INCB054329
/ Incyte
- LARVOL DELTA
Home
Next
Prev
1 to 25
Of
26
Go to page
1
2
June 26, 2025
Maturation of human cardiac organoids enables complex disease modeling and drug discovery.
(PubMed, Nat Cardiovasc Res)
- "Modeling of cardiomyopathy caused by a desmoplakin (DSP) mutation resulted in fibrosis and cardiac dysfunction and led to identifying the bromodomain and extra-terminal inhibitor INCB054329 as a drug mitigating the desmoplakin-related functional defect. These findings establish DM-hCOs as a versatile platform for applications in cardiac biology, disease and drug screening."
Journal • Cardiomyopathy • Cardiovascular • Fibrosis • Immunology • RYR2
May 16, 2025
SYNERGISTIC EFFECTS OF NOVEL PROTEIN KINASE CK2 AND BET PROTEIN INHIBITORS IN MANTLE CELL LYMPHOMA: TARGETING SURVIVAL AND TUMOR-INDUCED IMMUNOSUPPRESSIVE SIGNALS
(EHA 2025)
- "We tested CX4945 and SGC-CK2-1, or CK2 gene silencing, with BET inhibitors (JQ-1, INCB054329) on MCL cells, assessing cell survival, apoptosis, and proliferation. The combined inhibition of CK2 and BET proteins represents a promising therapeutic approach targeting both intrinsic survival pathways that drive MCL progression and TME-related immunosuppressive signals that may contribute to therapy resistance. This dual-targeted strategy may open new avenues for improving immunotherapeutic responses in MCL, offering a rational approach to overcome current treatment limitations."
IO biomarker • Hematological Malignancies • Immunology • Lymphoma • Mantle Cell Lymphoma • Oncology • BRD4 • IGF1 • IL10 • MYC • PPBP • TIMP2
April 02, 2024
Targeting Metabolic Dependencies Fueling the TCA Cycle to Circumvent Therapy Resistance in Acute Myeloid Leukemia.
(PubMed, Cancer Res)
- "Furthermore, following treatments such as cytarabine, a standard in AML treatment for over four decades, drug-persisting leukemic cells exhibit an enhanced reliance on mitochondrial metabolism. In this issue of Cancer Research, two studies investigated dependencies of AML cells on two respiratory substrates, α-ketoglutarate and lactate-derived pyruvate, that support mitochondrial oxidative phosphorylation (OXPHOS) following treatment with the imipridone ONC-213 and the BET inhibitor INCB054329, respectively...In summary, targeting these mitochondrial dependencies might be a promising strategy to kill therapy-naïve and treatment-resistant OXPHOS-reliant LSCs and to delay or prevent relapse. See related articles by Monteith et al., p. 1101 and Su et al., p. 1084."
Journal • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • ATF4 • MCL1 • MCT1
December 03, 2023
Combined Inhibition of Protein Kinase CSNK2 and BET Proteins As a Novel Therapeutic Strategy for Mantle Cell Lymphoma
(ASH 2023)
- "Currently available therapeutic approaches for Mantle Cell Lymphoma (MCL), including the Bruton Tyrosine Kinase (BTK) inhibitors ibrutinib, acalabrutinib and zanubrutinib, are not curative...In MCL, BET inhibitors, such as INCB054329 or JQ-1, have been shown to increase apoptosis through downregulation of the AKT-mTOR, ERK, and other B Cell Receptor (BCR)-triggered cascades...The most effective and tested CSNK2 chemical inhibitor is CX4945 (silmitasertib), but very recently a novel compound, SGC-CK2, has been developed...Remarkably, CK2 inactivation led to a robust reduction of the BET inhibitor-induced increase of Mcl1, and NF-kB Ser 529 phosphorylation, thus counteracting BET-inhibitors-evoked compensatory pathways that could favor apoptosis resistance. Therefore, combined CSNK2 and BET proteins inhibition could represent an innovative strategy for chemotherapy and BTKi-resistant MCL."
Hematological Malignancies • Lymphoma • Mantle Cell Lymphoma • Oncology • ANXA5 • BRD4 • MYC
April 01, 2017
BET inhibitors INCB054329 and INCB057643 display significant activity in androgen-independent prostate cancer models
(AACR 2017)
- P1/2; "These results provide evidence of activity of INCB054329 and INCB057643 in prostate cancer cell lines. Although short term assays suggest a preferential anti-proliferative effect in androgen sensitive prostate cancer cells, both compounds also exhibit significant activity in an androgen-independent model both in vitro and in vivo suggesting that they might represent a valid therapeutic option for treatment of castration-resistant prostate cancer."
