Afatinib (BIBW2992)

Name: Afatinib (BIBW2992)
Brand: Selleck Chemicals
SKU: S1011
Rating: 5 (279 reviews)

For research use only.

Catalog No.S1011

279 publications

CAS No. 850140-72-6

Afatinib (BIBW2992) inhibits EGFR/ErbB irreversibly in vitro with IC50 of 0.5, 0.4, 10, 14, 1 nM for EGFR^wt, EGFR^L858R, EGFR^L858R/T790M ErbB2 (HER2) and ErbB4 (HER4), respectively. Afatinib induces autophagy.

Selleck's Afatinib (BIBW2992) has been cited by 279 publications

Cancer Cell, 2021, S1535-6108(20)30609-7

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Nat Cell Biol, 2021, 23(4):377-390

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Nature, 2020, 584(7822):608-613

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Nature, 2019, 571(7763):127-131

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Nat Med, 2019, 25(1):111-118

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Cancer Discov, 2019, 9(7):926-943

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Cancer Cell, 2019, 36(2):179-193

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Cell, 2019, 36(2):179-193

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Cancer Cell, 2019, 10.1016/j.ccell.2019.09.001

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Nat Med, 2018, 24(7):968-977

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Nat Med, 2018, 24(5):638-646

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Cell, 2018, 172(1-2):373-386

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Nat Methods, 2018, 15(8):631-639

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Nat Med, 2017, 23(10):1167-1175

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Nature, 2016, 30;534(7609):647-51.

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Cancer Discov, 2015, 5(7):713-22

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Cancer Discov, 2013, 3(2):168-81

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Cancer Res, 2021, canres.2276.2020

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Cell Rep, 2021, 35(8):109181

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Mol Cancer, 2021, 20(1):17

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EBioMedicine, 2021, 64:103220

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Cells, 2021, 10(7)1647

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Pharmacol Res, 2021, 170:105701

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Front Oncol, 2021, 11:665045

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Biochem Pharmacol, 2021, 190:114642

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Int J Mol Sci, 2021, 22(2)E752

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Int J Mol Sci, 2021, 22(8)4005

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Drug Metab Dispos, 2021, 49(1):53-61

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Transl Oncol, 2021, 14(8):101110

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Onco Targets Ther, 2021, 14:3813-3820

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Thorac Cancer, 2021, 10.1111/1759-7714.13931

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Jpn J Clin Oncol, 2021, hyab048

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Oncol Lett, 2021, 21(5):418

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Lung Cancer, 2021, 154:84-91

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EBioMedicine, 2021, 64:103220

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Nat Nanotechnol, 2021, 10.1038/s41565-021-00872-w

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PLoS Pathog, 2021, 17(2):e1009303

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Mol Psychiatry, 2021, 10.1038/s41380-021-01137-7

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Toxicol Lett, 2021, S0378-4274(21)00043-6

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Acta Neuropathol, 2020, 17

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Cell Res, 2020, 10.1038/s41422-020-00409-1

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Nat Commun, 2020, 25;11(1):1556

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Clin Cancer Res, 2020, clincanres.3555.2020

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Clin Cancer Res, 2020, 10.1158/1078-0432

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Genome Med, 2020, 18;12(1):17

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Redox Biol, 2020, 38:101780

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Oncogene, 2020, 10.1038/s41388-020-01564-w

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Oncogene, 2020, 39(20):3997-4013

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Cancer Lett, 2020, 476:23-33

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J Invest Dermatol, 2020, 3 pii: S0022-202X(20)31407-X

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Cancers (Basel), 2020, 13;12(2) pii: E436

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Cell Death Dis, 2020, 11(10):882

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Cell Death Dis, 2020, 2;11(1):6

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Signal Transduct Target Ther, 2020, 5(1):214

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Cancer Discov, 2020, 10(5):674-687

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Oral Oncol, 2020, 112:105074

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J Virol, 2020, JVI.02001-20

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Antimicrob Agents Chemother, 2020, 1;AAC.00341-20

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Sci Rep, 2020, 10(1):17768

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Cancer Cell Int, 2020, 19;20:58

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BMC Cancer, 2020, 20(1):129

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J Cancer Res Clin Oncol, 2020, 146(3):605-619

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Am J Transl Res, 2020, 15;12(3):847-856 eCollection 2020

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Cancer Res Treat, 2020, 10.4143/crt.2020.585

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Toxicol In Vitro, 2020, 104928

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Oncol Rep, 2020, 44(6):2581-2594

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Hum Cell, 2020, 10.1007/s13577-020-00420-z

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Hum Cell, 2020, 10.1007/s13577-020-00425-8

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Anticancer Res, 2020, 40(4):1867-1874

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Korean J Parasitol, 2020, 58(3):249-255

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Radiat Oncol, 2020, 15(1):58

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Mol Cancer Res, 2020, 18(4):537-548

