CDK9 inhib News - LARVOL Sigma

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|||||||||| Journal: CDK9-mediated transcriptional activation of NEK7 promotes NLRP3-dependent podocyte Pyroptosis in diabetic kidney disease. (Pubmed Central) - Jan 18, 2026
This establishes a causal hierarchy wherein CDK9 knockdown suppresses NEK7/NLRP3 expression and pyroptosis, while CDK9 overexpression enhances these effects. These findings position CDK9 as a metabolic checkpoint governing NEK7-driven podocyte pyroptosis, offering a precision therapeutic strategy for DKD that selectively targets renal inflammation.

|||||||||| Journal: HEXIM1 inter-monomer autoinhibition governs 7SK RNA binding specificity and P-TEFb inactivation. (Pubmed Central) - Jan 16, 2026
This dual-site binding triggers a conformational rearrangement in Hexim1's disordered central region that unmasks the Cdk9-binding site, which is otherwise sequestered within an inter-monomer dimer interface. These findings reveal how Hexim autoinhibition dictates its specificity for 7SK RNA and prevents premature P-TEFb inhibition in the absence of 7SK, thereby providing a mechanistic understanding of Hexim/P-TEFb assembly into the 7SK RNP and further considerations for understanding Hexim-Tat competition during viral transcription.

|||||||||| Journal: Rtf1-dependent transcriptional pausing regulates cardiogenesis. (Pubmed Central) - Jan 15, 2026
Intriguingly, attenuating pause release by pharmacological inhibition or morpholino targeting of CDK9 improved RNA Pol II occupancy at the transcription start sites of key cardiac genes and restored cardiomyocytes in Rtf1-deficient embryos. Thus, our findings demonstrate the crucial role that Rtf1-mediated transcriptional pausing plays in controlling the precise spatiotemporal transcription programs that govern early heart development.

|||||||||| dinaciclib (MK-7965) / Merck (MSD), irinotecan / Generic mfg., vincristine / Generic mfg.
Journal, PARP Biomarker: Dinaciclib improves treatment response in chemoresistant hepatoblastoma. (Pubmed Central) - Jan 12, 2026
In our PDX model, treatment with VI?+?dinaciclib resulted in decreased tumor volume, viability and HB cell proliferation. Given these findings, combination treatment with VI and dinaciclib should be investigated further as a treatment for chemoresistant HB.

|||||||||| Journal: CDK9 is a dependency in GATA-3 driven and MCL-1 independent T-cell Lymphomas. (Pubmed Central) - Jan 8, 2026
We also identify novel mechanisms by which GATA-3 and CDK9 regulate rRNA transcription and processing, respectively, collaboratively promoting ribosome biogenesis. Therefore, CDK9 is a therapeutic vulnerability across genetically and transcriptionally diverse T-cell lymphomas, including those for which GATA-3 is oncogenic.

|||||||||| Journal: Phytochemical profiling and anticancer activity of the n-butanol fraction from Ardisia villosa extract: Inhibition of gastric cancer cell proliferation via cell cycle arrest and senescence induction. (Pubmed Central) - Jan 8, 2026
Molecular docking analyses further supported these findings by demonstrating strong binding affinities of phytochemicals to key cell cycle regulatory proteins, suggesting a direct molecular basis for their antiproliferative effects. In conclusion, the n-butanol fraction of Ardisia villosa displays potent anticancer activity, particularly in gastric cancer cells, through multi-targeted mechanisms involving cell cycle inhibition and senescence induction, and holds promise as a natural source for future anticancer therapeutics.

|||||||||| Journal: Disrupting CDK9 activity suppresses triple-negative breast cancer and is enhanced by EGFR Inhibition. (Pubmed Central) - Jan 8, 2026
In conclusion, the n-butanol fraction of Ardisia villosa displays potent anticancer activity, particularly in gastric cancer cells, through multi-targeted mechanisms involving cell cycle inhibition and senescence induction, and holds promise as a natural source for future anticancer therapeutics. Our results position CDK9 as a promising therapeutic target in TNBC, either alone or in combination with EGFR inhibition, provided that side effects associated with this combination treatment can be controlled.

