Chris De Savi

Woomera Therapeutics — United States

Biochemistry, Genetics and Molecular Biology · Life Sciences

19h-index1.6kcitations77works1.52yr avg
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Research Topics

Estrogen and related hormone effects(22), Cancer-related Molecular Pathways(9), Carbohydrate Chemistry and Synthesis(8), Cancer therapeutics and mechanisms(8), Synthetic Organic Chemistry Methods(6)

Publications76 total

Targeted degradation of MK2 is insufficient to block inflammatory cytokine production in human cells due to cooperativity with MK3 and MK5
Frontiers in Immunology·2026Open Access
Evaluation of STK17B as a cancer immunotherapy target utilizing highly potent and selective small molecule inhibitors
Frontiers in Immunology·2024· 3 citedOpen Access
Supplementary Methods from AZD9496: An Oral Estrogen Receptor Inhibitor That Blocks the Growth of ER-Positive and <i>ESR1</i>-Mutant Breast Tumors in Preclinical Models
2023Open Access
Data from AZD9496: An Oral Estrogen Receptor Inhibitor That Blocks the Growth of ER-Positive and <i>ESR1</i>-Mutant Breast Tumors in Preclinical Models
2023Open Access
Supplementary Figure Legends from AZD9496: An Oral Estrogen Receptor Inhibitor That Blocks the Growth of ER-Positive and <i>ESR1</i>-Mutant Breast Tumors in Preclinical Models
2023Open Access
Supplementary Methods from AZD9496: An Oral Estrogen Receptor Inhibitor That Blocks the Growth of ER-Positive and <i>ESR1</i>-Mutant Breast Tumors in Preclinical Models
2023Open Access
Supplementary Figure Legends from AZD9496: An Oral Estrogen Receptor Inhibitor That Blocks the Growth of ER-Positive and <i>ESR1</i>-Mutant Breast Tumors in Preclinical Models
2023Open Access
Supplementary Tables and Legends from AZD9496: An Oral Estrogen Receptor Inhibitor That Blocks the Growth of ER-Positive and <i>ESR1</i>-Mutant Breast Tumors in Preclinical Models
2023Open Access
Supplementary Figures from AZD9496: An Oral Estrogen Receptor Inhibitor That Blocks the Growth of ER-Positive and <i>ESR1</i>-Mutant Breast Tumors in Preclinical Models
2023Open Access
Supplementary Tables and Legends from AZD9496: An Oral Estrogen Receptor Inhibitor That Blocks the Growth of ER-Positive and <i>ESR1</i>-Mutant Breast Tumors in Preclinical Models
2023Open Access
Data from AZD9496: An Oral Estrogen Receptor Inhibitor That Blocks the Growth of ER-Positive and <i>ESR1</i>-Mutant Breast Tumors in Preclinical Models
2023Open Access
Supplementary Figures from AZD9496: An Oral Estrogen Receptor Inhibitor That Blocks the Growth of ER-Positive and <i>ESR1</i>-Mutant Breast Tumors in Preclinical Models
2023Open Access
Discovery of BLU-945, a Reversible, Potent, and Wild-Type-Sparing Next-Generation EGFR Mutant Inhibitor for Treatment-Resistant Non-Small-Cell Lung Cancer
Journal of Medicinal Chemistry·2022· 147 citedOpen Access
Abstract 2924: Target identification, selectivity profiling and mechanistic insights of a Cdk9 inhibitor using complementary proteomics methods
Cancer Research·2022
Phase 1 study of KT-333, a targeted protein degrader, in patients with relapsed or refractory lymphomas, large granular lymphocytic leukemia, and solid tumors.
Journal of Clinical Oncology·2022· 21 cited
STAT3 degraders inhibit cellular activation, cytokine production, and Th17 development, resulting in inhibition of autoimmunity in the MOG-EAE model of CNS inflammation.
The Journal of Immunology·2022· 1 cited
Mechanistic Insights into a CDK9 Inhibitor Via Orthogonal Proteomics Methods
ACS Chemical Biology·2021· 13 citedOpen Access
603 Targeted STAT3 degradation leads to remodeling of an immunosuppressive tumor microenvironment and subsequent sensitization to immune checkpoint therapy
Regular and Young Investigator Award Abstracts·2021Open Access
Discovery of a Series of 7-Azaindoles as Potent and Highly Selective CDK9 Inhibitors for Transient Target Engagement
Journal of Medicinal Chemistry·2021· 22 citedOpen Access
Discovery of AZD4573, a Potent and Selective Inhibitor of CDK9 That Enables Short Duration of Target Engagement for the Treatment of Hematological Malignancies
Journal of Medicinal Chemistry·2020· 98 citedOpen Access
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Frequent Co-authors

Craig S. Donald(9), Hazel M. Weir(8), Robert H. Bradbury(8), Rowena Callis(8), Jon Curwen(8), Richard A. Norman(8), Zena Wilson(8), Celina M. D’Cruz(8), Mandy Lawson(7), Alfred A. Rabow(7), David Buttar(7), Peter Ballard(7), Galith Karoutchi(7), Philip A. MacFaul(7), Michael Tonge(7), Graeme E. Walker(7), Rachel Rowlinson(6), Steve Powell(6), Graham H.P. Richmond(6), Brendon Ladd(6)