Technology ID
TAB-4524
LZK and DLK Inhibitors to Target LZK and Suppress MYC Expression, Inhibit AKT Activation, and Promote Cancer Cell Death and Tumor Regression
E-Numbers
E-196-2020-0
Lead Inventor
Brognard, John (National Cancer Institute (NCI))
Co-Inventors
Swenson, Rolf (NHLBI)
Funk, Amy (NCI)
Hitko, Carolyn (NHLBI)
Nyswaner, Katherine (NCI)
Applications
Therapeutics
Research Materials
Therapeutic Areas
Oncology
Development Stages
Pre-Clinical (in vitro)
Lead IC
NHLBI
ICs
NHLBI
NCI
This technology includes the use of LZK and DLK inhibitors to be used for the treatment of head and neck squamous cell carcinoma (HNSCC) or lung squamous cell carcinoma (LSCC). Specifically, we demonstrate that inhibitors that can be repurposed to target LZK suppresses LZK kinase-dependent stabilization of MYC and activation of the PI3K/AKT pathway. In vivo preclinical cell line xenograft mouse model demonstrates that targeting LZK will suppress tumor growth. We also demonstrate that several additional compounds potently inhibit LZK and could serve as new therapeutic modalities.
Commercial Applications
LZK inhibitors that serve as lead compounds could lead to new therapies for the treatment of LSCC and HNSCC and other cancers with amplified LZK that include prostate, ovarian and small cell lung cancer.
Competitive Advantages
We have discovered LZK as a novel therapeutic target in squamous cell carcinomas with amplified LZK; over 50% of HNSCC and LSCC patients have amplifications or gains in LZK.
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