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BMC Pharmacol Toxicol, 2020, 21(1):61

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NPJ Breast Cancer, 2020, 6:30

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Physiol Rep, 2020, 8(13):e14490

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Genome Biol, 2020, 21(1):181

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J Cancer, 2020, 11(1):241-250

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J Cell Physiol, 2020, 10.1002/jcp.30172

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Viruses, 2020, 12(11)E1294

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Rapid Commun Mass Spectrom, 2020, 10.1002/rcm.8955

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Cancer Cell Int, 2020, 20:376

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Neurooncol Adv, 2020, Dec;2(1):vdaa020

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Sci Rep, 2020, 10(1):12982

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Nat Commun, 2019, 10(1):2532

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Nano Lett, 2019, 19(10):7526-7533

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Clin Cancer Res, 2019, 10.1158/1078-0432

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Int J Cancer, 2019, 10.1002/ijc.32487

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Oncogene, 2019, 38(30):5890-5904

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Cancer Lett, 2019, 466:23-34

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J Exp Clin Cancer Res, 2019, 38(1):282

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J Exp Clin Cancer Res, 2019, 38(1):266

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Cancers (Basel), 2019, 11(1)

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Cancers (Basel), 2019, 11(6)

PubMed: 31181806 ( click the link to review the publication )

Cell Death Dis, 2019, 10(9):663

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Br J Cancer, 2019, 121(10):846-856

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Cancers (Basel), 2019, 11(2)

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Acta Pharm Sin B, 2019, 9(6):1193-1203

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Cells, 2019, 8(12)

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Oncoimmunology, 2019,

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Mol Cancer Ther, 2019, 18(4):733-742

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Mol Cancer Ther, 2019, 18(5):920-928

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J Cancer, 2019, 10(9):2063-2073

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Am J Cancer Res, 2019, 9(6):1282-1292

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Oncogenesis, 2019, 8(10):54

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Mol Cancer Res, 2019, 17(11):2233-2243

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Gynecol Oncol, 2019, 153(1):158-164

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J Cell Physiol, 2019, 10.1002/jcp.28881

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Cancer Sci, 2019, 110(11):3584-3594

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Sci Rep, 2019,

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Clin Lung Cancer, 2019, 20(3):167-177

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J Biol Chem, 2019, 294(12):4488-4497

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Mol Pharmacol, 2019, 95(5):528-536

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Respir Res, 2019, 20(1-:270

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Acta Pharmacol Sin, 2019, 10.1038/s41401-019-0248-2

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Front Physiol, 2019, 10:189

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Cancer Res Treat, 2019, 51(3):951-962

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Transl Oncol, 2019, 12(6):852-858

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Oncol Rep, 2019, 41(2):1059-1066

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Clin Otolaryngol, 2019, 10.1111/coa.13434

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Mol Med Rep, 2019, 20(4):3317-3325

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Pharmaceuticals (Basel), 2019, 12(4)

PubMed: 31703435 ( click the link to review the publication )

J Thorac Oncol, 2019, 14(9):1556-1566

PubMed: 31108249 ( click the link to review the publication )

JCI Insight, 2019, 4(4)

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Cell Mol Gastroenterol Hepatol, 2019, 8(1):37-60

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Oncotarget, 2019, 10(14):1440-1457

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JCI Insight, 2019, 4(21)

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Nat Struct Mol Biol, 2018, 25(6):454-462

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EMBO Mol Med, 2018, 10(9)

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EMBO Mol Med, 2018, 10(9):e8746

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Clin Cancer Res, 2018, 24(11):2594-2604

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Proc Natl Acad Sci U S A, 2018, 115(26):E6030-E6038

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Genes Dev, 2018, 32(17-18):1201-1214

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Cancer Immunol Res, 2018, 6(12):1511-1523

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Clin Cancer Res, 2018, 15;24(6):1436-1447

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Theranostics, 2018, 8(12):3176-3188

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Cancer Res, 2018, 78(24):6866-6880

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Oncogene, 2018, 37(12):1576-1593

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Sci Signal, 2018, 11(549)

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EBioMedicine, 2018, 29:112-127

PubMed: 29433983 ( click the link to review the publication )

Cancers (Basel), 2018, 10(6)

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Cell Death Dis, 2018,

PubMed: 29880898 ( click the link to review the publication )

Cancer Discov, 2018, 8(9):1087-1095

PubMed: 29802158 ( click the link to review the publication )

Mol Cancer Ther, 2018, 17(8):1648-1658

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Mol Cancer Ther, 2018, 17(10):2144-2155

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Mol Cancer Ther, 2018, 17(9):2024-2033

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Mol Oncol, 2018, 12(6):830-854

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Mol Oncol, 2018, 12(4):441-462

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Cancer Sci, 2018, 109(11):3657-3661

