Research findings of MYC/GSPT1 protein degrader GT19630 have been published in Blood, a top international journal in hematology
Release time：2026-08-24 17:14
Suzhou, 24 August, 2026-Kintor Pharmaceutical Limited (“Kintor Pharma”, HKEX: 9939), announced that a collaborative research paper with The University of Texas MD Anderson Cancer Center was published on August 17, 2026, in Blood, a premier journal in the field of international hematology. The findings demonstrate that GT19630, a novel MYC/GSPT1 degrader independently developed by Kintor, offers a promising therapeutic strategy for MYC-driven hematological malignancies.
The Blood is the official journal of the American Society of Hematology and the most authoritative premier journal in the field of hematology, providing an international forum for the publication of original articles describing basic, translational, and clinical research in hematology.
Research Background
c-Myc is a critical oncogenic transcription factor that plays a pivotal role in tumorigenesis, cancer cell survival, proliferation and immune evasion. As an intrinsically disordered protein (IDP), c-Myc lacks a defined binding pocket for small-molecule inhibitors, rendering it a historically "undruggable" target. To date, strategies directly targeting c-Myc or its regulatory pathways have not achieved clinical breakthroughs, and substantial unmet medical needs remain.
In recent years, targeted protein degradation (TPD) has emerged as a high interest area in drug discovery, providing novel intervention paradigms for "undruggable" targets. This technology enables the degradation of disease-causing proteins, addressing challenges that conventional small molecules or biologics cannot overcome. GT19630 is a novel dual protein degrader independently developed by Kintor Pharma, capable of simultaneously degrading c-Myc and GSPT1, and is currently in the preclinical research stage.
Mechanism of Action
GT19630 disrupts a novel feedforward loop of MYC and GSPT1, where MYC promotes transcription of GSPT1, and GSPT1 senses the stop codon of MYC to properly terminate its translation. The agent induces integrated stress response and abrogates oxidative phosphorylation through inhibition of the TCA cycle, resulting in apoptosis.
Superior Molecular Activity
Compared with other GSPT1-targeting molecular glue degraders, GT19630 has superior activity. GT19630 induces profound anti-proliferative effects and apoptosis at low nanomolar concentrations in a multitude of leukemia and lymphoma cell lines and primary samples, including those with TP53 mutations.
In Vivo Antitumor Efficacy
GT19630 is highly active in vivo in models of therapy-resistant hematologic malignancies, including Burkitt's lymphoma, acute myeloid leukemia (AML) and multiple myeloma.
Selectivity
CD34+ AML blasts overexpress MYC protein compared to normal hematopoietic stem/progenitor cells (HSPCs) and GT19630 induces greater cytotoxicity in AML cells compared to normal HSPCs.
Overcoming Drug Resistance
GT19630 restores sensitivity to venetoclax and profoundly prolongs survival in vivo in venetoclax-resistant AML.
Safety Profile
GT19630 was well tolerated in humanized CRBN mice.
In conclusion, these data strongly support GT19630 as a differentiated drug candidate with the potential to offer a novel therapeutic option for patients with MYC-driven malignancies.
Dr. Youzhi Tong, the founder, chairman and CEO of Kintor Pharma, said, GT19630 is a molecular glue protein degrader independently developed by Kintor Pharmaceutical over several years. Targeting both MYC and GSPT1, this drug molecule leverages its unique dual-target degradation mechanism, which not only endows it with standalone drug development potential but also enables conjugation with antibodies, peptides, or other molecules to further develop into ADCs, PDCs, or other XDC-based innovative therapeutics, offering broad expandability and multi-scenario development value. Kintor is now open to collaboration with innovative pharmaceutical companies worldwide, and sincerely invites industry partners to join forces in tackling the long‑regarded “undruggable” c‑Myc target. For cooperation inquiries, please contact us by BD@kintor.com.cn.
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