1. EED as a promising therapeutic target
(1) Dysregulations in polycomb repressive complex 2 (PRC2) have been found in a number of human cancers. PRC2 compromises four components, EED is a critical component of PRC2 complex and mediates allosteric activation of EZH2 by H3K27me3.
(2) EED inhibitor might overcome the long-term resistance of EZH2 inhibitors
- EED inhibition manifests comparable effects of EZH2 inhibition
- EED inhibition is not affected by EZH2 acquired resistant mutations
- EED inhibition also has an effect on EZH1, which has comparable function as EZH2, and maybe compensatively up-regulation while EZH2 inhibition
(3) EED inhibitor has the potential to treat advanced malignancies for whom no effective standard treatment is available.
(4) PRC2 inhibition profoundly modulates immune system, especially in T cell and tumor microenvironment, which provides strong rationale for combination trials with other immuno-therapies for blood cancer and solid tumor.
(5) EZH2 inhibitors face the risk of secondary toxicity, EED inhibitor could be a substitutional option for patients
2. A novel EED inhibitor with favorable features
(1) Asset vs MAK683
- Better drug-like properties (solubility, free plasma concentration)
- Better PK profiles (exposure) across species
- Comparable efficacy of tumor regression
- Potential better tolerability in toxicological study
(2) Asset vs EPZ6438
- Shows activity on EZH2-inhibitor Resistant Cell line
- Better efficacy of tumor regression
(3) Asset exhibits excellent efficacy in vivo: strong and complete tumor regression at 10 mpk BID on Karpas422 CDX model, with TGI 98.4%
MAK683 is an investigational EED inhibitor developed by Novartis
EPZ6438 is an approved first-in-class EZH2 inhibitor developed by Epizyme
1. Asset type: ActRIIB inhibitor
2. Indication: Cancer cachexia
3. Modality:Small molecule
5. Demands： License-out or co-development
IND approved by FDA and NMPA
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