Farydak (panobinostat) / Secura Bio - LARVOL DELTA

Synergy of a CDK4/6 inhibitor and an HDAC inhibitor in pancreatic cancer overcomes autophagy (AACR 2026) - "Our previous study demonstrated synergy and efficacy of Panobinostat (Pan), a pan-HDAC inhibitor, and Abemaciclib (Abe), a CDK4/6 inhibitor, in PDAC cells. Interestingly, the synergy of Pan-Abe from PDAC cells was confirmed in MIA PaCa-2 tumor xenograft model. Further studies are needed to understand the role of autophagic processes in the efficacy of Pan-Abe in PDAC."

Oncology • Pancreatic Cancer • Pancreatic Ductal Adenocarcinoma • Solid Tumor

Mechanistic basis of panobinostat, venetoclax, and anti-CD40 combination therapy in the immune elimination of cancer stem cells (AACR 2026) - "Interactions between CSCs and DCs/macrophages are elevated, and ligand-receptor analyses indicate that Mif-Cd74 and App-Cd74 signaling mediate CSC-immune cell communication. Collectively, these results provide a mechanistic framework for how Panobinostat-Venetoclax-Anti-CD40 triple combination therapy remodels the tumor microenvironment to eliminate breast CSCs and potentiate antitumor immunity."

Cancer stem • Combination therapy • Breast Cancer • Oncology • Solid Tumor • APOE • CD74

IL-1-driven signaling promotes resistance to PI3K and BCL2 inhibitors in B-cell lymphoma preclinical models (AACR 2026) - "A 1,400-compound FDA-approved library was used in combination with copanlisib/venetoclax. VL51 cells with acquired resistance to PI3K/BCL2 inhibitors were characterized by an upregulation of IL1α and IL1β, elevated ERK and STAT3 phosphorylation, and increased expression of pro-survival and cytokine-responsive proteins. IL-1-driven reprogramming promotes resistance to PI3K and BCL2 inhibition in B-cell lymphoma via activation of NF-κB, STAT3, and metabolic survival pathways. Targeting IL-1 signaling or downstream effectors may overcome resistance and offer a promising therapeutic strategy for relapsed or refractory B-cell lymphomas."

IO biomarker • Preclinical • B Cell Lymphoma • Diffuse Large B Cell Lymphoma • Hematological Malignancies • Lymphoma • Mantle Cell Lymphoma • Marginal Zone Lymphoma • Non-Hodgkin’s Lymphoma • Oncology • ALDH1A1 • AURKA • IL1A • IL1B

Single-cell multiomic drug response profiling of PRISM-multiplexed cancer cell lines sequenced with SBX (AACR 2026) - "We treated the PRISM pool with two RAS inhibitors (BI-2865 and RMC-6236), as well as a negative control (DMSO) and a positive control (Panobinostat), and collected cells at early time points (3h and 12h) to capture initial drug response dynamics. Importantly, these protein changes frequently lacked a corresponding significant change in the expression of their encoding RNA transcripts, underscoring the power of multi-modal profiling to more comprehensively illuminate functional mechanisms driving drug response.Our study establishes a scalable paradigm for linking genotype, transcriptome, and proteome to pharmacologic phenotype at single-cell resolution across genetically diverse human models. These data, enabled with massively high-throughput sequencing using SBX, provide a rich resource for mechanistic discovery and rational design of combination therapies targeting the RAS pathway."

Preclinical • Oncology

WEE1 reinforces C-MYC driven oncogenic programs through GSK3ß inhibition (AACR 2026) - "A high-throughput screen of 892 FDA-approved drugs identified Panobinostat as a synergistic partner of the WEE1 inhibitor MK1775. These findings define a WEE1-GSK3β-MYC signaling axis in which WEE1 stabilizes MYC and sustains MYC-driven oncogenic programs. WEE1 inhibition activates GSK3β, promoting proteasome-mediated MYC degradation. The combination of WEE1 inhibition and Panobinostat represents a promising therapeutic approach for MYC-driven EAC."

Esophageal Adenocarcinoma • Oncology • Solid Tumor • MYC • WEE1

Copy number variation in Sonic hedgehog-medulloblastoma with unique p53 mutations: Inhibition of PI3K/AKT/mTOR pathways with HDAC inhibitors can serve as therapeutic options (AACR 2026) - "Effects of small molecule inhibitors targeting PI3K (Buparlisib; BKM-120) and HDAC (LBH-589) in SHH-MB cells (Daoy), were assessed via functional assays, such as cell proliferation, migration, cell cycle, and drug resistance. Furthermore, small molecule PI3K and HDAC inhibitors suppressed PI3K/AKT/mTOR pathways inhibiting cell proliferation, migration, and tumor formation. These studies provide evidence of genomic anomalies as well as treatment options for SHH-MB."

