Javascript must be enabled to continue!
Abstract 5778: Preclinical evaluation of TQB3616, a highly potent and selective small-molecule CDK4/6 inhibitor
View through CrossRef
Abstract
Objective: The G1 restriction point is critical for regulating the cell cycle and is controlled by the retinoblastoma protein (Rb) pathway (CDK4/6-cyclin D1-Rb-p16/ink4a). Selective CDK4/6 inhibitors, such as palbociclib and ribociclib have been approved by US FDA in combination with letrozole to treat patients with HR+/Her2- breast cancer, and selective CDK4/6 inhibitor LY2835219 is in Phase 3 trials for the same and related indications. Here, we disclose TQB3616 for the first time, a novel selective, potent, oral inhibitor of CDK4/6.
Method: The anti-proliferative activity of TQB3616 was evaluated in a panel of 18 Rb-proficient cell lines in a 72-hour viability assay. Daily oral administration was used to evaluate in vivo antitumor activity of TQB3616 in the MCF-7 cell-derived xenograft (CDX) breast cancer model. Effect on CDK4/6-cyclin D1-Rb signaling was assessed by western blot analysis of downstream effector protein p-Rb. In vivo antitumor activity of TQB3616 was also tested in a patient-derived xenograft (PDX) lung cancer model LU-01-0393.
Result: TQB3616 displayed potent anti-proliferative activity in 8 of 18 Rb-proficient cancer cell lines (>50% inhibition at 0.3 µM). Inhibition of p-Rb in the tumor samples was verified by western blot analysis. TQB3616 showed in vivo antitumor activity in the MCF-7 CDX model with TGI of 60% @7.5 mpk and 93% @15 mpk, better than palbociclib (TGI = 52% @20 mpk, 80% @40 mpk) and LY2835219 (TGI = 45% @7.5 mpk, 76% @15 mpk). TQB3616 also showed good in vivo antitumor activity in the LU-01-0393 lung cancer PDX model with 65% of TGI @35 mpk.
Conclusion: TQB3616 is a potent and selective CDK4/6 inhibitor and shows excellent antitumor activity in preclinical tumor models. These results warrant TQB3616 going to the clinic for exploration of its potential for treating HR+/Her2-/Rb+ breast cancer as well as other Rb+ cancer types.
Citation Format: Xu Zhaobing, Hu Lihong, Liu Yingchun, Charles Z. Ding, Xiaoyu Zhu, Chen Chen, Yusong Zhu, Jiahu Wu, Dongdong Wu, Shuhui Chen, Xiquan Zhang, Ling Yang, Xin Tian. Preclinical evaluation of TQB3616, a highly potent and selective small-molecule CDK4/6 inhibitor [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5778.
American Association for Cancer Research (AACR)
Title: Abstract 5778: Preclinical evaluation of TQB3616, a highly potent and selective small-molecule CDK4/6 inhibitor
Description:
Abstract
Objective: The G1 restriction point is critical for regulating the cell cycle and is controlled by the retinoblastoma protein (Rb) pathway (CDK4/6-cyclin D1-Rb-p16/ink4a).
Selective CDK4/6 inhibitors, such as palbociclib and ribociclib have been approved by US FDA in combination with letrozole to treat patients with HR+/Her2- breast cancer, and selective CDK4/6 inhibitor LY2835219 is in Phase 3 trials for the same and related indications.
Here, we disclose TQB3616 for the first time, a novel selective, potent, oral inhibitor of CDK4/6.
Method: The anti-proliferative activity of TQB3616 was evaluated in a panel of 18 Rb-proficient cell lines in a 72-hour viability assay.
Daily oral administration was used to evaluate in vivo antitumor activity of TQB3616 in the MCF-7 cell-derived xenograft (CDX) breast cancer model.
Effect on CDK4/6-cyclin D1-Rb signaling was assessed by western blot analysis of downstream effector protein p-Rb.
In vivo antitumor activity of TQB3616 was also tested in a patient-derived xenograft (PDX) lung cancer model LU-01-0393.
Result: TQB3616 displayed potent anti-proliferative activity in 8 of 18 Rb-proficient cancer cell lines (>50% inhibition at 0.
3 µM).
Inhibition of p-Rb in the tumor samples was verified by western blot analysis.
TQB3616 showed in vivo antitumor activity in the MCF-7 CDX model with TGI of 60% @7.
