Cancer Drug Resistance

Cisplatin (CDDP) is an antineoplastic chemotherapy agent by cross-linking with DNA and causing DNA damage in cancer cells. Cisplatin activates ferroptosis and induces autophagy.

Dexamethasone (Hexadecadrol) is a glucocorticoid receptor agonist, apoptosis inducer, and common disease inducer in experimental animals, constructing models of muscle atrophy, hypertension, and depression. Dexamethasone can inhibit the production of inflammatory miRNA-155 exosomes in macrophages and significantly reduce the expression of inflammatory factors in neutrophils and monocytes. Dexamethasone also has potential for use in COVID-19 research.

Trametinib (GSK1120212; JTP-74057) is an orally active MEK inhibitor that inhibits MEK1 and MEK2 with IC₅₀s of about 2 nM. Trametinib activates autophagy and induces apoptosis, cross the blood-brain barrier (BBB), used in research related to subarachnoid hemorrhage (SAH).

Streptozotocin (Streptozocin; STZ) is an antibiotic widely used in experimental animal models of induced diabetes. Streptozotocin enters B cells via the glucose transporter (GLUT2) and causes the alkylation of DNA ( DNA-methylating ). Streptozotocin can induce the apoptosis of β cells.

Bleomycin sulfate is a DNA synthesis inhibitor. Bleomycin hydrochloride is a DNA damaging agent. Bleomycin sulfate is an antitumor antibiotic.

Osimertinib (AZD9291) is a covalent, orally active, irreversible, and mutant-selective EGFR inhibitor with an apparent IC₅₀ of 12 nM against L858R and 1 nM against L858R/T790M, respectively. Osimertinib overcomes T790M-mediated resistance to EGFR inhibitors in lung cancer.

Trastuzumab is a humanized IgG1 monoclonal antibody that selectively binds to HER2 with high affinity. Trastuzumab can be used for the research of HER2-positive metastatic breast cancer and gastric cancer. (Note: The product specifications below only indicate the effective content of Trastuzumab. The component ratio of this product is Trastuzumab : excipients = 1:0.6-1:0.9.)

Enzalutamide (MDV3100) is an androgen receptor (AR) antagonist with an IC₅₀ of 36 nM in LNCaP prostate cells. Enzalutamide is an autophagy activator.

Disulfiram (Tetraethylthiuram disulfide) is a specific inhibitor of aldehyde-dehydrogenase (ALDH1), used for the treatment of chronic alcoholism by producing an acute sensitivity to alcohol. Disulfiram inhibits gasdermin D (GSDMD) pore formation in liposomes and inflammasome-mediated pyroptosis and IL-1β secretion in human and mouse cells. Disulfiram, a copper ion carrier, with Cu²⁺ increases intracellular ROS levels and induces cuproptosis.

Verteporfin (CL 318952) is a photosensitizer for photodynamic therapy to eliminate the abnormal blood vessels in the eye associated with conditions such as age-related macular degeneration. Verteporfin is a YAP inhibitor which disrupts YAP-TEAD interactions. Verteporfin induces cell apoptosis. Verteporfinis an autophagy inhibitor that blocks autophagy at an early stage by inhibiting autophagosome formation.

Bleomycin hydrochloride is a DNA synthesis inhibitor. Bleomycin hydrochloride is a DNA damaging agent. Bleomycin hydrochloride is an antitumor antibiotic.

HP-β-CD ((2-Hydroxypropyl)-β-cyclodextrin) is a widely used drug delivery vehicle to improve the stability and bioavailability.

SN-38 is an active metabolite of the Topoisomerase I inhibitor Irinotecan. SN-38 can bind to RPL15. SN-38 inhibits DNA and RNA synthesis with IC₅₀s of 0.077 and 1.3 μM, respectively. SN-38 is a payload of sacituzumab govitecan (HY -132254).

Gefitinib (ZD1839) is a potent, selective and orally active EGFR tyrosine kinase inhibitor with an IC₅₀ of 33 nM. Gefitinib selectively inhibits EGF-stimulated tumor cell growth (IC₅₀ of 54 nM) and that blocks EGF-stimulated EGFR autophosphorylation in tumor cells. Gefitinib also induces autophagy and cell apoptosis, which can be used for cancer related research, such as Lung cancer and breast cancer .

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.

Pexidartinib (PLX-3397) is a potent, orally active, selective, and ATP-competitive colony stimulating factor 1 receptor (CSF1R or M-CSFR) and c-Kit inhibitor, with IC₅₀s of 20 and 10 nM, respectively. Pexidartinib (PLX-3397) exhibits 10- to 100-fold selectivity for c-Kit and CSF1R over other related kinases. Pexidartinib (PLX-3397) induces cell apoptosis and has anti-tumor activity. Pexidartinib has limited permeability to the blood-brain barrier, primarily through ABCB1.

Abemaciclib (LY2835219) is a selective and BBB-permeable CDK4/6 inhibitor with IC₅₀ values of 2 nM and 10 nM for CDK4 and CDK6, respectively.

Vadimezan (DMXAA), the tumor vascular disrupting agent (tumor-VDA), is a murine agonist of the stimulator of interferon genes (STING) and also a potent inducer of type I IFNs and other cytokines. Vadimezan is unable to activate human STING. Vadimezan has anti-influenza virus H1N1-PR8 activities.

Cytochalasin B is a cell-permeable mycotoxin binding to the barbed end of actin filaments, disrupting the formation of actin polymers, with K_d value of 1.4-2.2 nM for F-actin. Cytochalasin B blocks cell migration.

Erlotinib (CP-358774) is a selective, orally active EGFR tyrosine kinase inhibitor. Erlotinib also acts as a substrate and inhibitor of OATP2B1, with an IC₅₀ of approximately 0.079 μM for inhibiting OATP2B1-mediated uptake of estrone 3-sulfate. Erlotinib blocks EGFR phosphorylation, downstream signal transduction, as well as the growth and proliferation of cancer cells. Erlotinib inhibits MMP-10-mediated renal injury, fibrotic lesions, the ERK1/2, GSK-3β and β-catenin signaling pathways, fibronectin, α-SMA, collagen deposition, and renal injury markers. Erlotinib is metabolized via CYP3A to produce the active metabolite OSI-420. Erlotinib can be used in research related to non-small cell lung cancer, gastric cancer, papillary renal cell carcinoma, pancreatic cancer, renal fibrosis, and other conditions.