|||||||||| temozolomide / Generic mfg., zotiraciclib (TG02) / Cothera Biosci
Journal: Transcriptional condensates enrich phosphorylated PRMT2 to stimulate H3R8me2a deposition and hypoxic response in glioblastoma. (Pubmed Central) - Jan 7, 2026
Moreover, the combination of TG02 and temozolomide, the standard chemotherapy for GBM, significantly inhibits tumor progression in mouse xenograft models, an effect partially mediated by targeting PRMT2S12 phosphorylation. Our study uncovers the role of transcriptional condensation in enhancing PRMT activity, reveals a new mechanism for CDK9 inhibitors in modulating context-dependent transcriptional programs, and proposed a combinatorial therapeutic strategy against GBM.

|||||||||| Journal, BRCA Biomarker: ZMYM3 S464: a potential phospho-regulatory hub in epigenetic remodeling and oncogenesis. (Pubmed Central) - Jan 6, 2026
ZMYM3 S464 emerges as a phospho-regulatory hub that coordinates epigenetic silencing, HR repair, and mitotic fidelity. Its cancer-type-specific upregulation offers a novel biomarker for HR-deficiency stratification and a therapeutic entry point for modulating BRCA1 function or epigenetic drug sensitivity; functional validation in HR-deficient models is now warranted.

|||||||||| Journal: Novel biallelic CDK9 variants are associated with retinal dystrophy without CHARGE-like malformation syndrome. (Pubmed Central) - Jan 4, 2026
With respect to reduced kinase activity, the new variant could be ranked as WT?>?P321S?>?A288T. Thus, our study raises a possibility that retinal dystrophy can arise with or without a CHARGE-like malformation syndrome depending on the level of kinase activity associated with the combination of variant CDK9 alleles present.

|||||||||| Journal: Enhancer/Enhanceosome/Super-enhancer and the promoter-proximate RNA Polymerase II (Pol II) pausing are coupled. (Pubmed Central) - Dec 22, 2025
It is likely that the BRD4 docking site on nucleosomes is generated by p300/CBP. We conclude that enhancer/enhanceosome/super-enhancer and Pol II pausing regulation are coupled and could be the unique universal mechanism that differentiates animals from unicellular organisms.

|||||||||| Journal: Rational Design of Oxazolonylflavone Derivatives as Novel CDK4/9 Inhibitors with Potent Antitumor Efficacy and Oral Bioavailability. (Pubmed Central) - Dec 18, 2025
Furthermore, HS-36 possessed an excellent pharmacokinetic profile, including good oral bioavailability (F = 41.8%), which enabled solid and well-tolerated in vivo antitumor efficacy (TGI = 68.8%) in a MV-4-11 xenograft model. This work not only presents HS-36 as a promising lead compound but also validates our rational approach to optimizing natural product scaffolds.

|||||||||| Rinvoq (upadacitinib) / AbbVie
Spatially and functionally uncoupled cytokine responses differentially activate wound healing and keratinisation responses in a prognostically relevant manner in perianal fistulising Crohn (A10) - Dec 16, 2025 - Abstract #ECCOIBD2026ECCO_IBD_529;
This work not only presents HS-36 as a promising lead compound but also validates our rational approach to optimizing natural product scaffolds. Healthy control and pCD cytokine-treated organoids (n=4)

|||||||||| Journal: CDK11 activates CDK12 to trigger the elongation of RNA Polymerase II. (Pubmed Central) - Dec 11, 2025
Moreover, we find that CDK10 can partially compensate for the function of CDK11. Combining with earlier functional elucidation of CDK9 from us, the consequent roles of CDK7/8, CDK9, CDK10/11, and CDK12/13 in transcription regulation in metazoans are established.

|||||||||| HDAC and CDK inhibitor combinations suppress neutrophil activation in myeloma () - Dec 5, 2025 - Abstract #ASH2025ASH_9452;
These transcriptional changes, accompanied by increased re-expression of tumor suppressors (e.g.,p16) and TGF?/SMAD signaling components, would predict reprogramming of an anti-inflammatory microenvironment by these combination treatments in myeloma. These findings point to a promising but underdeveloped therapeutic avenue whereby suppressing neutrophil-driven inflammation enhances anti-myeloma immunity.