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Mol Cancer Res, 2018, 16(11):1773-1784

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Lung Cancer, 2018, 126:72-79

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Front Oncol, 2018, 8:432

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Sci Rep, 2018, 8(1):18043

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J Biol Chem, 2018, 293(42):16518-16527

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Am J Cancer Res, 2018, 8(8):1541-1550

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Ann Thorac Surg, 2018, 105(2):363-370

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Int J Oncol, 2018, 53(4):1544-1556

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Invest New Drugs, 2018, 36(6):999-1005

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Transl Oncol, 2018, 11(6):1406-1418

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Biosci Rep, 2018, 38(6)

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Onco Targets Ther, 2018, 11:8201-8209

PubMed: 30568455 ( click the link to review the publication )

J Craniomaxillofac Surg, 2018, 46(3):492-497

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Mol Cancer Ther, 2018, 17(8):1648-1658

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Bladder Cancer, 2018, 4(1):77-90

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J Am Chem Soc, 2018, 140(40):12785-12797

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Sci Rep, 2018, 8(1):14896

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Oncotarget, 2018, 9(9):8560-8572

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Nat Commun, 2017, 8(1):410

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Nat Commun, 2017, 8(1):823

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Nat Commun, 2017, 8:13897

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Theranostics, 2017, 7(4):974-986

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Elife, 2017, 10.7554/eLife.25946

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Oncogene, 2017, 36(47):6581-6591

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Oncogene, 2017, 36(13):1873-1886

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Oncogene, 2017, 36(48):6691-6700

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Cell Death Dis, 2017, 8(5):e2773

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Arch Toxicol, 2017, 91(8):2921-2938

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Mol Cancer Ther, 2017,

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Neoplasia, 2017, 19(12):1012-1021

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Sci Rep, 2017, 7:44206

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Sci Rep, 2017, 7:44089

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Cancer Prev Res, 2017, 10(1):76-88

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Toxicol Appl Pharmacol, 2017, 335:16-27

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BMC Cancer, 2017,

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Biochem Biophys Res Commun, 2017, 486(4):1027-1033

PubMed: 28366635 ( click the link to review the publication )

Biochem Biophys Res Commun, 2017, 491(3):656-661

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SLAS Discov, 2017, 22(7):915-922

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Oncol Lett, 2017, 14(4):4349-4354

PubMed: 28959367 ( click the link to review the publication )

Oncotarget, 2017, 8(3):4277-4288

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Oncotarget, 2017, 8(14):22414-22432

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Oncotarget, 2017,

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Oncotarget, 2017, 8(29):47305-47316

PubMed: 28521301 ( click the link to review the publication )

Oncotarget, 2017, 8(38):63901-63910

PubMed: 28969039 ( click the link to review the publication )
Oncotarget, 2017, 8(35):58771-58780

PubMed: 28938595 ( click the link to review the publication )

BMB Rep, 2017, 50(3):150-155

PubMed: 28256196 ( click the link to review the publication )

Oncotarget, 2017,

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Elife, 2017, 6

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Oncotarget, 2017,

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Gut, 2016, 1296-305

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Genome Biol, 2016, 17:80

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Elife, 2016, 10.7554/eLife.18489

PubMed: 27845624 ( click the link to review the publication )

Expert Opin Drug Deliv, 2016, 13(1):133-41

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PLoS Genet, 2016, 12(9):e1006279

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Mol Cancer Ther, 2016,

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Mol Cancer Ther, 2016,

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Cancer Sci, 2016, 107(8):1134-40

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Mol Pharm, 2016, 13(6):2117-25

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Am J Cancer Res, 2016, 6(8):1708-19

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Stem Cells Int, 2016, 2016:9601493

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PLoS One, 2016, 11(5):e0155230

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PLoS One, 2016, 11(1):e0146311

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Mol Med Rep, 2016, 13(3):2338-44

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Oncotarget, 2016, 7(28):42859-42872

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Cancer Immunol Res, 2016,

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Oncotarget, 2016, 7(36):58038-58050

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Cancer Immunol Res, 2016,

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Oncotarget, 2016, 7(4):3847-56

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Oncotarget, 2016, 7(26):40398-40417

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Oncotarget, 2016, 7(50):83424-83436

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Oncotarget, 2016,

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Gut, 2015, 10.1136/gutjnl-2014-309026

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Nat Commun, 2015, 6:8481

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J Thorac Oncol, 2015, 10(1):93-101

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Clin Cancer Res, 2015, 10.1158/1078-0432.CCR-14-2789

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Clin Cancer Res, 2015, 10.1158/1078-0432.CCR-15-0560

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Clin Cancer Res, 2015, 21(20):4597-606

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J Cell Biol, 2015, 211(2):391-405

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Int J Cancer, 2015, 136(11):2717-29

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J Med Chem, 2015, 58(16):6589-606