5 mpk and 93% @15 mpk, better than palbociclib (TGI = 52% @20 mpk, 80% @40 mpk) and LY2835219 (TGI = 45% @7.
5 mpk, 76% @15 mpk).
TQB3616 also showed good in vivo antitumor activity in the LU-01-0393 lung cancer PDX model with 65% of TGI @35 mpk.
Conclusion: TQB3616 is a potent and selective CDK4/6 inhibitor and shows excellent antitumor activity in preclinical tumor models.
These results warrant TQB3616 going to the clinic for exploration of its potential for treating HR+/Her2-/Rb+ breast cancer as well as other Rb+ cancer types.
Citation Format: Xu Zhaobing, Hu Lihong, Liu Yingchun, Charles Z.
Ding, Xiaoyu Zhu, Chen Chen, Yusong Zhu, Jiahu Wu, Dongdong Wu, Shuhui Chen, Xiquan Zhang, Ling Yang, Xin Tian.
Preclinical evaluation of TQB3616, a highly potent and selective small-molecule CDK4/6 inhibitor [abstract].
In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL.
Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 5778.
Related Results
Induction of Metabolic Impairment In Prolonged Early G1 Arrest Induced by CDK4/CDK6 Inhibition Sensitizes Myeloma Cells for Proteasome Inhibitor Killing During Subsequent S Phase Synchronization
Induction of Metabolic Impairment In Prolonged Early G1 Arrest Induced by CDK4/CDK6 Inhibition Sensitizes Myeloma Cells for Proteasome Inhibitor Killing During Subsequent S Phase Synchronization
Abstract
Abstract 2989
Sequential drug combination is a rational approach to maximize tumor killing and minimize side effects in cancer therapy. Howev...
Abstract 5814: Emergent functions of cyclin-dependent kinase 4 regulating aurora b and cenpp transcription
Abstract 5814: Emergent functions of cyclin-dependent kinase 4 regulating aurora b and cenpp transcription
Abstract
A better understanding of the precise molecular mechanisms that control cell proliferation is crucial for the identification of novel cancer therapeutic tar...
CDK4/6i treatment induces ferroptosis via downregulation of SLC7A11 mediated by SP1 for estrogen receptor positive breast cancers.
CDK4/6i treatment induces ferroptosis via downregulation of SLC7A11 mediated by SP1 for estrogen receptor positive breast cancers.
Abstract
Purpose: Cyclin-dependent kinase 4 and 6 inhibitors (CDK4/6is) can significantly extend tumor response in patients with metastatic estrogen receptor–positive (ER+)...
Abstract 2311: Determinants of CDK4 target engagement by palbociclib, ribociclib and abemaciclib
Abstract 2311: Determinants of CDK4 target engagement by palbociclib, ribociclib and abemaciclib
Abstract
Palbociclib, ribociclib and abemaciclib compose a class of ATP-competitive CDK4 and CDK6 inhibitors that have demonstrated preclinical and clinical efficacy...
Abstract 315: Identification of distinct and targetable mechanisms of acquired resistance to CDK4/6 inhibitors
Abstract 315: Identification of distinct and targetable mechanisms of acquired resistance to CDK4/6 inhibitors
Abstract
Recently, three CDK4/6 inhibitors were approved by FDA and became effective treatments for ER+ breast cancer patients. However, most if not all patients eve...
O-GlcNAcylation of MITF regulates its activity and CDK4/6 inhibitor resistance in breast cancer
O-GlcNAcylation of MITF regulates its activity and CDK4/6 inhibitor resistance in breast cancer
Abstract
Cyclin-dependent kinases 4 and 6 (CDK4/6) play a pivotal role in cell cycle and cancer development. Targeting CDK4/6 has demonstrated promising effects against bre...
Abstract 1001: Treatment of RB1-intact cancers with CDK4/6 inhibitor combination therapy
Abstract 1001: Treatment of RB1-intact cancers with CDK4/6 inhibitor combination therapy
Abstract
Synthetic CDK4/6 inhibitors exert anti-tumor effects by forcing RB1 in unphosphorylated status, causing not only cell cycle arrest but also cellular senesce...
Abstract 1769: A selective BRM (SMARCA2) inhibitor for the treatment of BRG1 (SMARCA4) mutant cancers
Abstract 1769: A selective BRM (SMARCA2) inhibitor for the treatment of BRG1 (SMARCA4) mutant cancers
Abstract
Background:
ATP-dependent BRG1/BRM associated factor complexes play a key role in regulating gene expression by remodel...