|||||||||| Therapeutic resistance in aggressive B-cell lymphoma is overcome through the reciprocal enhanced efficacy by CDK9 inhibitors and CAR-T cells () - Dec 5, 2025 - Abstract #ASH2025ASH_9036;
Collectively, these results underscore a synergistic dual-targeting approach that tackles both tumor-intrinsic survival mechanisms and the immunosuppressive TME. This combinatorial "one-two punch" strategy holds strong potential to more effectively eliminate minimal residual disease (MRD), prevent relapse, and drive complete and durable remissions in aggressive B-cell lymphomas.

|||||||||| tambiciclib (SLS009) / SELLAS Life Sciences
Tambiciclib (SLS009), a novel, potent CDK9 inhibitor is effective in killing ASXL1 mutated and TP53 knockout Acute Myeloid Leukemia cell lines () - Dec 5, 2025 - Abstract #ASH2025ASH_8741;
Inhibition of CDK9 with tambiciclib is a promising and effective approach for inducing cell death in AML. Our preliminary data warrants further investigation to optimize the therapeutic window for tambiciclib treatment in repeated doses and combination therapies.

|||||||||| Journal: Disrupting Integrator complex subunit INTS6 causes neurodevelopmental disorders and impairs neurogenesis and synapse development. (Pubmed Central) - Nov 17, 2025
Notably, CDK9i reversed neurosphere over-proliferation and rescued the abnormal dendritic spine phenotype caused by Ints6 deficiency. This work advances understanding of INTS-related NDD pathogenesis and highlights potential therapeutic targets for intervention.

|||||||||| Cognex (tacrine) / Shionogi
Journal: Fluorocyclopropyl-Containing Tacrine Derivatives as Potent and Selective Dual CDK2/CDK9 Inhibitors for the Treatment of Colorectal Cancer. (Pubmed Central) - Nov 15, 2025
Importantly, ZLMT-72 (10 mg/kg) displayed robust antitumor efficacy in both subcutaneous (TGI = 50.6%) and orthotopic (TGI = 84.3%) xenograft tumor models of HCT116, alongside favorable pharmacokinetic properties and a promising safety profile. Collectively, ZLMT-72, as a potent dual CDK2/9 inhibitor, holds substantial therapeutic potential for CRC treatment.

|||||||||| Review, Journal: Beyond Inhibition: Recent Advances of Heterobifunctional Molecules Targeting CDK9. (Pubmed Central) - Nov 13, 2025
Additionally, innovative approaches employing heterobifunctional molecules across various modalities have been extensively explored to target CDK9, expanding the therapeutic potential through multiple mechanisms. These advances hold promise for establishing a new paradigm in the treatment of transcriptionally addicted cancers.

|||||||||| Journal: CD73-enriched extracellular vesicles reduce cyclooxygenase 2 (COX-2)-mediated inflammation in activated macrophages. (Pubmed Central) - Nov 6, 2025
Our study demonstrated that eATP enhanced LPS-mediated inflammation in macrophages which could be significantly reduced upon addition of CD73-rich EVs. Such engineered EVs can, therefore, be explored therapeutically for their anti-inflammatory properties.

|||||||||| Neuropath-AI, a histopathology-based deep learning classifier for CNS tumors, achieves and improves human neuropathologist-level performance (Hawaii Convention Center, Kamehameha Exhibit Hall I) - Nov 5, 2025 - Abstract #WFNOS2025WFNOS_2075;
Our model provides the basis for a clinically applicable deep learning assistant to improve human efficiency and accuracy of CNS tumor diagnosis. The model will be made publicly available and can be readily implemented to assist human pathologists in clinical workflows, in further expanded prospective studies.

|||||||||| Nesprin-2 is upregulated in glioblastoma and contributes to tumor progression (Hawaii Convention Center, Kamehameha Exhibit Hall II & III) - Nov 5, 2025 - Abstract #WFNOS2025WFNOS_1388;
Compared to mice injected with control cells, both mice injected with either nesprin-2 knockdown cell lines exhibited reduced tumor growth and prolonged survival. These results show that nesprin-2 is a key factor in the progression of glioblastoma and suggest that the LINC complex may be a therapeutic target for the treatment of glioblastoma.