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Cancer Discov, 2015,

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Mol Cancer Ther, 2015, 14(1):298-306

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Mol Cancer Ther, 2015, 10.1158/1535-7163.MCT-13-0951

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Antimicrob Agents Chemother, 2015, 59(2):1088-99

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Antimicrob Agents Chemother, 2015, 59(2):1088-99

PubMed: 25487801 ( click the link to review the publication )

Drug Metab Dispos, 2015, 43(3):375-84

PubMed: ( click the link to review the publication )

Drug Metab Dispos, 2015, 43(3):375-84

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Cell Tissue Res, 2015, 359(3):799-816

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Oncol Rep, 2015,

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Arch Immunol Ther Exp, 2015, 10.1007/s00005-015-0330-5

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PLoS ONE, 2015,

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PLoS One, 2015, 10(4):e0123623

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Anticancer Res, 2015, 35(4):2005-8

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Purity & Quality Control

Choose Selective EGFR Inhibitors

Biological Activity

Description

Targets

EGFR (L858R) ^[1] (Cell-free assay)	EGFR (wt) ^[1] (Cell-free assay)	ErbB4 ^[2] (Cell-free assay)	EGFR (L858R/T790M) ^[1] (Cell-free assay)	HER2 ^[1] (Cell-free assay)
0.4 nM	0.5 nM	1 nM	10 nM	14 nM

In vitro

BIBW2992 shows potent activity against both wild-type and mutant forms of EGFR and HER2. It is similar to Gefitinib in potency against L858R EGFR, but about 100-fold more active against the Gefitinib resistant L858R-T790M EGFR double mutant. BIBW2992 exhibits potent effects on both EGFR and HER2 phosphorylation in vivo. It compares favorably to reference compounds (such as Lapatinib et al.) in all cell types tested, such as human epidermoid carcinoma cell line A431 expressing wt EGFR, murine NIH-3T3 cells transfected with wt HER2, as well as breast cancer cell line BT-474 and gastric cancer cell line NCI-N87, which express endogenous HER2. ^[1]

