MaSi auf Twitter hat folgende (pessimistische) These zu AFMDs ICE aufgestellt:
A tetravalent bispecific is much better then a bivalent bispecific.
But a proper executed, linked mAB has on the NK-linkage site a covalent bond, which will outcompete any noncovalent interaction.
On the antigen binding side, the mAB still has 2 valencies = identical to an ICE.
The benefit of $afmd ICE is the flexibility to:
1) apply ICE only, as long as patient NKs (or T-cells) are not exhausted, or
2) provide precomplexed effector cells if needed.
Auf eine Antwort hat er folgendes ergänzt:
mAB-NK bond mentioned here, is only via affinity (CD16a/Fc), which is weaker then the tetravalent{avidity}-bispecific ICE (CD16a/Fab) bond which itself is weaker as a covalent mAB-NK bond. Only equivalent to covalent is the "CAR-NK". AFMD "claim to fame" is equivalency to CAR-NK.
If ICE most of the time does the job without effector cell adding needed = perfect scenario for $AFMD.
If we will need in each case precomplexed effector cells, the competitive advantage will lean towards the suppliers of covalently linked mAB-effector cells.
Frage:
Weißt Du was Masi meint, und wie lautet deine Einschätzung?
Vielen Dank!
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