|||||||||| temozolomide / Generic mfg.
Combination therapies with CDK9 inhibitors as a promising strategy to overcome therapy resistance in glioblastomas (Hawaii Convention Center, Kamehameha Exhibit Hall II & III) - Nov 5, 2025 - Abstract #WFNOS2025WFNOS_1306;
A serendipitous finding was the increased expression of c-Myc upon CDK9 inhibitor treatment; while c-Myc increase did not appear to impede the efficacy of the CDK9 inhibitors, inclusion of a BRD4 inhibitor enhanced the sensitivity of the cells to the CDK9 inhibition. Ongoing studies include the use of temozolomide (TMZ)-resistant and sensitive DGCs and GSCs to identify specific drug-induced epigenetic modifications and elucidate the mechanisms by which CDK9 inhibition brings about its anti-tumor and neuroprotective effects, while overcoming therapy resistance.

|||||||||| zotiraciclib (TG02) / Cothera Biosci
Phase I/II study of zotiraciclib for recurrent malignant gliomas with IDH mutations: results of the phase I study (Hawaii Convention Center, Kamehameha Exhibit Hall II & III) - Nov 5, 2025 - Abstract #WFNOS2025WFNOS_1256;
ZTR at the RP2D of 200mg, q3D, 3wks on/1wk off in a 28-day cycle is well tolerated. Objective responses suggest activity of this regimen in IDH-mutant gliomas, supporting continued investigation.

|||||||||| Clinically Applicable Molecular Grouping of Intracranial Meningiomas Based on High-Risk Copy Number Alterations and NF2/22q Status (Hawaii Convention Center, Kamehameha Exhibit Hall II & III) - Nov 5, 2025 - Abstract #WFNOS2025WFNOS_415;
Molecular classification based on high-risk CNAs and NF2/22q status offers a clinically actionable framework for prognostic stratification in meningiomas. This grouping can be assessed using targeted assays and may enhance WHO grading to inform postoperative monitoring and therapeutic strategies.

|||||||||| Membrane proteomic profiling to identify candidate therapy targets for glioblastoma infiltration (Hawaii Convention Center, Kamehameha Exhibit Hall II & III) - Nov 5, 2025 - Abstract #WFNOS2025WFNOS_379;
Furthermore, nine of these ubiquitously upregulated proteins were undetectable in astrocyte cells.Analysis of correlation between protein abundance ratio and survival time in GBM clinical samples retrieved from the CPTAC study on cBioPortal showed that ROBO1, LOXL1 and DYSF conferred a negative correlation with survival, which suggests that these membrane proteins could exhibit a functional role in GBM survival and progression.These findings suggest that targeting membrane proteins offers promise for developing effective GBM therapies predicated on the most clinically accurate intra-tumour region. Future work utilises molecular docking techniques to identify suitable repurposed drugs against the membrane proteins observed.

|||||||||| Targeting transcriptional elongation by BRD4 and CDK9 inhibition for the treatment of diffuse midline glioma (Hawaii Convention Center, Kamehameha Exhibit Hall II & III) - Nov 5, 2025 - Abstract #WFNOS2025WFNOS_350;
Combination therapy in mice bearing DMG PDX also inhibited tumor growth and extended survival. This study has shown promising results demonstrating that this combined therapy is a potentially effective strategy for treating DMG.

|||||||||| zotiraciclib (TG02) / Cothera Biosci
Phase I/II study of zotiraciclib for recurrent malignant gliomas with IDH mutations: results of the phase I study (Hawaii Convention Center, Kamehameha Exhibit Hall II & III) - Nov 5, 2025 - Abstract #WFNOS2025WFNOS_316;
ZTR at the RP2D of 200mg, q3D, 3wks on/1wk off in a 28-day cycle is well tolerated. Objective responses suggest activity of this regimen in IDH-mutant gliomas, supporting continued investigation.

|||||||||| PRT2527 / Prelude Therap
Results from the Phase 1 Study of PRT2527, a Selective and Potent CDK9 Inhibitor, as Monotherapy and in Combination With Zanubrutinib in Patients with Relapsed/Refractory Lymphoid Malignancies (S / T (Confex)) - Nov 5, 2025 - Abstract #DGHO2025DGHO_1524;
P1
Most common TEAE was neutropenia, manageable with growth factor support. Data supports further evaluation of PRT2527 as mono in PTCL and in combo with zanu in aggressive B cell lymphoma.

