Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

TP-0184 inhibits FLT3/ACVR1 to overcome FLT3 inhibitor resistance and hinder AML growth synergistically with venetoclax.

Leukemia - 1 Jan 2024

Tyagi Anudishi, Jaggupilli Appalaraju, Ly Stanley, Yuan Bin, El-Dana Fouad, Hegde Venkatesh L, Anand Vivek, Kumar Bijender, Puppala Mamta, Yin Zheng, Wong Stephen T C, Mollard Alexis, Vankayalapati Hariprasad, Foulks Jason M, Warner Steven L, Daver Naval, Borthakur Gautam, Battula V Lokesh

Abstract excerpt

We identified activin A receptor type I (ACVR1), a member of the TGF-β superfamily, as a factor favoring acute myeloid leukemia (AML) growth and a new potential therapeutic target. ACVR1 is overexpressed in FLT3-mutated AML and inhibition of ACVR1 expression sensitized AML cells to FLT3 inhibitors. We developed a novel ACVR1 inhibitor, TP-0184, which selectively caused growth arrest in FLT3-mutated AML cell...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Activin Receptors, Type I
Share to Apoptosis

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Cell Line, Tumor

Share to fms-Like Tyrosine Kinase 3

Share to Leukemia, Myeloid, Acute

Share to Molecular Docking Simulation

Share to Mutation

Share to Protein Kinase Inhibitors

Source

Identifiers

PMID: 38007585
DOI: 10.1038/s41375-023-02086-6

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

TP-0184 inhibits FLT3/ACVR1 to overcome FLT3 inhibitor resistance and hinder AML growth synergistically with venetoclax.PMID 38007585Read ↗

Anlotinib Induced Venetoclax-resistant Acute Myeloid Leukemia Stem Cells Apoptosis through Downregulating Mcl-1-mediated Anti-apoptoeic PathwaySemantic proximity Read ↗

Romaciclib, a CDK8/CDK19 inhibitor, can overcome venetoclax resistance through a combinatorial strategySemantic proximity Read ↗

CK2 inhibitor, CX-4945, enhances BH3 priming and promotes apoptosis of venetoclax-resistant AML by targeting antiapoptotic proteinsSemantic proximity Read ↗

Rewired Neuroactive Ligand-Receptor Signaling Confers Adaptive Resistance to BCL-2 Inhibition in AMLSemantic proximity Read ↗

Off-target based drug repurposing opportunities for tivantinib in acute myeloid leukemiaSemantic proximity Read ↗

Multi-selective RAS(ON) Inhibition Targets Oncogenic RAS Mutations and Overcomes RAS/MAPK-Mediated Resistance to FLT3 and BCL2 Inhibitors in Acute Myeloid LeukemiaSemantic proximity Read ↗

Targeting MCL-1 and MAPK overcomes venetoclax resistance in FLT3-ITD-positive AML cells harbouring activating PTPN11 (SHP-2) mutations.Semantic proximity Read ↗

Targeting tumour vasculature by inhibiting activin receptor-like kinase (ALK)1 functionSemantic proximity Read ↗

Combining the novel FLT3 and MERTK dual inhibitor MRX-2843 with venetoclax results in promising antileukemic activity against FLT3-ITD AML.Semantic proximity Read ↗

Venetoclax overcomes resistance to all‐trans retinoic acid in a variant acute promyelocytic leukemia with TNRC18::RARA fusionSemantic proximity Read ↗

A Phase II Study of Azacitidine, Venetoclax, and Trametinib in Relapsed or Refractory Acute Myeloid Leukemia Harboring RAS Pathway-Activating Mutations.Semantic proximity Read ↗

ACC010, a novel BRD4 inhibitor, synergized with homoharringtonine in acute myeloid leukemia with FLT3-ITD.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.