Biosimilar • Genito-urinary Cancer • Hematological Malignancies • Oncology • Prostate Cancer
February 13, 2021
Safety and Efficacy of Bromodomain and Extra-Terminal Inhibitors for the Treatment of Hematological Malignancies and Solid Tumors: A Systematic Study of Clinical Trials.
(PubMed, Front Pharmacol)
- " We retrieved and reviewed published reports on the clinical trials of twelve BET inhibitors including AZD5153, ABBV-075, BMS-986158, CPI-0610, GSK525762, OTX-015, PLX51107, INCB054329, INCB057643, FT-1101, CC-90010, and ODM-207 for patients with hematological malignancies and solid tumors and summarized their published target genes. All BET inhibitors reviewed in our study exhibited exposure-dependent thrombocytopenia, which may limit their clinical application. Moreover, further efforts are necessary to explore the optimal dosing schemes and combinations to maximize the efficacy of BET inhibitors."
Clinical • Journal • Review • Fatigue • Hematological Malignancies • Infectious Disease • Neutropenia • Oncology • Pneumonia • Respiratory Diseases • Solid Tumor • Thrombocytopenia
November 06, 2020
BET inhibition enhances the antileukemic activity of low-dose Venetoclax in acute myeloid leukemia.
(PubMed, Clin Cancer Res)
- "Our findings suggest low dose combinations of VEN and BETi may be more efficacious for AML patients than either monotherapy, potentially providing a longer, more tolerable dosing regimen."
Journal • Acute Myelogenous Leukemia • Hematological Malignancies • Leukemia • Oncology • BAX
November 01, 2020
BRDT is a novel regulator of eIF4EBP1 in renal cell carcinoma.
(PubMed, Oncol Rep)
- "Taken together, these data suggested that blocking of BRDT by PLX51107, INCB054329 or BRDT knockdown suppressed the growth of RCC via decreasing eIF4EBP1, thereby leading to decreased c‑myc transcription levels. Considering the regulatory function of BET proteins in gene transcription, the present study suggested that there is a novel mechanism underlying eIF4EBP1 regulation by BRDT, and subsequently decreased c‑myc in RCC, and further identified a new approach by regulating eIF4EBP1 or c‑myc for enhancing BRDT‑targeting RCC therapy."
Journal • Genito-urinary Cancer • Nephrology • Oncology • Renal Cell Carcinoma • Renal Disease • Solid Tumor • EIF4E • EIF4EBP1 • MYC
January 13, 2016
Incyte: J.P. Morgan Healthcare Conference
(Incyte)
- Anticipated data from P1/2 trial (NCT02431260) in advanced malignancies in 2016
Anticipated P1/2 data • Oncology
November 03, 2017
Phase 1/2 study of INCB054329, a bromodomain and extraterminal (BET) protein inhibitor, in patients (pts) with advanced malignancies
(EORTC-NCI-AACR 2017)
- P1/2; "Initial data show that INCB054329 has preliminary activity and is reasonably well tolerated. Thrombocytopenia, an on-target effect of BET inhibition, was the only DLT and was associated with exposure. Updated data in all enrolled cohorts including the intrapatient dose titration cohort will be presented."
P1/2 data • Colorectal Cancer • Gastrointestinal Cancer • Hematological Malignancies • Lung Cancer • Lymphoma • Non Small Cell Lung Cancer • Oncology • Solid Tumor
February 17, 2017
INCB054329: Anticipated dose escalation data from P1/2 trial (NCT02431260) in advanced malignancies later in 2017
(Incyte)
- Q4 & Year-End FY 2016 Results
Anticipated P1/2 data • Oncology
April 23, 2020
Radiosynthesis and in vivo evaluation of a new positron emission tomography radiotracer targeting bromodomain and extra-terminal domain (BET) family proteins.
(PubMed, Nucl Med Biol)
- "The imaging results in rodents in vivo demonstrate that [C]PB003 binds to BET with high selectivity and specificity and has favorable uptake in peripheral organs. However, the low brain uptake of [C]PB003 limits the visualization of brain regions indicating the efforts are still needed to discover the new BET imaging probes for brain visualization."
Journal • Preclinical
September 14, 2018
The Novel Bromodomain and Extraterminal Domain Inhibitor INCB054329 Induces Vulnerabilities in Myeloma Cells That Inform Rational Combination Strategies.
(PubMed, Clin Cancer Res)
- "Preclinical data reveal insights into vulnerabilities created in myeloma cells by BET protein inhibition and potential strategies that can be leveraged in clinical studies to enhance the activity of INCB054329."
