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Table 1 Brief summary of anti-cancer compounds that are ABCG2 substrates

From: New trends for overcoming ABCG2/BCRP-mediated resistance to cancer therapies

Compound Mechanism of action Note (see below) Reference
Traditional cytotoxics
  Mitoxantrone Topoisomerase II poison   [4]
  Etoposide Topoisomerase II poison   [11, 12]
  Doxorubicin DNA intercalator; Topo II poison 1 [27, 29]
  Daunarubicin DNA intercalator; Topo II poison 1 [27, 29]
  Epirubicin DNA intercalator; Topo II poison 1 [29]
  Topotecan Topoisomerase I poison   [22]
  Irinotecan Topoisomerase I poison   [27]
  SN-38 Topoisomerase I poison 2 [21]
  5-fluorouracil Thymidylate synthase inhibitor   [26]
  Methotrexate Dihydrofolate reductase inhibitor   [24]
  Cladribine Nucleoside analogue   [28]
  Clofarabine Nucleoside analogue   [28]
  6-mercaptopurine Nucleoside analogue   [28]
  Flavopiridol CDK9 inhibitor   [25]
Tyrosine kinase inhibitors
  Imatinib Bcr-Abl inhibitor   [13, 89]
  Dasatinib Bcr-Abl inhibitor 3 [14, 40]
  Nilotinib Bcr-Abl inhibitor   [14]
  Sorafenib Multi-kinase inhibitor 4 [91, 93]
  Sunitinib Multi-kinase inhibitor 5 [87, 92]
  Gefitinib EGFR inhibitor   [15]
  Erlotinib EGFR inhibitor   [16]
  Rucaparib PARP inhibitor 6 [37, 38]
PDT agents
  Pheophorbide a Photosensitizer   [39]
  Chlorin e6 Photosensitizer   [41]
  HPPH Photosensitizer   [42, 43]
  5-aminolevulinic acid Photosensitizer   [48]
  Porfimer sodium Photosensitizer 7 [49]
  1. 1, Requires gain-of-function mutation at ABCG2 R482
  2. 2, SN-38 is the active metabolite of irinotecan
  3. 3, One study suggests ABCG2 expression correlates with poor patient response
  4. 4, Phase I/II trial of sorafenib plus irinotecan recently completed
  5. 5, Phase III trial of sunitinib plus FOLFIRI found no benefit over FOLFIRI alone
  6. 6, ABCG2 also limits rucaparib oral bioavailability
  7. 7, ABCG2 correlates with poor response to porfimer sodium in NSCLC patients