Replies to post #135164 on Biotech Values

[mcbio]

As for provenge, the earlier papers by Vuk-Pavlovic showed very weak T cell responses. And as we know, the response was largely against the fusion point of the constructed peptide cassette. I won't deny that provenge has demonstrated some efficacy, but I think we can agree that the mechanism through which that efficacy is manifest depends on a pathway very different than rindo.

Any comments on Bavarian Nordic's potentially improved Provenge? See: http://investorshub.advfn.com/boards/read_msg.aspx?message_id=38279562 .

[BTH]

Rindopepimut is simply a 13 amino acid peptide attached to a carrier protein (KLH in this case). So the body has to ramp up an immune response against this peptide. This has historically been a relatively failing proposition in producing an adaptive immune response: you get low titre B-cell derived antigen specific antibodies and a weak T cell response. This is very similar to BLP25.

Is there any way these two drugs you mention are doing something to the tumor, despite not ramping a very strong T cell response?

[iwfal]

CLDX -

Rindopepimut is simply a 13 amino acid peptide attached to a carrier protein (KLH in this case). So the body has to ramp up an immune response against this peptide. This has historically been a relatively failing proposition in producing an adaptive immune response: you get low titre B-cell derived antigen specific antibodies and a weak T cell response. This is very similar to BLP25.

Thanks for the discussion. Comments back: One key difference is that Rind is attempting to stimulate immune response to a mutated peptide (vs, for instance, BLP25 which is against wild-type MUC1). It should be much easier to excite an immune response against a non-wild type peptide.

Also note that I find the clearance rate of the EGFRviii at disease recurrence to be interesting. (I'd consider it to be much more than interesting if I fully trusted the company)

All that said I'd agree that any immunotherapy enough different from the two primary proven ones should be treated with substantial skepticism proportionate to their distance from the proven immunotherapies.

I won't deny that provenge has demonstrated some efficacy, but I think we can agree that the mechanism through which that efficacy is manifest depends on a pathway very different than rindo.

My comment is that it is not clear to me that we understand what arm(s) of the immune system are responsible of efficacious immunotherapy vs cancers.