Yes, mice would have it made if it wasn't for ending up in out labs getting various cancers. But so much works for them but never seems to work out for us. But no telling how many years, if ever, until this will be checked out in humans in the old RCT. Here is, I think, the actual study:/www.ncbi.nlm.nih.gov/pubmed/26649526
Antioxid Redox Signal. 2016 Apr 10;24(11):575-89. doi: 10.1089/ars.2015.6418. Epub 2016 Jan 26.
Nimbolide-Induced Oxidative Stress Abrogates STAT3 Signaling Cascade and Inhibits Tumor Growth in Transgenic Adenocarcinoma of Mouse Prostate Model.
Zhang J1, Ahn KS2, Kim C2, Shanmugam MK1, Siveen KS1, Arfuso F3, Samym RP4,5,6, Deivasigamanim A7, Lim LH6, Wang L1,8, Goh BC1,8, Kumar AP1,8,9,10, Hui KM7, Sethi G1,9.
Prostate cancer (PCa) is one of the most commonly diagnosed cancers worldwide. Currently available therapies for metastatic PCa are only marginally effective, hence novel treatment modalities are urgently required. Considerable evidence(s) suggest that deregulated activation of oncogenic transcription factor, signal transducer and activator of transcription 3 (STAT3) plays a pivotal role in the development and progression of PCa. Thus, agents that can abrogate STAT3 activation could form the basis of novel therapy for PCa patients. In the present study, we analyzed whether the potential anticancer effects of nimbolide (NL), a limonoid triterpene derived from Azadirachta indica, against PCa cell lines and transgenic adenocarcinoma of mouse prostate (TRAMP) model are mediated through the negative regulation of STAT3 pathway.
Data from the in vitro studies indicated that NL could significantly inhibit cell viability, induce apoptosis, and suppress cellular invasion and migration. Interestingly, NL also abrogated STAT3 activation and this effect was found to be mediated via an increased production of reactive oxygen species (ROS) due to GSH/GSSG imbalance. Oral administration of NL significantly suppressed the tumor growth and metastasis in TRAMP mouse model without exhibiting any significant adverse effects.
The present study demonstrates the critical role of GSH/GSSG imbalance-mediated ROS production contributing to the STAT3 inhibitory and tumor-suppressive effect of NL in PCa.
Overall, our findings indicate that NL exhibits significant anticancer effects in PCa that may be primarily mediated through the ROS-regulated inhibition of STAT3 signaling cascade.