Dacomitinib | pan-ErbB inhibitor

Dacomitinib chemical structure

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Dacomitinib (1110813-31-4) is a potent, irreversible second generation pan-ErbB inhibitor (IC50s= 6, 45.7 and 73.7 nM for EGFR, ERBB2 and ERBB4 respectively).1 It inhibits wild-type and mutant forms of ErbB including EGFR T780M and is highly effective for both the wild-type ERBB2 and the gefitinib-resistant oncogenic mutation identified in lung cancers. It is also effective against EGFR L858R2 and L747P3 mutations. It was also shown to be an inhibitor of 4-hydroxyphenylpyruvate dioxygenase, a copper-binding protein, (HPD) triggering an interaction between HPD and dihydrolipoamide S-acetyltransferase and consequently inducing cuproptosis in colorectal cancer.4

References/Citations:

  1. Engelman et al. (2007), PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib; Cancer Res. 67 11924
  2. Wang et al. (2026), Dacomitinib for EGFR-L858R-mutated non-small cell lung cancer following acquired resistance to third-generation EGFR-TKIs: a retrospective real-world study; Transl. Lung Cancer Res. 15 121
  3. Su et al. (2026), Dacomitinib in Combination with chemotherapy is effective in lung adenocarcinoma with rare EGFR L747P mutation and bone metastases: a case report; Front. Oncol. 16 1762855
  4. Dai et al. (2026), HPD is a copper-binding protein that interacts with DLAT to promote colorectal cancer cuproptosis under copper stress.; Cell Rep. 45 117633
1110813-31-4, Dacomitinib, Dacomitinib supplier, ErbB inhibitor, pan-ErbB inhibitor, PF00299804, PF299
Alternate Name:
PF299; PF00299804

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Dacomitinib (1110813-31-4) is a potent, irreversible second generation pan-ErbB inhibitor (IC50s= 6, 45.7 and 73.7 nM for EGFR, ERBB2 and ERBB4 respectively).1 It inhibits wild-type and mutant forms of ErbB including EGFR T780M and is highly effective for both the wild-type ERBB2 and the gefitinib-resistant oncogenic mutation identified in lung cancers. It is also effective against EGFR L858R2 and L747P3 mutations. It was also shown to be an inhibitor of 4-hydroxyphenylpyruvate dioxygenase, a copper-binding protein, (HPD) triggering an interaction between HPD and dihydrolipoamide S-acetyltransferase and consequently inducing cuproptosis in colorectal cancer.4

References/Citations:

  1. Engelman et al. (2007), PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib; Cancer Res. 67 11924
  2. Wang et al. (2026), Dacomitinib for EGFR-L858R-mutated non-small cell lung cancer following acquired resistance to third-generation EGFR-TKIs: a retrospective real-world study; Transl. Lung Cancer Res. 15 121
  3. Su et al. (2026), Dacomitinib in Combination with chemotherapy is effective in lung adenocarcinoma with rare EGFR L747P mutation and bone metastases: a case report; Front. Oncol. 16 1762855
  4. Dai et al. (2026), HPD is a copper-binding protein that interacts with DLAT to promote colorectal cancer cuproptosis under copper stress.; Cell Rep. 45 117633