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Table 3 Drug target and molecular mechanism in lung cancer

From: Quantitative proteomics in lung cancer

Target

Mechanism

Ref.

ALK

Alectinib (C30H34N4O2) is an inhibitor of ALK, which binds to and inhibits not only ALK kinase but also the L1196M mutant.

Ceritinib (C28H36ClN5O3S) is a ATP-competitive, tyrosine kinase inhibitor of ALK, especially for ALK-rearranged NSCLC.

Crizotinib (C21H22Cl2FN5O) is a kinase inhibitor for ALK, c-Met, and ROS1, especially for ROS1-rearranged NSCLC.

[59]

[58]

[60]

ATP synthase

Citreoviridin (C23H30O6) inhibits the mitochondrial ATP synthetase system. It has been used to target ectopic ATPase activity in lung cancer cells in order to modulate the metabolic activity associated with tumorigenesis.

[64]

BRAF

Vemurafenib (C23H18ClF2N3O3S) selectively binds to the ATP-binding site of BRAF (V600E) kinase, since most BARF gene mutations exist at residue 600 which has been found to be over-activates the MAPK signaling pathway.

[83]

EGFR

Afatinib (C24H25ClFN5O3) selectively inhibits ErbB1, ErbB2, ErbB4 and EGFR mutants (L858R and T790M). It may inhibit tumor progression and angiogenesis.

Erlotinib (C22H23N3O4) is a protein kinase inhibitor which inhibits EGFR phosphorylation and blocks signal transduction. However, the FDA-approval is limited to EGFR mutations.

Gefitnib (C22H24ClFN4O3) inhibits the catalytic activity of tyrosine kinase that competes with the binding affinity of ATP to the tyrosine kinase domain of EGFR. It inhibits signal transduction by inhibiting the receptor for phosphorylation.

[55]

[54]

[53]