Monday, January 27, 2020 6:30:55 AM
Science of drugs doesnt happen overnight
Everyone should Know what they own here!
January 21, 2020[color=red][/color]
https://link.springer.com/article/10.1007/s12015-019-09942-y
Conventional chemo-radiotherapies are not effective against quiescent, slowly (or non-) dividing CSCs, thereby become resistant and subsequently repopulate the tumour [112]. Interestingly, it was found that a compound named thapsigargin targets highly plastic CSCs in a proliferation independent fashion and can thus effectively target quiescent cells [113, 114]. However, thapsigargin is not selective for cancer cells, but recent efforts to modify it as a tumour-targeted pro-drug have greatly improved the specificity profile and undergoing phase II trials (NCT01056029) [115].
Update on Clinical Trial NCT01056029 - April 26th, 2016[color=red][/color]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4984914/
Update on Clinical Trial NCT01777594 - June 17, 2019[color=red][/color]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627768/
Conclusions:
In conclusion, mipsagargin is a first-in-class PSMA-targeted prodrug that may be an effective therapeutic strategy in patients with HCC, a disease characterized as highly vascularized. Infusion of 40 mg/m2 mipsagargin over a 1-hour period on Days 1, 2 and 3 of 28-day cycles was relatively well tolerated and resulted in disease stabilization, decreased tumor blood flow as observed by decrease Ktrans, and prolonged TTP in a population of patients who had progressed on prior treatment with sorafenib. These observations importantly suggest that mipsagargin may have clinical activity in HCC, including in the population of patients with advanced, refractory HCC. In this study, exploratory analyses suggested that mipsagargin decreased blood flow in HCC lesions and in metastatic sites relative to baseline examination within two cycles of exposure to mipsagargin. These findings warrant a larger clinical study to further characterize the activity of mipsagargin in advanced HCC.
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