- |||||||||| TriptoSar (triptolide) / Pierre Fabre
Journal: Triptolide induces autophagy of ovarian granulosa cells via PI3K/AKT/m TOR pathway (Pubmed Central) - Oct 24, 2019 At the same time,TP could significantly inhibit the expression of p-PI3 K,p-AKT,p-mTOR protein,and the inhibitory effect of TP was better than that of NVP-BEZ235 group. This study suggests that 100 nmol·L-1 TP could induce OGCs autophagy successfully in cultured rat ovary for 12 h; TP may induce OGCs autophagy by inhibiting PI3 k/Akt/m TOR signaling pathway.
- |||||||||| Afinitor (everolimus) / Novartis
Clinical, Journal: TORC1 inhibition enhances immune function and reduces infections in the elderly. (Pubmed Central) - Oct 9, 2019 In addition, we observed an up-regulation of antiviral gene expression and an improvement in the response to influenza vaccination in this treatment group. Thus, selective TORC1 inhibition has the potential to improve immune function and reduce infections in the elderly.
- |||||||||| dactolisib (RTB101) / Novartis, PureTech
Clinical, Journal, PARP Biomarker: Maintenance BEZ235 Treatment Prolongs the Therapeutic Effect of the Combination of BEZ235 and Radiotherapy for Colorectal Cancer. (Pubmed Central) - Aug 22, 2019 Cleaved caspase-3, cleaved poly (ADP-ribose) polymerase (PARP), 53BP1, and γ-H2AX expression in the HCT116 xenograft tissue and three CRC cell lines were significantly upregulated after RT + BEZ235 + mBEZ235 treatment. Maintenance BEZ235 treatment in CRC cells prolonged the inhibition of cell viability, enhancement of apoptosis, attenuation of mTOR signaling, impairment of the DNA-DSB repair mechanism, and downregulation of angiogenesis that occurred due to concurrent BEZ235 and RT treatment.
- |||||||||| AZD8055 / AstraZeneca, navitoclax (ABT 263) / AbbVie, Roche, dactolisib (RTB101) / Novartis, PureTech
Clinical, Journal: Downregulation of MCL-1 and upregulation of PUMA using mTOR inhibitors enhance antitumor efficacy of BH3 mimetics in triple-negative breast cancer. (Pubmed Central) - Aug 3, 2019 The specific changes of MCL-1 and PUMA facilitated the release of the apoptotic regulators, such as BIM, BAX, and BAK, to induce the activation of mitochondrial apoptotic pathway, thereby sensitizing the ABT263 activity in TNBC. Therefore, our findings provided evidences that mTOR inhibitors can enhance antitumor efficacy of BH3 mimetics via downregulating MCL-1 and upregulating PUMA in TNBC; it could be a promising therapeutic strategy to treat TNBC.
- |||||||||| Journal: Targeting BCR-ABL-Independent TKI Resistance in Chronic Myeloid Leukemia by mTOR and Autophagy Inhibition. (Pubmed Central) - Aug 1, 2019
Additionally, we show that catalytic mTOR inhibitors induce autophagy and demonstrate that genetic or pharmacological inhibition of autophagy sensitizes ponatinib-resistant CML cells to death induced by mTOR inhibition in vitro (% number of colonies of control[SD], NVP-BEZ235 vs NVP-BEZ235+HCQ: 45.0[17.9]% vs 24.0[8.4]%, P = .002) and in vivo (median survival of NVP-BEZ235- vs NVP-BEZ235+HCQ-treated mice: 38.5 days vs 47.0 days, P = .04). Combined mTOR and autophagy inhibition may provide an attractive approach to target BCR-ABL-independent mechanism of resistance.
- |||||||||| rabeximod (ROB 803) / Cyxone, dactolisib (RTB101) / Novartis, PureTech
Journal, PARP Biomarker: Identification of 7-(4'-Cyanophenyl)indoline-1-benzenesulfonamide as a mitotic inhibitor to induce apoptotic cell death and inhibit autophagy in human colorectal cancer cells. (Pubmed Central) - Jul 19, 2019 Conversely, the autophagy inducer NVP-BEZ235 shows a synergistic interaction with B220 in HCT116 cells, indicating autophagy was required for the observed cell death. In summary, these results indicate B220 combined with the induction of autophagy using the dual PI3K/mTOR inhibitor, NVP-BEZ235, might be an attractive strategy for cancer therapy, and provides a framework for further development of B220 as a new therapeutic agent for colon cancer treatment.
- |||||||||| dactolisib (RTB101) / Novartis, PureTech
Preclinical, Journal, PARP Biomarker: MicroRNA-223 protects neonatal rat cardiomyocytes and H9c2 cells from hypoxia-induced apoptosis and excessive autophagy via the Akt/mTOR pathway by targeting PARP-1. (Pubmed Central) - Jun 28, 2019 We found that miR-223 overexpression and PARP-1 silencing positively regulated the Akt/mTOR pathway and that treating cells with NVP-BEZ235 (BEZ235), a novel dual Akt/mTOR inhibitor, could reverse the inhibitory effects of both the miR-223 mimics and PARP-1 siRNA on hypoxia-induced apoptosis and autophagy. Taken together, our findings showed that miR-223 protects NRCMs and H9c2 cells from hypoxia-induced apoptosis and excessive autophagy via the Akt/mTOR pathway by targeting PARP-1; thus, miR-223 may be a potential target in the treatment of MI in the future.