Cell Data

Cell Lines	Assay Type	Activity Description	PMID
HDLM-2	MmXYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NH\DUXhKSzVyPUCuNFA2PzJizszN	M37PZ\|xiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
KASUMI-1	NHLN[YtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MW\JR\|UxRTBwMEC5NVEh\|ryP	MYe8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNVc{PjV3Lze+V2FPT0WUPD;hQi=>
HCC2218	MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MWjJR\|UxRTBwMEC5PFch\|ryP	M163bFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
KARPAS-45	M3rU[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NIfa[oVKSzVyPUCuNFE3PzFizszN	MnTWQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
HSC-4	MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M1nZU2lEPTB;MD6wNVc1QCEQvF2=	NXnQNnhERGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTF5M{[1OU8oRlODTlfFVlww[T5?
CHL-1	M2fuZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	Mn\ITWM2OD1yLkCxPFM6KM7:TR?=	M2LNc\|xiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
KY821	MWTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MYTJR\|UxRTBwMEKwOkDPxE1?	M4rqVlxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
NCI-N87	M4LZ[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M1ztSGlEPTB;MD6wNlc4OyEQvF2=	NWXpRm9NRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTF5M{[1OU8oRlODTlfFVlww[T5?
DOK	NXH4RY5IT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NWjhS\|dGUUN3ME2wMlA{OTl2IN88US=>	MUS8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNVc{PjV3Lze+V2FPT0WUPD;hQi=>
DSH1	NXfhdFhNT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NHq1S4tKSzVyPUCuNFM{OTRizszN	M37t[\|xiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
MDA-MB-175-VII	MlzNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NXnwbnkzUUN3ME2wMlA{PDF4IN88US=>	MX28ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNVc{PjV3Lze+V2FPT0WUPD;hQi=>
NCI-H2170	NWT2fpdmT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M1vncmlEPTB;MD6wN\|czQCEQvF2=	MVK8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNVc{PjV3Lze+V2FPT0WUPD;hQi=>
BT-474	NHzNOYpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NWGwSFl1UUN3ME2wMlA1QTh4IN88US=>	NYOwW2tXRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTF5M{[1OU8oRlODTlfFVlww[T5?
EFO-27	M4exUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NGryWG9KSzVyPUCuNFUyQDJizszN	MlHPQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
NCI-H720	M1fUS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NW\PSG5QUUN3ME2wMlA2OzJ3IN88US=>	NE\xTpg9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOTd\|NkW1M{c,W0GQR1XSQE9iRg>?
PC-14	NEfMWZNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MY\JR\|UxRTBwMEW2Olgh\|ryP	MVi8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNVc{PjV3Lze+V2FPT0WUPD;hQi=>
EC-GI-10	MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	Mlq5TWM2OD1yLkC1PVEzKM7:TR?=	M1TCUFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
KYSE-450	NHPFTYdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MUHJR\|UxRTBwMEW5O\|gh\|ryP	NX\zOHpjRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTF5M{[1OU8oRlODTlfFVlww[T5?
BPH-1	MnfZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NFHi[3RKSzVyPUCuNFU6QDhizszN	M3O5e\|xiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
NCI-H292	NWTBVlhzT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MkLsTWM2OD1yLkC2NFkh\|ryP	MnLVQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
H9	MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MnLyTWM2OD1yLkC3NVMzKM7:TR?=	Mne1QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
NCI-H526	M4PFOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MnLPTWM2OD1yLkC3PFI{KM7:TR?=	NF;IWFk9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOTd\|NkW1M{c,W0GQR1XSQE9iRg>?
NCI-H1623	MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MXLJR\|UxRTBwMEiwNlUh\|ryP	MUm8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNVc{PjV3Lze+V2FPT0WUPD;hQi=>
KYSE-140	M2PB[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NGDaVHBKSzVyPUCuNFg{OyEQvF2=	NFX5TI49[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOTd\|NkW1M{c,W0GQR1XSQE9iRg>?
Ca9-22	NYPQTGJRT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MnfPTWM2OD1yLkC4N\|U{KM7:TR?=	M13FeVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
AU565	NFu1e\|dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MUnJR\|UxRTBwMEi1NFQh\|ryP	NIiwWGM9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOTd\|NkW1M{c,W0GQR1XSQE9iRg>?
ZR-75-30	MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M1u5PGlEPTB;MD6wPVU1PSEQvF2=	NFm4b5U9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOTd\|NkW1M{c,W0GQR1XSQE9iRg>?
NCI-H1770	NEjsPFNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NEPWd\|RKSzVyPUCuNVAzQCEQvF2=	NGD3O4w9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOTd\|NkW1M{c,W0GQR1XSQE9iRg>?
LB2241-RCC	NH\qdYZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MlmzTWM2OD1yLkGwPFg1KM7:TR?=	NVzaNpAxRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTF5M{[1OU8oRlODTlfFVlww[T5?
CAL-39	MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MVLJR\|UxRTBwMUG3PVIh\|ryP	NEfUXFY9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOTd\|NkW1M{c,W0GQR1XSQE9iRg>?
UACC-893	NFTNNoZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MkLRTWM2OD1yLkGxPFg2KM7:TR?=	MlXPQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
LU-65	MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NYezOpJoUUN3ME2wMlEzPjN\|IN88US=>	MUO8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNVc{PjV3Lze+V2FPT0WUPD;hQi=>
HN	NH[2dWlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NVm2UoZjUUN3ME2wMlE{ODd5IN88US=>	M{PDPFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
TI-73	NVXMPItqT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MkPRTWM2OD1yLkG0O\|E2KM7:TR?=	MVy8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNVc{PjV3Lze+V2FPT0WUPD;hQi=>
KU812	Mm\US5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NEmwSmdKSzVyPUCuNVU1PTZizszN	NXLK[IlxRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTF5M{[1OU8oRlODTlfFVlww[T5?
SW13	NWHab5BtT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NV[0[WtuUUN3ME2wMlE3OjF4IN88US=>	Mk[1QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
BB30-HNC	M{HzOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MX3JR\|UxRTBwMU[1O\|Yh\|ryP	NGXwSnI9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;3e5cv\WKrLnHjMpVsN2OqZX3icE9kd22yb4Xu[H9z\XCxcoTfZ4Fz\C:FSFXNRmwyOTd\|NkW1M{c,W0GQR1XSQE9iRg>?
HSC-2	M1HoR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NEe2[JhKSzVyPUCuNVY5OzdizszN	Ml3SQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
BV-173	MmW2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M{HLcmlEPTB;MD6xO\|U6PiEQvF2=	NXPBSmdJRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTF5M{[1OU8oRlODTlfFVlww[T5?
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COR-L88	NWjMXpBMT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MomyTWM2OD1yLk[0NVE{KM7:TR?=	MVu8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNVc{PjV3Lze+V2FPT0WUPD;hQi=>
CTV-1	MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MW\JR\|UxRTBwNkSzPVIh\|ryP	MoH5QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
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HAL-01	NFXIOo9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MXPJR\|UxRThwNUG5NUDPxE1?	MmjpQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
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BALL-1	NVu3UXdQT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MlHsTWM2OD17LkKxPVA4KM7:TR?=	M2PTRVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
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MHH-PREB-1	NITsOldIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NGiwNYRKSzVyPUGwMlE6QTlizszN	NU\2VGszRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTF5M{[1OU8oRlODTlfFVlww[T5?
DEL	NF\HS3NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MoeyTWM2OD1zMD6zPVQ3KM7:TR?=	M2LKUFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
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OVCAR-4	MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MVTJR\|UxRTFyLki4N\|Uh\|ryP	NWHFXpB[RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTF5M{[1OU8oRlODTlfFVlww[T5?
CAL-72	NWLqc2NiT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MXjJR\|UxRTFyLkmzPVEh\|ryP	Ml7jQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
HCC1954	MkTsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NGq0UmtKSzVyPUGxMlA4PTRizszN	MnPjQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
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NCI-H226	M4jNS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NXHxPZo5UUN3ME20PU44Pzh3IN88US=>	MofUQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xd4f3MoVjcS6jYz71b{9kcGWvYnyvZ49ueG:3bnTfdoVxd3K2X3PhdoQwS0iHTVLMNVE4OzZ3NT:nQnNCVkeHUkyvZV4>
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LB2518-MEL	NIjBe\|BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NED0foJKSzVyPUS5Mlg4OjNizszN	MXG8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:5d4eu[YJqNmGlLoXrM4Np\W2kbD;jc41xd3WwZG;y[ZBwenShY3Hy[E9EUEWPQlyxNVc{PjV3Lze+V2FPT0WUPD;hQi=>
A101D	MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MVnJR\|UxRTR7Lkm0NlUh\|ryP	M4\4bVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4f3e{5m[mlwYXOueYsw[2inbXLsM4NwdXCxdX7kY5JmeG:{dG;jZZJlN0OKRV3CUFEyPzN4NUWvK\|5USU6JRWK8M4E,
NCI-H2087	Mmj2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M2\lNGlEPTB;NEmuPVY5OiEQvF2=	NXnKW5FWRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:ve5d4NmWkaT7hZ{52cy:laHXtZoww[2:vcH;1coRgemWyb4L0Y4NiemRxQ1jFUWJNOTF5M{[1OU8oRlODTlfFVlww[T5?

