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Article ; Online: Inhibitors of bromodomain and extra-terminal proteins for treating multiple human diseases.

Kulikowski, Ewelina / Rakai, Brooke D / Wong, Norman C W

2020 Volume 41, Issue 1, Page(s) 223–245

Abstract: Clinical development of bromodomain and extra-terminal (BET) protein inhibitors differs from the traditional course of drug development. These drugs are simultaneously being evaluated for treating a wide spectrum of human diseases due to their novel ... ...

Abstract	Clinical development of bromodomain and extra-terminal (BET) protein inhibitors differs from the traditional course of drug development. These drugs are simultaneously being evaluated for treating a wide spectrum of human diseases due to their novel mechanism of action. BET proteins are epigenetic "readers," which play a primary role in transcription. Here, we briefly describe the BET family of proteins, of which BRD4 has been studied most extensively. We discuss BRD4 activity at latent enhancers as an example of BET protein function. We examine BRD4 redistribution and enhancer reprogramming in embryonic development, cancer, cardiovascular, autoimmune, and metabolic diseases, presenting hallmark studies that highlight BET proteins as attractive targets for therapeutic intervention. We review the currently available approaches to targeting BET proteins, methods of selectively targeting individual bromodomains, and review studies that compare the effects of selective BET inhibition to those of pan-BET inhibition. Lastly, we examine the current clinical landscape of BET inhibitor development.
MeSH term(s)	Cell Cycle Proteins ; Humans ; Neoplasms/drug therapy ; Nuclear Proteins ; Protein Domains ; Transcription Factors
Chemical Substances	BRD4 protein, human ; Cell Cycle Proteins ; Nuclear Proteins ; Transcription Factors
Language	English
Publishing date	2020-09-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603210-2
ISSN	1098-1128 ; 0198-6325
ISSN (online)	1098-1128
ISSN	0198-6325
DOI	10.1002/med.21730
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Article: Apabetalone, a Clinical-Stage, Selective BET Inhibitor, Opposes DUX4 Target Gene Expression in Primary Human FSHD Muscle Cells.

Sarsons, Christopher D / Gilham, Dean / Tsujikawa, Laura M / Wasiak, Sylwia / Fu, Li / Rakai, Brooke D / Stotz, Stephanie C / Carestia, Agostina / Sweeney, Michael / Kulikowski, Ewelina

Biomedicines

2023 Volume 11, Issue 10

Abstract: Facioscapulohumeral dystrophy (FSHD) is a muscle disease caused by inappropriate expression of the double homeobox 4 (DUX4) gene in skeletal muscle, and its downstream activation of pro-apoptotic transcriptional programs. Inhibitors ... ...

Abstract	Facioscapulohumeral dystrophy (FSHD) is a muscle disease caused by inappropriate expression of the double homeobox 4 (DUX4) gene in skeletal muscle, and its downstream activation of pro-apoptotic transcriptional programs. Inhibitors of
Language	English
Publishing date	2023-09-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11102683
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Article: Apabetalone Downregulates Fibrotic, Inflammatory and Calcific Processes in Renal Mesangial Cells and Patients with Renal Impairment.

Gilham, Dean / Wasiak, Sylwia / Rakai, Brooke D / Fu, Li / Tsujikawa, Laura M / Sarsons, Christopher D / Carestia, Agostina / Lebioda, Kenneth / Johansson, Jan O / Sweeney, Michael / Kalantar-Zadeh, Kamyar / Kulikowski, Ewelina

Biomedicines

2023 Volume 11, Issue 6

Abstract: Epigenetic mechanisms are implicated in transcriptional programs driving chronic kidney disease (CKD). Apabetalone is an orally available inhibitor of bromodomain and extraterminal (BET) proteins, which are epigenetic readers that modulate gene ... ...

Abstract	Epigenetic mechanisms are implicated in transcriptional programs driving chronic kidney disease (CKD). Apabetalone is an orally available inhibitor of bromodomain and extraterminal (BET) proteins, which are epigenetic readers that modulate gene expression. In the phase 3 BETonMACE trial, apabetalone reduced risk of major adverse cardiac events (MACE) by 50% in the CKD subpopulation, indicating favorable effects along the kidney-heart axis. Activation of human renal mesangial cells (HRMCs) to a contractile phenotype that overproduces extracellular matrix (ECM) and inflammatory cytokines, and promotes calcification, frequently accompanies CKD to drive pathology. Here, we show apabetalone downregulated HRMC activation with TGF-β1 stimulation by suppressing TGF-β1-induced α-smooth muscle actin (α-SMA) expression, α-SMA assembly into stress fibers, enhanced contraction, collagen overproduction, and expression of key drivers of fibrosis, inflammation, or calcification including thrombospondin, fibronectin, periostin, SPARC, interleukin 6, and alkaline phosphatase. Lipopolysaccharide-stimulated expression of inflammatory genes
Language	English
Publishing date	2023-06-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11061663
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Article ; Online: Dual mechanism: Epigenetic inhibitor apabetalone reduces SARS-CoV-2 Delta and Omicron variant spike binding and attenuates SARS-CoV-2 RNA induced inflammation.

