RE:RE:RE:RE:RE:RE:RE:AACR - late breaking absracts text posted by noon todayThis is the problem with both the NASH program and TH1902. In both cases, they have proof something does what you think you would want, but in both cases, they cannot prove it. There is no intrerest. It's all inferred with 10 years of HIV people using the drug and 10 years of safety data which seems to also show results that 'may' point to it being good for NASH. However that programm cannot find a partner to move ahead. In the case of TH1902, where it 'may' be working to make a cold tumor a hot tumor, but they do not know if or how. And are they on the path today to prove how, or are they on the path to show results, but will not know how anyhow? So to summarize that, we have two nice programs without anything investors or partners that can sink their teeth into either one. With NASH, we cannot connect the dots. With TH1902, we cannot connect the dots. NASH has been 4 years of trying to connect the dots, without ever really trying the way it's needed to prove it up.
Wino115 wrote: I think it may be far more likely with someone trying to both get in to the anti PD-L1 market with their drug and to take some market share away or differentiating themselves in the market versus the Mercks and BMS's. Given the number of big/mid/small firms chasing the immunotherapy jaugernauts, it may make more sense.
I totally agree successful monotherapy results for TH1902 would help immeasurably, but it may not completely shut down a trial that would be an offshot. I guess what they are hinting at in the paper is that their peptide seems to be able to deliver into the cell, not stay on the surface where the PD-L1 hides the cancer cell from the immune system thus making it not susceptible, or cold. We know docetaxel may not be the best toxin in it all, but it may be the delivery mechanism purely that is opening up the tumor cell to all the sudden be suceptible. I really don't know enough at all about it, but my layman's reading is they combined these two drugs and found t-cells, immune system cells and readings inside these tumors that they know could not be penetrated with just the anti PD-L1 drug. So they're just concluding that someone TH1902 in the mix either took down the defenses of the cold tumor cells or got around the disguise it puts on so immunce cells walk past it. Somehow those t-cells got in there to fight that tumor and the only difference was the PDC was also used.
It could be what you are saying - saturating sort1 receptors -- or any number of other things. They can't point to an MOA yet it seems and only state that somehow they are "modulating" the ability for the immune cells to get in there somehow. It's definitely interesting and you'd think someone wanting in would follow up on it to further the understanding of the MOA. At least that's my hope prior to actually seeing the numbers which could change it depending on their strength.