Replies to post #76121 on Avid Bioservices Inc (CDMO)

[freethemice]

This is exactly why I made the comment that I think Bavi + chemo will work
even better, relative to the second-line chemo, than Bavi + chemo will work
relative to the front-line chemo.
Which would imply that Bavi should go after all the second-line SOC treatments,
like in CRPC.

[entdoc]

RRdog, I'm not certain paclitaxel and carboplatin, being anti-mitotic, i.e inhibitory to rapid cellular division, are necessarily "somewhat apoptotic,"as you assert, but maybe. Don't remember seeing that in the package insert anyway. It is such a shame Bavi must be used with such losers as pacli- and carbo-, and oxy and toxi, because Bavi's "uregulation of the immune system" consists, in part, of goading the body to rapidly reproduce specialized immune-system cells, monocytes (body garbage collectors). Unfortunately the anti-mitotic chemotherapeutic agents the decrease cellular production probably have a "down-regulatory" effect on Bavi mechanism of action. I think I have seen that dilemma in print, and posted it here a few weeks ago.
The end of the Bavi narrative imo is that, in some iteration, Bavi will almost certainly be used to upregulate the immune system--Bavi-in-your-tea, or a Bavi nasal spray--aimed at micro-sepsis and micro-tumors. Chimeric Bavi is already last year's flavor (compared to Affitech's all-human Bavi). And our naked and chimeric Bavi isn't even through trials yet. I repeat. What a monstrous mistake Bavi trials did not commence with Bavi + irradiation therapy, or surgery. Now THERE you've got sumpin'!

[Thurly]

The question to me is, is there a particularly good synergistic effect when bavi and docetaxel are used in combo? Or does that combo efficacy specific to breast cancer? New trial data from the NSCLC and CRPC trials will tell us a lot about that.

2005 Abstract
http://cancerres.aacrjournals.org/content/65/10/4408.abstract
In the present study, we tested the hypothesis that docetaxel, which is known to have antivascular effects on tumors, might induce exposure of anionic phospholipids on tumor vasculature and, thus, enhance the antitumor activity of 3G4. Treatment of human umbilical vascular endothelial cells with subtoxic concentrations of docetaxel (20 pmol/L) in vitro caused anionic phospholipids to be externalized without inducing apoptosis. Docetaxel treatment of mice increased the percentage of tumor vessels that expose anionic phospholipids from 35% to 60%. No induction of phosphatidylserine was observed on vessels in normal tissues even after systemic treatment with docetaxel. Treatment of mice bearing orthotopic MDA-MB-435 human breast tumors with 3G4 plus docetaxel inhibited tumor growth by 93%. Treatment of mice bearing disseminated MDA-MB-435 tumors with 3G4 plus docetaxel reduced the average number of tumor colonies in the lungs by 93% and half the animals did not develop tumors.

Considering the later PII ABC trial results, (http://www.marketwire.com/press-release/new-progression-free-survival-data-from-peregrines-bavituximab-phase-ii-refractory-breast-nasdaq-pphm-1267852.htm) combo therapy with docetaxel looks like a protocol that merits further study with other tumor types.

Two trials testing bavi/docetaxel combos are listed on clinicaltrials.gov: 2nd line NSCLC and CRPC.