Fu, Li / Gilham, Dean / Stotz, Stephanie C / Sarsons, Christopher D / Rakai, Brooke D / Tsujikawa, Laura M / Wasiak, Sylwia / Johansson, Jan O / Sweeney, Michael / Wong, Norman C W / Kulikowski, Ewelina

International immunopharmacology

2023 Volume 117, Page(s) 109929

Abstract: The SARS-CoV-2 virus initiates infection via interactions between the viral spike protein and the ACE2 receptors on host cells. Variants of concern have mutations in the spike protein that enhance ACE2 binding affinity, leading to increased virulence and ...

Abstract	The SARS-CoV-2 virus initiates infection via interactions between the viral spike protein and the ACE2 receptors on host cells. Variants of concern have mutations in the spike protein that enhance ACE2 binding affinity, leading to increased virulence and transmission. Viral RNAs released after entry into host cells trigger interferon-I (IFN-I) mediated inflammatory responses for viral clearance and resolution of infection. However, overreactive host IFN-I responses and pro-inflammatory signals drive COVID-19 pathophysiology and disease severity during acute infection. These immune abnormalities also lead to the development of post-COVID syndrome if persistent. Novel therapeutics are urgently required to reduce short- and long-term pathologic consequences associated with SARS-CoV-2 infection. Apabetalone, an inhibitor of epigenetic regulators of the BET protein family, is a candidate for COVID-19 treatment via a dual mechanism of action. In vitro, apabetalone downregulates ACE2 gene expression to limit SARS-CoV-2 entry and propagation. In pre-clinical models and patients treated for cardiovascular disease, apabetalone inhibits expression of inflammatory mediators involved in the pathologic cytokine storm (CS) stimulated by various cytokines. Here we show apabetalone treatment of human lung epithelial cells reduces binding of viral spike protein regardless of mutations found in the highly contagious Delta variant and heavily mutated Omicron. Additionally, we demonstrate that apabetalone counters expression of pro-inflammatory factors with roles in CS and IFN-I signaling in lung cells stimulated with SARS-CoV-2 RNA. Our results support clinical evaluation of apabetalone to treat COVID-19 and post-COVID syndrome regardless of the SARS-CoV-2 variant.
MeSH term(s)	Humans ; SARS-CoV-2 ; RNA, Viral ; COVID-19 ; Angiotensin-Converting Enzyme 2/genetics ; COVID-19 Drug Treatment ; Spike Glycoprotein, Coronavirus/genetics ; Inflammation/drug therapy ; Interferons ; Antibodies ; Cytokine Release Syndrome/drug therapy ; Epigenesis, Genetic
Chemical Substances	RNA, Viral ; apabetalone (8R4A7GDZ1D) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23) ; Spike Glycoprotein, Coronavirus ; Interferons (9008-11-1) ; Antibodies ; spike protein, SARS-CoV-2
Language	English
Publishing date	2023-02-23
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2043785-7
ISSN	1878-1705 ; 1567-5769
ISSN (online)	1878-1705
ISSN	1567-5769
DOI	10.1016/j.intimp.2023.109929
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Article ; Online: Pharmacologic epigenetic modulators of alkaline phosphatase in chronic kidney disease.

Haarhaus, Mathias / Gilham, Dean / Kulikowski, Ewelina / Magnusson, Per / Kalantar-Zadeh, Kamyar

Current opinion in nephrology and hypertension

2019 Volume 29, Issue 1, Page(s) 4–15

Abstract: Purpose of review: In chronic kidney disease (CKD), disturbance of several metabolic regulatory mechanisms cause premature ageing, accelerated cardiovascular disease (CVD), and mortality. Single-target interventions have repeatedly failed to improve the ...