|||||||||| sunaciclib (AU-07) - Qianhong Bio / Pharma, Aucentra
QHRD107 (CDK9 Inhibitor), venetoclax, and azacitidine combination therapy (107VA regimen) in relapsed/refractory Acute Myeloid Leukemia: Data updates and subgroup analysis (OCCC - West Halls B3-B4) - Nov 4, 2025 - Abstract #ASH2025ASH_7705;
P2
The 107VA regimen demonstrated high response rates in VEN-AZA relapse or refractoryAML, particularly in patients with TP53 mutations and myelodysplasia-related features. Based on thesedata, a phase 2b randomized controlled study comparing 107VA with other salvage regimens is currentlybeing conducted for patients who relapse after VEN-AZA treatment.

|||||||||| Venclexta (venetoclax) / Roche, AbbVie, tambiciclib (SLS009) / SELLAS Life Sciences
Phase 2 study of SLS009 in combination with azacitidine and venetoclax for relapsed/refractory AML with MDS-related changes (AML-MR) after prior venetoclax treatment (OCCC - West Halls B3-B4) - Nov 4, 2025 - Abstract #ASH2025ASH_5817;
Clinicalefficacy was seen in pts with AML-MR, with a signal of activity in pts with ASXL1 mutated AML. Pts withonly 1 line of ven-based prior therapy experienced the greatest benefit in terms of response and longterm survival, implying a role in patients progressing after HMA + ven.

|||||||||| Disruption of NEAT1-transcriptional network identifies targetable non-genetic dependencies in multiple myeloma (OCCC - West Halls B3-B4) - Nov 4, 2025 - Abstract #ASH2025ASH_4923;
In conclusion, our data demonstrated that NEAT1 contributes to overt phases of MM and to the clinicalaggressive behaviour of the disease, by orchestrating a mitotic transcriptional program. Furthermore,through the application of a multi-dimensional approach, we revealed that the dual inhibition of NEAT1and transcriptional regulators as CDK9 may offer a promising strategy for novel combinatorial anti-MMtherapies.

|||||||||| Identifying novel 'druggable' targets via Npm1A-turboid fusion and mass spectrometry to overcome genetic or adaptive resistance to menin inhibitors in mtNPM1 AML (OCCC - West Halls B3-B4) - Nov 4, 2025 - Abstract #ASH2025ASH_2685;
Treatment with revumenib may also cause emergenceof hot spot mutations in menin (e.g., S160T, M327V, M327I, G331D, G331R, and T349M) exhibitingreduced affinity to MI-binding...OCI-AML3 MEN1-M327I cells were resistant toSNDX-50469, ziftomenib, and DS1594b, but sensitive to the second-generation MI, bleximenib, aspreviously reported.To identify novel 'druggable' targets in mtNpm1 AML cells either sensitive or resistant to MI, we knockedin TurboID by CRISPR/Cas9 into the C-terminus of the mtNpm1 gene in OCI-AML3 cells...When combined with a BET inhibitor (pelabresib) ora novel dual BET/HAT inhibitor (NEO2734/EP31670), both RocA and talazoparib induced synergisticlethality in the sensitive OCI-AML3 and OCI-AML2-Npm1A KI, as well as the MI-resistant (OCI-AML3-Menin-M327I or the OCI-AML3 MITR) cells...Exvivo treatment with EP31670 and RocA or talazoparib induced synergistic loss of viability in MI (SNDX-50469)-resistant, patient-derived (N = 3) mtNpm1 AML cells. In the PDX model of luciferized mtNpm1 +FLT3-ITD AML cells engrafted in NSG mice, compared to vehicle control, monotherapy with EP31670 (7.5mg/kg QD), talazoparib (0.25 mg/kg QD) or RocA (0.5 mg/kg 3x/wk) significantly reduced AML burden.Collectively, these findings highlight the newly discovered, preclinical efficacy of inhibitors of eIF4A andPARP against mtNpm1 AML cells and support the rationale for further evaluating the efficacy ofcombinations involving these agents.