... Click to View More Cell Line Experimental Data

Assay

Methods	Test Index	PMID
Western blot	CIP2A / p-AKT / AKT / PARP; PubMed: 25537503 Oncotarget Time-dependent effects of afatinib on CIP2A, p-AKT and apoptosis-related proteins in the sensitive H358 and resistant H460 cells. Cells were exposed to 10 μM afatinib for up to 48 hours. Immunoblots were scanned and quantitated to determine the ratio of the level of CIP2A to actin. Data are mean ± SD. n = 3 for the different time intervals. p-EGFR / p-IGF1R / p-ERK / p-AKT; PubMed: 26052929 Mol Carcinog Effects of afatinib on EGFR and IGF1R Signaling Pathways. H1975 cells were treated with afatinib with various doses and cell lysates were subjected to Western blot analysis. Afatinib effectively inhibits p-EGFR and p-ERK while p-AKT was partially inhibited. IGF1R phosphorylation was increased upon afatinib treatment in H1975 cells. p-VEGFR2 / VEGFR2 / JAG1 / DLL4 / NICD1 ; PubMed: 28533486 Oncotarget HUVECs were cultured in the presence of Vatalanib (100 nM) or DBZ (10 nM) for 1 h and then treated for 15 min with rhgal-3 (37 nM) and cultured for additional 6 hrs. After this period, the total protein was isolated and the protein levels of galectin-3, NICD1, DLL4, JAG1, VEGFR2 and VEGFR2-p were assessed by Western blot. β-actin was used as a loading control.	25537503 26052929 28533486
Growth inhibition assay	Cell apoptosis; PubMed: 25537503 Oncotarget Dose-dependent effects of afatinib on apoptosis. Data are mean ± SD. n = 3 for each concentration. , p < 0.05, *, p < 0.01, vs. no afatinib. Cell viability; PubMed: 26515464 Oncotarget A. MTS assay for Ba/F3 cells harboring EGFR exon 19 deletion and L858R. The proportional cell viability is shown. B. MTS assay for Ba/F3 cells harboring EGFR exon 19 deletion+T790M and L858R+T790M. The proportional cell viability is shown. C. MTS assay for Ba/F3 cells harboring wild type EGFR. The proportional cell viability is shown. Erlotinib, afatinib, osimertinib, and rociletinib were used as EGFR-TKIs. Error bars indicate standard deviation.	25537503 26515464
Immunofluorescence	p65; PubMed: 26317651 Oncotarget Effects of different treatments on the nuclear translocation of the NF-κB subunit p65. A2780T cells were treated with 2.5 μM afatinib for 48 hours, or 10 μM PDTC for 2 hours. Subsequently, the NF-κB subunit p65 (red) was localized by immunofluorescence and a confocal microscopy. Nuclei were stained with DAPI (blue). Scale bar = 10 μM. vacuoles; PubMed: 29713246 Cancer Cell Int Autophagy activation upon treatment with Afatinib and Sorafenib was validated using immunofluorescence in order to visualize a creation of autophagosomes; ×60 magnification. DMSO treatment was used as control. Green—autophagy vacuoles; Blue—Hoechst, nuclear staining.	26317651 29713246

