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Formula | C23H28N8O4 |
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Molecular Weight | 480.52 | CAS No. | 1032568-63-0 | ||||
Solubility (25°C)* | In vitro | DMSO | Insoluble | ||||
Water | Insoluble | ||||||
Ethanol | Insoluble | ||||||
In vivo (Add solvents to the product individually and in order) |
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* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.) |
Description | Copanlisib is a potent pan-class I PI3K with IC50 of 0.5, 3.7, 6.4, and 0.7 nM in cell-free assays for PI3Kα/β/γ/δ , respectively. Phase 3.This product has poor solubility, animal experiments are available, cell experiments please choose carefully! | ||||||||
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Targets |
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In vitro | In both KPL4 cells and LPA-stimulated PC3 cells, BAY 80-6946 reduces pAKT levels. In a subset of human cancer cell lines with PIK3CA mutations and/or overexpression of HER2, BAY 80-6946 shows antiproliferative activity and induces apoptosis. [1] The combination of HER2-targeted therapies and BAY 80-6946 inhibits growth more effectively than either therapy used alone, and can restore sensitivity to trastuzumab and lapatinib in cells. [2] |
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In vivo | In rat KPL4 or HCT116 tumor xenograft model, BAY 80-6946 (6 mg/kg, i.v.) induces 100% complete tumor regression. In nude mice with Lu7860 erlotinib-resistant, patient-derived NSCLC and MAXF1398 patient-derived luminal breast tumor models, BAY 80-6946 (14 mg/kg, i.v.) also causes tumor growth inhibition. [1] |
Kinase Assay: |
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Cell Assay: |
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Animal Study: |
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, , Dr. Antonino Maria Spartà from University of Bolog
, , Dr. Antonino Maria Spartà from University of Bolog
Data from [Data independently produced by , , Oncol Rep, 2017, 37(5):3137-3145]
Assessments of prostate cancer cell functions highlight differences between a pan-PI3K/mTOR inhibitor, gedatolisib, and single-node inhibitors of the PI3K/AKT/mTOR pathway [ Mol Oncol, 2024, 10.1002/1878-0261.13703] | PubMed: 39092562 |
Targeting CD25+ lymphoma cells with the antibody-drug conjugate camidanlumab tesirine as a single agent or in combination with targeted agents [ Br J Haematol, 2024, 10.1111/bjh.19658] | PubMed: 39080847 |
Functional Assessments of Gynecologic Cancer Models Highlight Differences Between Single-Node Inhibitors of the PI3K/AKT/mTOR Pathway and a Pan-PI3K/mTOR Inhibitor, Gedatolisib [ Cancers (Basel), 2024, 16(20)3520] | PubMed: 39456616 |
Targeting N-linked Glycosylation for the Therapy of Aggressive Lymphomas [ Cancer Discov, 2023, 13(8):1862-1883] | PubMed: 37141112 |
UHRF1 is a mediator of KRAS driven oncogenesis in lung adenocarcinoma [ Nat Commun, 2023, 14(1):3966] | PubMed: 37407562 |
Leveraging molecular structure and bioactivity with chemical language models for de novo drug design [ Nat Commun, 2023, 14(1):114] | PubMed: 36611029 |
Single-cell dissection of Merkel cell carcinoma heterogeneity unveils transcriptomic plasticity and therapeutic vulnerabilities [ Cell Rep Med, 2023, 4(7):101101] | PubMed: 37421947 |
Subtype-selective induction of apoptosis in translocation-related sarcoma cells induced by PUMA and BIM upon treatment with pan-PI3K inhibitors [ Cell Death Dis, 2023, 14(2):169] | PubMed: 36849535 |
Protein Tyrosine Phosphatase Non-Receptor 11 (PTPN11/Shp2) as a Driver Oncogene and a Novel Therapeutic Target in Non-Small Cell Lung Cancer (NSCLC) [ Int J Mol Sci, 2023, 24(13)10545] | PubMed: 37445722 |
Protein Tyrosine Phosphatase Non-Receptor 11 (PTPN11/Shp2) as a Driver Oncogene and a Novel Therapeutic Target in Non-Small Cell Lung Cancer (NSCLC) [ Int J Mol Sci, 2023, 24(13)10545] | PubMed: 37445722 |
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