|||||||||| enzomenib (DSP-5336) / Sumitomo Pharma, Kyoto University
Preclinical activity of investigational menin inhibitor DSP-5336 (Enzomenib)-based combinations against MLL1-rearranged (MLL-r) or mutant-NPM1 AML models (OCCC - West Halls B3-B4) - Nov 4, 2025 - Abstract #ASH2025ASH_2682;
Previously reported preclinical data showed that treatment with Menin inhibitor (MI),e.g., SNDX-5613 (revumenib) or KO-539 (ziftomenib), disrupts binding of Menin to MLL1/2 and MLL1-FP,leading to reduced MLL1/2 and MLL1-FP target gene expression, as well as induction of differentiationand apoptosis in AML cells expressing MLL-FP or mtNPM1c...Notably, in the cell lines and PD AML cells with MLLr ormtNPM1c AML, in vitro treatment with DSP-5336 in combination with CDK9 inhibitor (CDK9i) AZD4573 orBAY1251152 for 48 to 96 hours induced synergistic apoptosis or loss of viability, as discovered by the ZIPmethod with SynergyFinder...In vivo co-treatment with DSP-5336 and BAY1251152 showedsignificantly greater reduction in AML burden than treatment with each agent alone (p< 0.05), withoutinducing weight loss or other toxicities. These preclinical findings underscore the anti-AML activity of DSP-5336 and its molecular correlates, aswell as demonstrate synergistic in vitro and in vivo activity of DSP-5336-based combination with CDK9iagainst AML harboring MLL1-FP or mtNPM1c.

|||||||||| Discovery of first-in-class calr-targeted precision ADCs delivering a CDK9degrader payload for the treatment of calr-mutated MPNs (OCCC - W414AB) - Nov 4, 2025 - Abstract #ASH2025ASH_1454;
Treatmentwas well tolerated, with no off-target effects observed in healthy hematopoietic cells.In summary, we describe a first-in-class CALR-targeted ADC that delivers a novel CDK9 degrader payload,selectively eliminating CALR-mutant MPN progenitors. These results support further development of amutant CALR x CDK9 degrader pADC as a potential disease-modifying therapeutic for CALR-mutantMPNs.

|||||||||| lenalidomide / Generic mfg., thalidomide / Generic mfg., pomalidomide / Generic mfg.
Journal: Orthogonal IMiD-Degron Pairs Induce Selective Protein Degradation in Cells. (Pubmed Central) - Nov 2, 2025
In proof-of-concept studies, this system was applied to induce degradation of the optimum degron fused to CDK9, HPRT1, NanoLuc, or TRIM28. We anticipate that this system will be a valuable addition to the current arsenal of degron systems for use in target validation.

|||||||||| Review, Journal: The 7SK snRNP complex: a critical regulator in carcinogenesis. (Pubmed Central) - Nov 1, 2025
Emerging evidence implicates 7SK snRNP deregulation in cancer progression. This review explores the intricate interplay between 7SK snRNP and CDK9, highlighting how disruptions in individual 7SK snRNP components drive transcriptional imbalances, amplify oncogenic programs, and promote a tumorigenic environment.

|||||||||| Preclinical, Journal: The CDK9-targeting degrader PO-8 alleviates LPS-induced inflammation by inhibiting JAK-STAT signaling in vitro and in vivo. (Pubmed Central) - Oct 30, 2025
Mechanistic studies revealed that PO-8-mediated CDK9 degradation disrupts the JAK2-STAT3 signaling pathway, thereby mitigating inflammation. To the best of our knowledge, this study is the first to establish the anti-inflammatory efficacy of a small-molecule CDK9 degrader, highlighting PROTAC-based CDK9 targeting as a promising therapeutic strategy for inflammatory diseases.

|||||||||| Journal: New Assay Systems to Characterize the Broad-Spectrum Antiherpesviral and Non-Herpesviral Activity of Cyclin-Dependent Kinase (CDK) 8 Inhibitors. (Pubmed Central) - Oct 29, 2025
This suggests that CDK8 may play several different roles in viral replication. The option of a refined CDK8-specific antiviral drug targeting is discussed.

|||||||||| Preclinical, Journal: Discovery of dCDK9-202 as a Highly Potent and Selective PROTAC CDK9 Degrader with Strong In Vivo Antitumor Activity. (Pubmed Central) - Oct 23, 2025
Moreover, intravenous administration of dCDK9-202 effectively inhibits TC-71 tumor growth without any signs of toxicity in mice. This promising CDK9 degrader dCDK9-202 has a high potential for advanced preclinical development in the treatment of CDK9-addicted human cancers.

