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Fig. 2 | Journal of Hematology & Oncology

Fig. 2

From: Recent advances in therapeutic strategies for triple-negative breast cancer

Fig. 2

Potential therapeutic targets and appropriate drugs in TNBC. The schematic shows several major abnormal signaling pathways (green), excessive activated receptors (purple), and other key molecules involved in proliferation and progression (blue) in TNBC. Drugs specifically targeting molecules are indicated by red arrows, and the number represents the following agents: (1) VEGFR inhibitors (cediranib, apatinib, lenvatinib) and VEGFR mAb (bevacizumab); (2) EGFR inhibitors (afatinib, gefitinib), EGFR mAbs (nimotuzumab, panitumumab, cetuximab, and SCT200) and ADCs (anti-EGFR-IL-dox and U3-1402); (3) IGF1R blocking drugs (linsitinib, NVP-AEW541, and BMS-754807); (4) CXCR4 antagonists (balixafortide) and CXCR4-binding peptide (DV1); (5) Src inhibitors (dasatinib and BJ-2302); (6) MEK inhibitors (trametinib and binimetinib); (7) ERK inhibitors (BL-EI001 and nifetepimine); (8) PI3K inhibitors (alpelisib and buparlisib); (9) AKT inhibitors (ipatasertib and capivasertib); (10) mTOR inhibitors (everolimus and MLN0128); (11) CYP17 inhibitors (abiraterone acetate and orteronel); (12) AR inhibitors (bicalutamide, enzalutamide, and enobosarm); (13) microtubule stabilizer (taxanes, vincristine, and eribulin); multiple target inhibitors (AMXI-5001 and ixabepilone); and ADCs (mirvetuximab, soravtansine, CX-2009, and SAR566658); (14) endocrinotherapy (tamoxifen and letrozole); (15) HDAC inhibitors (panobinostat, belinostat, chidamide, romidepsin, entinostat, and CUDC-907); (16) PARPi (olaparib, veliparib, talazoparib, niraparib, and rucaparib) and platinum-based agents (cisplatin and carboplatin); (17) CDK inhibitors (trilaciclib, palbociclib, abemaciclib, ribociclib, dinaciclib, and PF-06873600); and (18) p53 agonist (PRMIA-1 and APR-246). ADCs, antibody‒drug conjugates; AR: androgen receptor; AXL: AXL receptor tyrosine kinase; BRCA: breast cancer susceptibility gene; BRD4: bromodomain containing 4; CDK: cyclin-dependent kinases; CXCR4: C-X-C chemokine receptor type 4; CYP17: 17-[α]-hydroxylase/17:20-lyase (CYP17); ER: estrogen receptor; DHT: dihydrotestosterone; EGFR: epidermal growth factor receptor; FGFR: fibroblast growth factor receptor; HDAC: histone deacetylase; IGF1R: type 1 insulin-like growth factor receptor; PARP: poly-adenosine diphosphate ribose polymerase; and VEGFR: vascular endothelial growth factor receptor

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