EPDeg™ bioPROTAC is composed of a target binder (nanobody) and a modified E3 protein as a form of direct fusion protein between the two, providing the following advantages.
EPDeg™ vs. | Main advantage of EPDeg™ bioPROTAC(proved by data) |
---|---|
PROTAC |
Possible to degrade novel targets that cannot be degraded by small-molecule based PROTAC at this moment & There is no need to have the linker used in PROTAC synthesis → We proved that EPDeg™ bioPROTAC can potently degrade currently intractable targets by PROTAC (ex. SOX2, ATXN1) |
Possible to show higher potency by utilizing new E3 ligases that cannot be recruited by small molecule E3 ligands at this moment → We proved that EPDeg™ bioPROTAC can have much higher potency than PROTAC for the same target (ex. STAT3) |
|
siRNA / ASO | Much higher level of down-regulation and much faster therapeutic effects were observed with the use of EPDeg™ bioPROTAC |
Other bioPROTACs | Possible to improve TPD efficiency by using EPD’s own engineered E3 proteins We proved substantially enhanced STAT3 degradation when one of engineered E3s was used to generate EPDeg™ |
siRNA / shRNA | bioPROTAC | |
---|---|---|
Target selectivity | Off-target knock down often reported (2D sequence-based selectivity) | Potentially lower off-target effect (3D structure-based selectivity) |
Subpopulation specific effect | Subpopulation specific knock down possible |
Subpopulation specific degradation possible
|
Kinetics | Impossible to degrade target protein that was already created before drug injection. If the protein has a long half-life and is stable, it may take a long time for the drug effect to be observed. |
Able to degrade target proteins that have already been generated before drug injection. The drug effect can be expected in a faster time. |
Applicability to aggregated proteins | Not applicable to insoluble protein aggregates observed in degenerative brain diseases | Applicable to insoluble protein aggregates |