|||||||||| Preclinical, Journal, IO biomarker: p-Cymene Targets Multiple Oncogenic Pathways in Hepatocellular Carcinoma: Insights From Network Pharmacology and In (Pubmed Central) - Oct 20, 2025
Additionally, BCL2 and VEGF were downregulated, suggesting inhibition of cell survival and angiogenesis. These findings highlight p-cymene's multi-targeted anticancer effects in HCC cells, supporting its further evaluation in in

|||||||||| Discovery of a first-in-class CDK9 degrader targeting oncogenic transcription networks in hematologic and solid tumors (Level 2' Exhibit Hall D; In-Person Only) - Oct 13, 2025 - Abstract #AACRNCIEORTC2025AACR_NCI_EORTC_491;
These findings highlight p-cymene's multi-targeted anticancer effects in HCC cells, supporting its further evaluation in in Available on Wednesday, October 22, 2025 at 01:00pm EDT.

|||||||||| OBP-004 / OncoBone Therapeutics
OBP-004, a novel small-molecule dual inhibitor of CDK9/13, reduces bone, brain, lung and lymph node metastases in vivo, with highest potency on bone metastases (Level 2' Exhibit Hall D; In-Person Only) - Oct 13, 2025 - Abstract #AACRNCIEORTC2025AACR_NCI_EORTC_284;
Available on Wednesday, October 22, 2025 at 01:00pm EDT. Available on Wednesday, October 22, 2025 at 01:00pm EDT.

|||||||||| Integrative multiomic analysis identifies EIF4A1 and CDK9 as key therapeutic targets in oligodendrogliomas (Forum Hall Foyer 3) - Oct 12, 2025 - Abstract #EANO2025EANO_796;
Our multiomic study provides a comprehensive molecular and clinical landscape of oligodendrogliomas and reveals that targeting the regulation of transcription and translation initiation could improve the prognosis of oligodendroglioma. CDK9 and EIF4A inhibitors, currently evaluated in clinical trials for other cancers, represent attractive new therapeutic targets for aggressive oligodendrogliomas.

|||||||||| Journal, PD(L)-1 Biomarker, IO biomarker: GBP1-CDK9-STAT3 signaling axis promotes osteosarcoma PD-L1 expression and immune escape. (Pubmed Central) - Oct 11, 2025
Specifically, our results reveal that GBP1 regulates PD-L1 expression by activating CDK9 and promoting STAT3 phosphorylation. These findings suggest that targeting GBP1 may represent a promising therapeutic strategy for the treatment of osteosarcoma by impairing tumor immune evasion.

|||||||||| Journal: Targeting CDK9 with Molegro Virtual Docker. (Pubmed Central) - Oct 11, 2025
The necessary inputs are binding affinity data available in BindingDB and the atomic coordinates of the target found in the protein data bank. All CDK9 datasets and Jupyter Notebooks discussed in this work are available at GitHub: https://github.com/azevedolab/docking#readme .

|||||||||| CDK9 inhibition as a promising therapy to counteract brain dysfunction in sepsis (Hall 2 - Van Gogh; Virtual & In-person) - Oct 10, 2025 - Abstract #ECNP2025ECNP_1346;
doi: 10.1016/j.gene.2020.145200. No conflict of interest

|||||||||| Preclinical, Journal: Determination of the In Vitro Cytotoxic Activities of Several Coumarin Derivatives on Neuroblastoma Cell Lines With In Silico Inhibitory Effects on CDK9, VEGFR2 and EGFR Proteins and ADME Studies. (Pubmed Central) - Oct 7, 2025
These compounds demonstrated selective cytotoxicity against SH-SY5Y neuroblastoma cells and a favorable multi-target binding profile, highlighting a distinct hydrophobic volume-based SAR. As a result, the obtained data exhibited that all used molecules may be good multitarget drug alternatives for the treatment of neuroblastoma.

|||||||||| A scalable, proteome-wide protein profiling platform with absolute quantification of 1000 proteins (Poster Hall (Exhibit Halls AB); Virtual) - Oct 3, 2025 - Abstract #SITC2025SITC_1495;
They simultaneously resulted in increased secretion of chemokines CXCL2, CXCL3, CXCL5, and maintained CCL2 and IL-8 expression, possibly promoting additional immune involvement parallel to direct cell killing. These findings underscore Omni 1000's capacity to profile functional heterogeneity in tumor immune microenvironments and support development of precision medicine with immunotherapeutic potential.Conclusions Together, we demonstrate a novel 1000-plex solution, Omni 1000, with content balancing critical targets and biological breadth, and demonstrated real-world utility in early detection of disease and high throughput cancer drug development.



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