P53mut • Brain Cancer • Medulloblastoma • Oncology • Solid Tumor • IDH2 • KRAS • PTEN • TP53

Age-stratified therapeutic strategies targeting tumor cell subclones that drive chemoresistance and immunosuppression in triple-negative breast cancer (AACR 2026) - "Mice were treated with standard therapy consisting of chemotherapy (paclitaxel, PTX) and immunotherapy (anti-PD-L1)...Finally, we treated young and aged mice with Panobinostat, a pan-HDACi that was the top hit in the screen, in combination with anti-PDL1...Further, specific subclones of tumor cells can drive transcriptional programs impacting age-associated differences in tumor progression, but they can be therapeutically targeted. This work sets the stage for the development of age-stratified therapeutic strategies that do not rely on toxic chemotherapy to improve outcomes for TNBC patients of all ages."

Tumor cell • Breast Cancer • Oncology • Solid Tumor • Triple Negative Breast Cancer • CD8

A Non-canonical RNA-Binding Function of NQO1 Drives Angiogenesis in Esophageal Squamous Cell Carcinoma via Extracellular Vesicle-Mediated AGRN Transfer. (PubMed, Cancer Res) - "Importantly, combined treatment with panobinostat and the anti-angiogenic agent anlotinib resulted in superior inhibition of tumor growth and vascularization compared with either monotherapy in patient-derived organoid xenograft models. Together, these findings uncover an enzymatic activity-independent RNA regulatory function of NQO1 in ESCC and provide a mechanistic rationale for targeting the NQO1/AGRN axis."

Journal • Esophageal Squamous Cell Carcinoma • Oncology • Squamous Cell Carcinoma • AGRN • NQO1

Inhibitory effect of vemurafenib combined with panobinostat on human anaplastic thyroid cancer cells. (PubMed, Pak J Pharm Sci) - "Ve combined with Pa exerts a synergistic inhibitory effect on the growth and metastasis of FRO and ARO cells, while promoting apoptosis and cellular redifferentiation. This combination may provide a potential therapeutic strategy for ATC."

Journal • Oncology • Solid Tumor • Thyroid Gland Anaplastic Carcinoma • Thyroid Gland Carcinoma • SLC2A1

Single-cell profiling of HDAC inhibitor-induced EBV lytic heterogeneity defines abortive and refractory states in B lymphoblasts. (PubMed, PLoS Pathog) - "We therefore characterized the impact of pan-HDAC inhibitor, panobinostat, and class I HDAC inhibitor, nanatinostat, on the growth, survival, and lytic reactivation of four EBV-positive cell lines: P3HR1-ZHT BL, Jijoye BL, IBL-1 immunoblastic lymphoma, and de novo infection derived lymphoblastoid cell lines (LCL). Functional validation through a Cas9-RNP approach revealed that the CD137 receptor is indeed involved in preventing successful lytic reactivation. These data have important implications for how we approach oncolytic therapies for EBV-associated malignancies."

Heterogeneity • IO biomarker • Journal • Burkitt Lymphoma • Epstein-Barr Virus Infections • Gastric Cancer • Hematological Malignancies • Hodgkin Lymphoma • Infectious Disease • Lymphoma • Nasopharyngeal Carcinoma • Oncology • Solid Tumor • TNFRSF9

IL3RA identified as novel biomarker and therapeutic target for ER+ breast cancer through plasma proteome-wide mendelian randomization and TCGA database analysis. (PubMed, Clin Proteomics) - "Our study identified IL3RA as novel biomarker and therapeutic target for ER+ breast cancer. Further validation and mechanistic studies are warranted to advance precision oncology strategies for ER+ breast cancer management."

Biomarker • Journal • Breast Cancer • Estrogen Receptor Positive Breast Cancer • Hormone Receptor Breast Cancer • Oncology • Solid Tumor • CD123 • CD8 • ER • IL3RA

WEE1 Stabilizes MYC to Promote Therapeutic Resistance in Esophageal Adenocarcinoma. (PubMed, Cancer Lett) - "These findings reveal a novel cytoplasmic function of WEE1 in sustaining MYC stability and chemoresistance. Targeting WEE1 destabilizes MYC and enhances therapeutic response, supporting the combination of MK-1775 and Panobinostat as a promising treatment strategy for EAC."

Journal • Esophageal Adenocarcinoma • Oncology • Solid Tumor • Targeted Protein Degradation • ABCC1 • CDK1 • MSH3

High-throughput 3D phenotypic screening identifies repurposed MEK inhibitors as drivers of chondrogenesis for cartilage regeneration. (PubMed, Front Bioeng Biotechnol) - "Trametinib, along with Panobinostat, SAHA, and Brefeldin A, was further evaluated via dose-response analyses and molecular assays to determine their impact on chondrogenic differentiation...These findings support the potential of MEK inhibitors like Trametinib, and other selected bioactive compounds, as promising agents for cartilage regeneration. Their repurposing could offer innovative therapeutic strategies for treating cartilage-related disorders, including osteoarthritis."