In vivo

Daily oral administration of BIBW2992 at 20 mg/kg for 25 days results in dramatic tumor regression with a cumulative treated/control tumor volume ratio (T/C ratio) of 2%. Reduced phosphorylation of EGFR and AKT is confirmed by immunohistochemical staining of tissue sections. Therefore, like lapatinib and neratinib, BIBW2992 is a next generation tyrosine kinase inhibitor (TKI) that inhibits human epidermal growth factor receptor 2 (Her2) and epidermal growth factor receptor (EGFR) kinases irreversibly. BIBW2992 is not only active against EGFR mutations targeted by first generation TKIs like Erlotinib or Gefitinib, but also against those insensitive to these standard therapies. ^[1]

Protocol

Kinase Assay: ^[1]	- Collapse In vitro kinase activity assays: The wild type tyrosine kinase domain of the human EGFR as well as that of the EGFR L858R/T790M double mutant are fused to Glutathione-S-transferase (GST), and extracted. Enzyme activity is then assayed in the presence of the inhibitor BIBW2992, serially diluted in 50% DMSO. A random polymer pEY (4:1) is used as substrate and biotinylated pEY (bio-pEY) is added as a tracer substrate. The kinase domain of HER2 is cloned using the baculovirus system and extracted similarly to that of EGFR kinase. Details of assays for EGFR, HER2, SRC, BIRK and VEGFR2 kinase activity are available in Supplementary information.
Cell Research: ^[1]	- Collapse Cell lines: NSCLC cells Concentrations: 0-10 μM Incubation Time: 1 hour Method: 1 × 10⁴ NSCLC cells are transferred into each well of a 96-well plate and cultured overnight in serum-free media for the EGFR phosphorylation assay. After addition of BIBW2992 on the next day, the plates are incubated at 37 °C for 1 hour. EGF-stimulation is done using 100 ng/mL for 10 min at room temperature. Cells are washed with ice cold PBS, extracted with 120 μL HEPEX buffer per well and shaken at room temperature for 1 hour. In all 2 × 10⁴ cells per well is used for the HER2 phosphorylation assay. Streptavidin precoated plates are coated with anti-EGFR-biotin at 1:100 dilution in blocking buffer and c-erb2/HER2 oncoprotein Ab-5(Clone N24)-Biotin. Cell extracts is then transferred to the antibody-coated wells and incubated at room temperature for 1 hour. Extinction is measured at 450 nm. (Only for Reference)
Animal Research: ^[1]	- Collapse Animal Models: Athymic NMRI-nu/nu female mice Dosages: 20 mg/kg Administration: Oral administration (Only for Reference)

References

Solubility (25°C)

In vitro	DMSO	97 mg/mL (199.61 mM)
	Ethanol	15 mg/mL (30.86 mM)
	Water	Insoluble
In vivo	Add solvents to the product individually and in order(Data is from Selleck tests instead of citations): 2% DMSO+30% PEG 300+5% Tween 80+ddH2O For best results, use promptly after mixing.	10mg/mL

* 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.

Chemical Information Download Afatinib (BIBW2992) SDF

Molecular Weight	485.94
Formula	C₂₄H₂₅ClFN₅O₃
CAS No.	850140-72-6
Storage	3 years-20°C powder 2 years-80°C in solvent
Synonyms	N/A
Smiles	CN(C)CC=CC(=O)NC1=C(C=C2C(=C1)C(=NC=N2)NC3=CC(=C(C=C3)F)Cl)OC4CCOC4

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Method for preparing DMSO master liquid: ： mg drug pre-dissolved in μL DMSO (Master liquid concentration mg/mL， Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation：Take μL DMSO master liquid, next addμL PEG300， mix and clarify, next addμL Tween 80，mix and clarify, next add μL ddH₂O，mix and clarify.

Note：1.Please make sure the liquid is clear before adding the next solvent.
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The Serial Dilution Calculator Equation

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Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

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Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2021-05-17)

NCT Number	Recruitment	interventions	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT04497584	Not yet recruiting	Drug: Afatinib + Prednisone	Advanced Squamous Non Small Cell Lung Cancer	University of Texas Southwestern Medical Center	June 1 2021	Phase 2
NCT04795245	Not yet recruiting	Drug: afatinib	Non-squamous Non-Small Cell Lung Cancer	Boehringer Ingelheim	May 19 2021	--
NCT04413201	Recruiting	Drug: Afatinib\|Drug: Osimertinib	Non-squamous NSCLC	Michael Hopp\|Boehringer Ingelheim\|Johannes Gutenberg University Mainz	September 11 2020	Phase 4
NCT04206787	Recruiting	Drug: Afatinib	Non-squamous Non-Small Cell Lung Cancer	Boehringer Ingelheim	May 20 2020	--
NCT04158947	Recruiting	Drug: Afatinib\|Drug: T-DM1	HER2-positive Breast Cancer\|Brain Metastases	xuexin he\|Second Affiliated Hospital School of Medicine Zhejiang University	May 10 2020	Phase 2

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

Frequently Asked Questions

Question 1:
What’s the recommendation about reconstitution of the compound for in vivo animal study?
Answer:
For in vivo experiment of afatinib, we recommend 0.5% methylcellulose/0.2% Tween 80 as vehicle.