- |||||||||| Zytiga (abiraterone acetate) / J&J, dactolisib (RTB101) / Novartis, PureTech
Preclinical, Journal: Combinatorial Effect of Abiraterone Acetate and NVP-BEZ235 on Prostate Tumor Progression in Rats. (Pubmed Central) - Jun 26, 2019 Conversely, when used in combination, the drugs impaired the inflammatory response, decreased hyperplastic lesions, and blocked tumor progression from premalignant to a malignant stage. Our data showed that the strategy to block the androgenic and PI3K/AKT/mTOR pathway is an effective therapeutic option and should be investigated including distinct PI3K pathway inhibitors.
- |||||||||| metformin / generics
Journal: Role of Metformin and AKT Axis Modulation in the Reversion of Hypoxia Induced TMZ-Resistance in Glioma Cells. (Pubmed Central) - Jun 21, 2019 Nevertheless, the administration of the dual PI3K/mTOR inhibitor BEZ235 potentiated the effect of TMZ plus MET on cell viability, inducing a pro-apoptotic phenotype during hypoxic condition also in T98 cells, suggesting the block of the PI3K/AKT/mTOR pathway as a complementary target to further overcome GBM resistance during hypoxia. In conclusion, we proposed TMZ plus MET as suitable treatment to revert TMZ-resistance also during hypoxia, an effect potentiated by the inhibition of PI3K/mTOR axis.
- |||||||||| dactolisib (RTB101) / Novartis, PureTech
Journal, Cancer stem cells, PD(L)-1 Biomarker, IO Biomarker: Insluin and epithelial growth factor (EGF) promote programmed death ligand 1(PD-L1) production and transport in colon cancer stem cells. (Pubmed Central) - Jun 15, 2019 Our findings reveal that PIK3CA mutations have a key role in the pathogenesis of VM and PIK3CA-driven experimental lesions can be effectively treated by PI3K/mTOR inhibitors. Apart from the essential roles in metabolism and stemness, insulin and EGF involve in up-regulation of PD-L1 expression in colon CSCs, therefore the inhibition of insulin and EGF/EGFR pathways can be considered for cancer immunotherapy or combined with PD-1/PD-L1 antibody-based cancer immunotherapy to eliminate CSCs.
- |||||||||| Xalkori (crizotinib) / Pfizer, dactolisib (RTB101) / Novartis, PureTech
Preclinical, Journal: Prolonged MEK inhibition leads to acquired resistance and increased invasiveness in KRAS mutant gastric cancer. (Pubmed Central) - May 22, 2019 We also showed that migration and invasion of resistant cells were promoted, and crizotinib and BEZ235 could inhibit this malignant phenotype. Overall, our results indicate that prolonged MAPK pathway inhibition could result in acquired resistance which is associated with increased malignant phenotype in KRAS mutant GC and pharmacological targeting c-MET and PI3K/mTOR could overcome this problem.
- |||||||||| Odomzo (sonidegib) / Sun Pharma, dactolisib (RTB101) / Novartis, PureTech
Journal, PARP Biomarker, IO Biomarker: Inhibition of sonic hedgehog and PI3K/Akt/mTOR pathways cooperate in suppressing survival, self-renewal and tumorigenic potential of glioblastoma-initiating cells. (Pubmed Central) - Apr 20, 2019 Finally, the combination of NVP-LDE-225 and NVP-BEZ-235 was superior in inhibiting tumor growth, regulating the expression of pluripotency promoting factors, stem cell markers, cell cycle, and cell proliferation, and modulating EMT compared to single agent alone. In conclusion, the combined inhibition of PI3K/Akt/mTOR and SHH pathways was superior to single pathway inhibition in suppressing glioblastoma growth by targeting GICs.
- |||||||||| dactolisib (RTB101) / Adicet Bio
Journal: Heat Stress and Hepatic Laser Thermal Ablation Induce Hepatocellular Carcinoma Growth: Role of PI3K/mTOR/AKT Signaling. (Pubmed Central) - Sep 12, 2018 Experiments were repeated with rats randomly assigned to receive either the adjuvant phosphoinositide 3-kinase (PI3K)/mammalian target of rapamycin (mTOR) inhibitor (NVP-BEZ235) or the vehicle control...Moderate heat stress induced expression of growth factors in HCC cells and hepatocytes, including heparin-binding growth factor, fibroblast growth factor 21, and nerve growth factor (range, 2.9-66.9-fold; P < .05). Conclusion Moderate heat stress and laser thermal ablation induce hepatocellular carcinoma growth, which is prevented with adjuvant PI3K/mTOR/protein kinase B inhibition.
- |||||||||| AZD8055 / AstraZeneca, Erbitux (cetuximab) / Eli Lilly, EMD Serono, dactolisib (RTB101) / Adicet Bio
Biomarker, Journal: Co-targeting mTORC and EGFR signaling as a therapeutic strategy in HNSCC. (Pubmed Central) - Mar 30, 2018 While single agent therapy was largely ineffective in vivo, improved response of combination treatment in an array of PDXs suggests the potential for adding a catalytic mTORC inhibitor to cetuximab therapy. Overall, these results add to a growing body of evidence suggesting approaches that attempt to match biomarkersin HNSCC remains complex and challenging.
- |||||||||| dactolisib (RTB101) / Adicet Bio
Phase classification, Enrollment change, Trial termination, Trial primary completion date, Metastases: Safety Study of BEZ235 With Everolimus in Subjects With Advanced Solid Tumors (clinicaltrials.gov) - Aug 23, 2017 P1b, N=19, Terminated, BEZ235 twice daily resulted in significant toxicity without objective responses; further development of this compound will not be pursued in this disease. Phase classification: P1/2 --> P1b | N=54 --> 19 | Recruiting --> Terminated | Trial primary completion date: Dec 2014 --> Feb 2014; funding
|