Journal • Immunology • Osteoarthritis • Pain • Rheumatology • ACAN

Drug screening on tumor organoids exposes therapeutic vulnerabilities of meningiomas to HDAC1/2i panobinostat. (PubMed, Sci Transl Med) - "In search of the molecular mechanism underlying a potentially intrinsic panobinostat resistance, we identified up-regulation of the HDAC8-transforming growth factor-β (TGFβ)-epithelial-to-mesenchymal transition (EMT) axis in the TO model, whereas subsequent HDAC8 depletion increased the sensitivity to panobinostat. These data highlight the utility of personalized drug screenings on TOs to identify suitable drug targets and inhibitors for more effective treatment of clinically aggressive meningiomas and to help advance our understanding of counteracting resistance mechanisms."

Journal • Brain Cancer • Meningioma • Oncology • Solid Tumor • HDAC1 • HDAC8 • TGFB1

ORBIT: Optimizing Reversal of HIV Latency With Combination Therapy (clinicaltrials.gov) - P1/2 | N=49 | Active, not recruiting | Sponsor: Erasmus Medical Center | Recruiting ➔ Active, not recruiting

Enrollment closed • Human Immunodeficiency Virus • Infectious Disease • CD4

CITED2 is a druggable epigenetic switch coupling neuronal maturation to regenerative decline. (PubMed, EMBO Mol Med) - "Pharmacogenomic screening identified CITED2 as a target of the clinically approved HDAC inhibitor Panobinostat, which promoted axonal growth, sprouting, and functional recovery post-injury. These findings position CITED2 as a key regulator of sensory neuron plasticity and a novel therapeutic target for CNS repair."

Journal • CNS Disorders • Orthopedics • CITED2

Boosting CAR T-cell Therapy in Multiple Myeloma Combining in silico Perturbation Predictions and Drug Repurposing (EHA-EBMT-CART 2026) - "Methods : Longitudinal single-cell RNA and TCR sequencing were performed on over 100,000 CAR⁺ and endogenous (CAR⁻) T cells from infusion product (IP) and post-infusion (Peak) samples of 11 MM patients treated with the academic anti-BCMA CAR T therapy ARI0002h ( Figure A )...In silico perturbation screening further identified Panobinostat, a histone deacetylase (HDAC) inhibitor, as a top-ranked compound predicted to attenuate IFN-driven dysfunction and restore functional transcriptional states in non-responder T cells ( Figure F–G ). Conclusions : This study establishes a precision immunotherapy framework integrating single-cell multi-omics profiling, ML and virtual pharmacogenomics to identify predictive biomarkers and rational drug combinations. Future integration of in vivo CRISPR knockout screens will enable systematic refinement of drug targets that enhance CAR T-cell fitness, paving the way for bioinformatics-driven clinical optimization of tailored cell therapies."

CAR T-Cell Therapy • IO biomarker • Hematological Malignancies • Multiple Myeloma • IFNG • SLAMF7

Dual Proteasome and Histone Deacetylase Inhibition Overcomes Tyrosine Kinase Inhibitor Resistance in Breakpoint Cluster Region: Abelson 1-Driven Leukaemia Cell Lines. (PubMed, J Cell Mol Med) - "Viability, cytotoxicity, and caspase-3/7 activity were assessed following single-agent treatment with asciminib, ponatinib, bortezomib, or panobinostat. Co-inhibition of proteasomes and histone deacetylases eliminates TKI-refractory BCR::ABL1-driven leukaemia cells by inducing mitochondrial apoptosis and loss of clonogenic potential. These findings indicate a clinically actionable, TKI-independent strategy for the salvage treatment of multidrug-resistant CML."

Journal • Preclinical • Chronic Myeloid Leukemia • Hematological Malignancies • Leukemia • Oncology • ABL1 • BCR • CASP3 • CASP7

Traditional Medicine Extracts of Gnidia sericocephala and Product Nkabinde in HIV-1 Latency Reversal: Insights from J-Lat Subtype B and J-Lat Subtype C Models. (PubMed, Int J Mol Sci) - "Reactivation potential was further tested in combination with established LRAs: panobinostat, SAHA, and TNF-α...Ex vivo, PN and G. sericocephala induced limited increases in HIV-1 gag RNA without substantial cytotoxicity. These findings demonstrate that G. sericocephala effectively reverses HIV-1 latency and potentiates TNF-α-induced reactivation, supporting its potential as a plant-derived LRA for future "shock and kill" HIV-1 cure strategies."