Journal
November 07, 2019
Bromodomain and Extra Terminal Domain (BET) Inhibitors Sensitize Chronic Myelomonocytic Leukemia (CMML) to PIM Inhibition Via Downregulation of Mir-33a
(ASH 2019)
- "Surprisingly, we identified that PIM1 was increased following treatment with INCB54329, other BETi, or a JQ1-derived PROTAC (Fig...Consistent with this, isogenic SKM1 leukemia cells engineered to overexpress PIM1 were resistant to INCB54329 and were more sensitive to INCB53914 versus controls cells...Collectively, these studies established BET and PIM inhibition as a novel and potent combination therapy for CMML that is mediated by miR-33a-dependent upregulation of PIM1(Fig. 1E)."
May 11, 2017
An Open-Label, Dose-Escalation Study of INCB054329 in Patients With Advanced Malignancies
(clinicaltrials.gov)
- P1/2; N=69; Active, not recruiting; Sponsor: Incyte Corporation; Recruiting ➔ Active, not recruiting; N=340 ➔ 69
Clinical • Enrollment change • Enrollment closed
February 05, 2018
An Open-Label, Dose-Escalation Study of INCB054329 in Patients With Advanced Malignancies
(clinicaltrials.gov)
- P1/2; N=69; Completed; Sponsor: Incyte Corporation; Active, not recruiting ➔ Completed; Trial completion date: Feb 2018 ➔ Jan 2018
Clinical • Trial completion • Trial completion date
April 12, 2017
An Open-Label, Dose-Escalation Study of INCB054329 in Patients With Advanced Malignancies
(clinicaltrials.gov)
- P1/2; N=340; Recruiting; Sponsor: Incyte Corporation; N=155 ➔ 340
Clinical • Enrollment change
June 14, 2019
An Open-Label, Dose-Escalation Study of INCB054329 in Patients With Advanced Malignancies
(clinicaltrials.gov)
- P1/2; N=69; Terminated; Sponsor: Incyte Corporation; Completed ➔ Terminated; As of 31 JAN 2018, the study was terminated by the sponsor due to PK variability.
Clinical • Trial termination
November 21, 2017
An Open-Label, Dose-Escalation Study of INCB054329 in Patients With Advanced Malignancies
(clinicaltrials.gov)
- P1/2; N=69; Active, not recruiting; Sponsor: Incyte Corporation; Trial primary completion date: Oct 2017 ➔ Jan 2018
Clinical • Trial primary completion date
April 30, 2015
An Open-Label, Dose-Escalation Study of INCB054329 in Patients With Advanced Malignancies
(clinicaltrials.gov)
- P1; N=65; Not yet recruiting; Sponsor: Incyte Corporation
Clinical • New P1 trial
August 28, 2015
An Open-Label, Dose-Escalation Study of INCB054329 in Patients With Advanced Malignancies
(clinicaltrials.gov)
- P1/2; N=155; Recruiting; Sponsor: Incyte Corporation; Phase classification: P1 ➔ P1/2; N=65 ➔ 155; Trial primary completion date: May 2017 ➔ Oct 2017
Clinical • Enrollment change • Phase classification • Trial primary completion date
June 10, 2015
An Open-Label, Dose-Escalation Study of INCB054329 in Patients With Advanced Malignancies
(clinicaltrials.gov)
- P1; N=65; Recruiting; Sponsor: Incyte Corporation; Not yet recruiting ➔ Recruiting
Clinical • Enrollment open
September 19, 2019
Development of 2 Bromodomain and Extraterminal Inhibitors With Distinct Pharmacokinetic and Pharmacodynamic Profiles for the Treatment of Advanced Malignancies.
(PubMed, Clin Cancer Res)
- P1/2; "INCB057643 exhibited a more favorable PK profile versus INCB054329; exposure-dependent thrombocytopenia was observed with both drugs which limited the target inhibition that could be safely maintained. Further efforts are required to identify patient populations that can benefit most, and an optimal dosing scheme to maximize therapeutic index."
Journal • PK/PD data
August 14, 2019
Efficacy of Novel Bromodomain and Extraterminal Inhibitors in Combination with Chemotherapy for Castration-Resistant Prostate Cancer.
(PubMed, Eur Urol Oncol)
- "Collectively, these results provide the first evidence of the therapeutic benefit obtainable by combining BETis with non-androgen receptor-targeted therapies for the treatment of mCRPC."
Clinical • Combination therapy • Journal
May 08, 2019
Assessing the link between epigenetics and metabolism in acute myeloid leukemia
(AAI 2019)
- "...We profiled three different AML cell lines’ metabolic responses to INCB54329, an inhibitor of bromodomain proteins...The precise function of glutaminolysis in hematopoiesis remains unclear. Unraveling the link between glutamine metabolism, epigenetic modifications, and stem cell function presents a novel therapeutic opportunity for various hematologic malignancies, chief among them acute myeloid leukemia"
1 to 25
Of
26
Go to page
1
2