EGFR Signaling Pathway Map

EGFR Inhibitors with Unique Features

Selective EGFR Inhibitor

Erlotinib HCl (OSI-744) : EGFR-selective, IC50=2 nM.
FDA-approved EGFR Inhibitor

Lapatinib : Approved by FDA for breast cancer.
Newest EGFR Inhibitor

CO-1686 (AVL-301) ^New : Irreversible, mutant-selective EGFR inhibitor with K_i of 21.5 nM and 303.3 nM for EGFRL858R/T790M and EGFRWT, respectively.

Related EGFR Products

Erlotinib (OSI-774) ^New

Erlotinib (OSI-774, CP358774, NSC 718781, Tarceva) is an EGFR inhibitor with IC50 of 2 nM, >1000-fold more sensitive for EGFR than human c-Src or v-Abl. Erlotinib induces autophagy.
Afatinib (BIBW2992) Dimaleate ^New

Afatinib (BIBW2992) Dimaleate irreversibly inhibits EGFR/HER2 including EGFR(wt), EGFR(L858R), EGFR(L858R/T790M) and HER2 with IC50 of 0.5 nM, 0.4 nM, 10 nM and 14 nM, respectively; 100-fold more active against Gefitinib-resistant L858R-T790M EGFR mutant. Afatinib (BIBW2992) Dimaleate induces autophagy.
Poziotinib (HM781-36B) ^New

Poziotinib (HM781-36B, NOV120101) is an irreversible pan-HER inhibitor with IC50 of 3.2 nM, 5.3 nM and 23.5 nM for HER1, HER2, and HER4, respectively. Poziotinib also induces apoptosis and G1 cell cycle arrest. Phase 2.
Gefitinib (ZD1839)

Gefitinib (ZD-1839, Iressa) is an EGFR inhibitor for Tyr1173, Tyr992, Tyr1173 and Tyr992 in the NR6wtEGFR and NR6W cells with IC50 of 37 nM, 37nM, 26 nM and 57 nM, respectively. Gefitinib promotes autophagy and apoptosis of lung cancer cells via blockade of the PI3K/AKT/mTOR pathway.

Features:A potent EGFR tyrosine kinase inhibitor.
Erlotinib HCl (OSI-744)

Erlotinib HCl (OSI-744, CP358774, NSC 718781) is an EGFR inhibitor with IC50 of 2 nM in cell-free assays, >1000-fold more sensitive for EGFR than human c-Src or v-Abl.
Osimertinib (AZD9291)

Osimertinib (AZD9291) is an oral, irreversible, and mutant-selective EGFR inhibitor with IC50 of 12.92, 11.44 and 493.8 nM for Exon 19 deletion EGFR, L858R/T790M EGFR, and WT EGFR in LoVo cells, respectively. Phase 3.
Lapatinib (GW-572016)

Lapatinib (GW-572016, GSK572016, GW2016), used in the form of Lapatinib Ditosylate, is a potent EGFR and ErbB2 inhibitor with IC50 of 10.8 and 9.2 nM in cell-free assays, respectively. Lapatinib induces ferroptosis and autophagic cell death.
AG-490 (Tyrphostin B42)

AG-490 (Tyrphostin B42, Zinc02557947) is an inhibitor of EGFR with IC50 of 0.1 μM in cell-free assays, 135-fold more selective for EGFR versus ErbB2, also inhibits JAK2 with no activity to Lck, Lyn, Btk, Syk and Src.
Rociletinib (CO-1686)

Rociletinib (CO-1686, AVL-301) is an irreversible, mutant-selective EGFR inhibitor with K_i of 21.5 nM and 303.3 nM for EGFR^L858R/T790M and EGFR^WT in cell-free assays, respectively. Phase 2.
AG-1478 (Tyrphostin AG-1478)

AG-1478 (Tyrphostin AG-1478, NSC 693255) is a selective EGFR inhibitor with IC50 of 3 nM in cell-free assays, almost no activity on HER2-Neu, PDGFR, Trk, Bcr-Abl and InsR. AG-1478 (Tyrphostin AG-1478) inhibits encephalomyocarditis virus (EMCV) and hepatitis c virus (HCV) by targeting phosphatidylinositol 4-kinase IIIα (PI4KA).

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Afatinib (BIBW2992)