Journal • Human Immunodeficiency Virus • Infectious Disease • TNFA

Panobinostat Potentiates the Antitumor Efficacy of 5-Fluorouracil in Gastric Cancer by Suppressing Thymidylate Synthase Expression. (PubMed, Int J Mol Sci) - "Furthermore, panobinostat downregulated a network of oncogenes and cell cycle regulators, including c-Myc and key cyclins. These findings indicate that panobinostat can enhance 5-FU cytotoxicity by targeting TS expression and reprogramming oncogenic transcriptional networks, supporting its potential as a complementary strategy for overcoming fluoropyrimidine resistance in GC therapy."

Journal • Gastric Cancer • Oncology • Solid Tumor • MYC • TYMS

Evaluation of antitumor response to HDAC inhibitors in advanced head and neck cancer: A proportional meta-analysis of clinical trials. (PubMed, J Oncol Pharm Pract) - "Out of these 7 studies, the average proportion of antitumor response was calculated to be 0.758 among HNC patients who received HDACi concurrently with chemotherapy, chemoradiotherapy, and targeted therapy, whereas the average proportion of antitumor response rate to HDACi was 0.485 among priorly treated HNC patients. Vorinostat was the most used HDACi, where the proportion of favorable response was 0.49 compared to the non-vorinostat HDACi (0.77), like valproic acid, panobinostat, and romidepsin.ConclusionThe overall antitumor response to HDACi was found to be 0.65 (65%), which supports the use of HDACi among advanced HNC patients, particularly along with the concurrent chemo/chemoradiotherapy or targeted therapy."

Journal • Retrospective data • Review • Head and Neck Cancer • Oncology • Solid Tumor

Rationalising the inclusion of HDAC inhibitors with standard-of-care chemotherapy for high-risk neuroblastoma (LCC 2026) - "Within treatment naïve neuroblastomas, priming with the histone deacetylase (HDAC) inhibitor Vorinostat could overcome this chemoresistance and sensitise tumours to treatment with specific standard-of-care chemotherapies...A key observation from this study was that the HDAC inhibitors Romidepsin and Panobinostat led to increased apoptosis...These mechanistic insights are now being leveraged to design rationalised treatment regimens that combine these HDAC inhibitors with standard-of-care chemotherapies. This includes the addition of a priming step with Belinostat, which we have now demonstrated is capable of significantly reducing tumour growth and doubling median survival times in patient-derived xenograft models treated with topotecan and cyclophosphamide."

Neuroblastoma • Solid Tumor

Synergistic targeting of the ARID2-MYC axis by pomalidomide and panobinostat overcomes intrinsic IMiD resistance in multiple myeloma. (PubMed, Sci Rep) - "This finding highlights the functional relevance of IMiD's inherent polypharmacology in circumventing primary resistance mechanisms at the cellular level. Together, our results identify the ARID2-containing PBAF complex as a critical vulnerability in resistant myeloma cells and provide a mechanistic rationale for designing combination strategies that co-target this complex, with the potential to enhance therapeutic efficacy by overcoming drug resistance."

Journal • Hematological Malignancies • Multiple Myeloma • Oncology • ARID2 • IKZF1 • IRF4

Functional precision approach in patients with very high risk acute lymphoblastic leukaemia in India: a single-centre cohort study. (PubMed, Lancet Reg Health Southeast Asia) - "Drug sensitivity scores from DRP performed on 112 samples identified panobinostat (median DSS 23.4), venetoclax (20.7), daunorubicin (17.9), selinexor (12.7) and bortezomib (12.1) as effective in VHR or relapsed ALL. These findings support prospective evaluation of DRP-guided treatment regimens in VHR ALL. DBT-Wellcome India Alliance, Tata Consultancy Services."

Journal • Acute Lymphocytic Leukemia • Hematological Malignancies • Leukemia • Oncology • Pediatrics • T Acute Lymphoblastic Leukemia

MIG-6 Regulates HDAC1-Mediated Angiogenesis and Tumorigenesis in PTEN-Deficient Endometrioid Endometrial Cancer. (PubMed, Mol Cancer Res) - "Pharmacologic inhibition of HDAC1 with panobinostat recapitulated the tumor-suppressive effects observed with MIG-6 overexpression. These findings suggest that HDAC1 may represent a potential therapeutic target in EEC and that HDAC inhibition can attenuate early tumor progression and angiogenic signaling in preclinical models. Implications: This study identifies the MIG-6/HDAC1 axis as a key regulator of angiogenesis in EEC, highlighting HDAC1 inhibition as a promising targeted therapeutic strategy for early tumor suppression."

Journal • Endometrial Cancer • Gynecologic Cancers • Oncology • Solid Tumor • ERRFI1 • HDAC1 • HIF1A • PTEN