$PPHM SKing/1-18-16 explains PPHM's PS-Targeting
Post# of 7017
Posted On: 02/08/2016 8:05:55 PM
$PPHM SKing/1-18-16 explains PPHM's PS-Targeting advantage vs. the
“individual-receptors” PS-binding approach of others, like: Axl MerTIM-3 RAGE Tyro3 GAS6 CD300a BAI1 MFG-E8 etc etc. (maybe why Dr. Raymond Birge is spending lots of time with Dr.Brekken & Peregrine these days?? => http://tinyurl.com/j3whbx3 )
CEO S.King/1-18-16/NobleConf Slide11 7:54: “It turns out that the PS receptors are very well studied, and a number of companies are going after the individual receptors [ex: Axl Mer TIM-3 RAGE Tyro3 GAS6 CD300a BAI1 MFG-E8...], depicted on Slide11 as the little pacman symbols. But, the bottom-line is that other companies are going after the individual receptors – our approach is to go after the ligand itself, PS (phosphatidylserine). So, effectively by blocking PS with a good safety profile, we're now able to affect the entire PS-signaling pathway, and we think that's a real advantage over other approaches, since basically we can simultaneously impact the ability of PS to shutdown the immune system.”
1-18-16: CEO Steve King's 1-18-16 presentation at Noble-Financial's Investor Conf. (21min replay, 31 slides) http://tinyurl.com/j9dkekm
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I ASKED A SCIENTIST FRIEND TO EXPLAIN THIS FURTHER – HIS 1-28-16 REPLY:
“Look at SK's Slide11 at Noble/1-18-16. The apoptotic or tumor cells, also the blood vessel cells of tumors, have PS expressed on their surface, this is the ligand. All those other cells, macrophages, dentritic cells etc, have receptors that bind the ligand (PS) on their surface. So if you have an antibody (bavi) which binds to PS it blocks the binding of PS with ANY of those receptors on the cells on which those receptors are expressed. The alternative is to develop antibodies which bind to each of those receptors, so you would need to develop a lot of different antibodies to accomplish the same result, i.e. blocking the ligation (binding) of PS to all the receptors. This is also true for receptors that don't bind to PS directly. For example, the receptor MerTK binds to the protein Gas6 (its ligand), not to PS, but Gas6 in turn binds with PS on apoptotic cells. So you can block the activation of MerTK by blocking PS with bavi so that Gas6 can't bind to PS and complete the chain with MerTK.”
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BY MASSHYSTERIA 1-29-16 IHUB #250754
“...evidence is strongly mounting support your comments from complimentary sources. In a type of concurrence with importance of PS blockade - except across its receptors on the T-Cell side of things. Many are aware that TIM-3 & LAG-3 are 2 of several checkpoints that bind to PS. Not sure how many are aware that the rate of clinical trials evaluating these two checkpoint inhibitors is rising, and that multiple smaller scale trials are showing great results using that combo. That is driving the greater investment and expansion of trials. Why is that a good thing? All these combo trials are conducted by large pharma companies who are seeing supporting signals to increase investment. Peregrine holds the molecule that achieves the complimentary results (blocking at PS site) holistically and without having to chase a multitude of checkpoints that bind to PS to stop/reduce immune response. BP's excitement about TIM-3 and LAG-3 should be a very good cause for upbeat expectations from bavituximab, and a likely reason that world-class institutions and AZN are in the game. The beauty is having a single solution that blocks PS, vs. possibly dozens that block the several other T-Cell checkpoints with which it binds. Commercially, clinically and logistically, there is no better winner in this competition if one can do the work of many. Provided this mechanism works and is shown to do what so many diverse professionals seem to be suggesting - its becoming a game of timing and finesse. The more good news I hear from Industry on TIM-3 & LAG-3, the happier I get. Definitely happier now than 12mos ago.”
“individual-receptors” PS-binding approach of others, like: Axl MerTIM-3 RAGE Tyro3 GAS6 CD300a BAI1 MFG-E8 etc etc. (maybe why Dr. Raymond Birge is spending lots of time with Dr.Brekken & Peregrine these days?? => http://tinyurl.com/j3whbx3 )
CEO S.King/1-18-16/NobleConf Slide11 7:54: “It turns out that the PS receptors are very well studied, and a number of companies are going after the individual receptors [ex: Axl Mer TIM-3 RAGE Tyro3 GAS6 CD300a BAI1 MFG-E8...], depicted on Slide11 as the little pacman symbols. But, the bottom-line is that other companies are going after the individual receptors – our approach is to go after the ligand itself, PS (phosphatidylserine). So, effectively by blocking PS with a good safety profile, we're now able to affect the entire PS-signaling pathway, and we think that's a real advantage over other approaches, since basically we can simultaneously impact the ability of PS to shutdown the immune system.”
1-18-16: CEO Steve King's 1-18-16 presentation at Noble-Financial's Investor Conf. (21min replay, 31 slides) http://tinyurl.com/j9dkekm
- - - - - - - - - - - - - - - - - - - -
I ASKED A SCIENTIST FRIEND TO EXPLAIN THIS FURTHER – HIS 1-28-16 REPLY:
“Look at SK's Slide11 at Noble/1-18-16. The apoptotic or tumor cells, also the blood vessel cells of tumors, have PS expressed on their surface, this is the ligand. All those other cells, macrophages, dentritic cells etc, have receptors that bind the ligand (PS) on their surface. So if you have an antibody (bavi) which binds to PS it blocks the binding of PS with ANY of those receptors on the cells on which those receptors are expressed. The alternative is to develop antibodies which bind to each of those receptors, so you would need to develop a lot of different antibodies to accomplish the same result, i.e. blocking the ligation (binding) of PS to all the receptors. This is also true for receptors that don't bind to PS directly. For example, the receptor MerTK binds to the protein Gas6 (its ligand), not to PS, but Gas6 in turn binds with PS on apoptotic cells. So you can block the activation of MerTK by blocking PS with bavi so that Gas6 can't bind to PS and complete the chain with MerTK.”
- - - - - - - - - - - - - - - - - - - -
BY MASSHYSTERIA 1-29-16 IHUB #250754
“...evidence is strongly mounting support your comments from complimentary sources. In a type of concurrence with importance of PS blockade - except across its receptors on the T-Cell side of things. Many are aware that TIM-3 & LAG-3 are 2 of several checkpoints that bind to PS. Not sure how many are aware that the rate of clinical trials evaluating these two checkpoint inhibitors is rising, and that multiple smaller scale trials are showing great results using that combo. That is driving the greater investment and expansion of trials. Why is that a good thing? All these combo trials are conducted by large pharma companies who are seeing supporting signals to increase investment. Peregrine holds the molecule that achieves the complimentary results (blocking at PS site) holistically and without having to chase a multitude of checkpoints that bind to PS to stop/reduce immune response. BP's excitement about TIM-3 and LAG-3 should be a very good cause for upbeat expectations from bavituximab, and a likely reason that world-class institutions and AZN are in the game. The beauty is having a single solution that blocks PS, vs. possibly dozens that block the several other T-Cell checkpoints with which it binds. Commercially, clinically and logistically, there is no better winner in this competition if one can do the work of many. Provided this mechanism works and is shown to do what so many diverse professionals seem to be suggesting - its becoming a game of timing and finesse. The more good news I hear from Industry on TIM-3 & LAG-3, the happier I get. Definitely happier now than 12mos ago.”
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