome this issue by presenting the targeting molecule on the surface of EVs [116]. EV membrane-bound proteins used include lysosome-associated membrane glycoprotein 2b (Lamp2b), lactadherin (C1C2), platelet-derived growth factor receptor (PDGFR), -phosphatidylinositol-anchored protein (GPI) and tetraspanin. To produce surface-modified EVs, cells are transfected with plasmid vectors encoding the targeting peptide, antibody, and ligand/glycan, and the secreted EVs are purified. For example, we have shown that engineered EVs prepared from HEK293T cells transfected with the peptide and monobody [117,118]. This method can enhance the targeting ability of EVs by fusing the target protein with the EV transmembrane protein. However, it remains unclear how this modification accurately directs the targeting, and whether the amount of modification can be controlled.