Anyone,
Last week, while the family had gotten together for vacation, I showed my sister Xoma's most recent annual report. My sister does microbiology type stuff (high throughput drug screening) for Proctor and Gamble in Cincinnati. She asked me some questions that I couldn't answer.
How, exactly, does Nueprex, by binding to LPS, "neutralize" the toxic effects of LPS that's loose in the bloodstream? Just because LPS has something attached to it, doesn't necessarily mean it changes it's molecular biology to be non-toxic.
How, exactly, does Nueprex, by binding to LPS, "facilitate" the clearance of the combined molecules from the bloodstream?
Since LPS only exist on gram-negative bacteria, why aren't the clinic trials beyond meningococcemia, designed for indications that known to be caused by gram-negative pathogens? Especially since most infections contracted in the hospital are gram-positive.
The report showed a nice electron microscope picture of rBPI21 attached to some bacteria and a nice diagram that showed rBPI21 in conjuction with antibiotics killing a bacterium. Wouldn't an electron microscope picture of a dying bacteria covered with rBPI21 be a more powerful illustration of rBPI21's effectiveness? Does the lack of such a picture mean that one doesn't exist, thereby casting doubt on the statements that say that it does?
My sister will be asking her colleagues about rBPI21. When she gets back to me on their insights, I'll pass them along here.
Ed. |