Abstract	Purpose of review: In chronic kidney disease (CKD), disturbance of several metabolic regulatory mechanisms cause premature ageing, accelerated cardiovascular disease (CVD), and mortality. Single-target interventions have repeatedly failed to improve the prognosis for CKD patients. Epigenetic interventions have the potential to modulate several pathogenetic processes simultaneously. Alkaline phosphatase (ALP) is a robust predictor of CVD and all-cause mortality and implicated in pathogenic processes associated with CVD in CKD. Recent findings: In experimental studies, epigenetic modulation of ALP by microRNAs or bromodomain and extraterminal (BET) protein inhibition has shown promising results for the treatment of CVD and other chronic metabolic diseases. The BET inhibitor apabetalone is currently being evaluated for cardiovascular risk reduction in a phase III clinical study in high-risk CVD patients, including patients with CKD (ClinicalTrials.gov Identifier: NCT02586155). Phase II studies demonstrate an ALP-lowering potential of apabetalone, which was associated with improved cardiovascular and renal outcomes. Summary: ALP is a predictor of CVD and mortality in CKD. Epigenetic modulation of ALP has the potential to affect several pathogenetic processes in CKD and thereby improve cardiovascular outcome.
MeSH term(s)	Alkaline Phosphatase/antagonists & inhibitors ; Alkaline Phosphatase/genetics ; Alkaline Phosphatase/physiology ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/etiology ; Epigenesis, Genetic ; Gene Expression Regulation, Enzymologic ; Humans ; Quinazolinones/therapeutic use ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/enzymology
Chemical Substances	Quinazolinones ; apabetalone (8R4A7GDZ1D) ; Alkaline Phosphatase (EC 3.1.3.1)
Language	English
Publishing date	2019-11-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000570
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Article: The BET inhibitor apabetalone decreases neuroendothelial proinflammatory activation

Wasiak, Sylwia / Fu, Li / Daze, Emily / Gilham, Dean / Rakai, Brooke D / Stotz, Stephanie C / Tsujikawa, Laura M / Sarsons, Chris D / Studer, Deborah / Rinker, Kristina D / Jahagirdar, Ravi / Wong, Norman C W / Sweeney, Michael / Johansson, Jan O / Kulikowski, Ewelina

Translational neuroscience

2023 Volume 14, Issue 1, Page(s) 20220332

Abstract: Brain vascular inflammation is characterized by endothelial activation and immune cell recruitment to the blood vessel wall, potentially causing a breach in the blood - brain barrier, brain parenchyma inflammation, and a decline of cognitive function. ... ...

Abstract	Brain vascular inflammation is characterized by endothelial activation and immune cell recruitment to the blood vessel wall, potentially causing a breach in the blood - brain barrier, brain parenchyma inflammation, and a decline of cognitive function. The clinical-stage small molecule, apabetalone, reduces circulating vascular endothelial inflammation markers and improves cognitive scores in elderly patients by targeting epigenetic regulators of gene transcription, bromodomain and extraterminal proteins. However, the effect of apabetalone on cytokine-activated brain vascular endothelial cells (BMVECs) is unknown. Here, we show that apabetalone treatment of BMVECs reduces hallmarks of
Language	English
Publishing date	2023-12-31
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2581219-1
ISSN	2081-6936 ; 2081-3856
ISSN (online)	2081-6936
ISSN	2081-3856
DOI	10.1515/tnsci-2022-0332
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Article ; Online: Reduction in the risk of major adverse cardiovascular events with the BET protein inhibitor apabetalone in patients with recent acute coronary syndrome, type 2 diabetes, and moderate to high likelihood of non-alcoholic fatty liver disease.

Toth, Peter P / Schwartz, Gregory G / Nicholls, Stephen J / Khan, Aziz / Szarek, Michael / Ginsberg, Henry N / Johansson, Jan O / Kalantar-Zadeh, Kamyar / Kulikowski, Ewelina / Lebioda, Ken / Wong, Norman C W / Sweeney, Michael / Ray, Kausik K

American journal of preventive cardiology

2022 Volume 11, Page(s) 100372

Abstract: Background: Nonalcoholic fatty liver disease (NAFLD) is common among patients with type 2 diabetes mellitus (T2DM) and is associated with increased risk for coronary atherosclerosis and acute cardiovascular (CV) events. We employed the validated, non- ... ...

Abstract	Background: Nonalcoholic fatty liver disease (NAFLD) is common among patients with type 2 diabetes mellitus (T2DM) and is associated with increased risk for coronary atherosclerosis and acute cardiovascular (CV) events. We employed the validated, non-invasive Angulo NAFLD fibrosis score (FS) in an intervention study in patients with T2DM and recent acute coronary syndrome (ACS) to determine the association of FS with CV risk and treatment response to apabetalone. Apabetalone is a novel selective inhibitor of the second bromodomain of bromodomain and extra-terminal (BET) proteins, epigenetic regulators of gene expression. Methods: The Phase 3 BETonMACE trial compared apabetalone with placebo in 2,425 patients with T2DM and recent ACS. In this Results: In 73.7% of patients, FS was elevated and consistent with a moderate-to-high likelihood of advanced liver fibrosis (FS+); 26.3% of patients had a lower FS (FS Conclusions: Amongst patients with T2DM, recent ACS, and a moderate-to-high likelihood of advanced liver fibrosis, apabetalone was associated with a significantly lower rate of ischemic MACE and HHF and attenuated the increase in hepatic FS over time.
Language	English
Publishing date	2022-08-08
Publishing country	Netherlands
Document type	Journal Article
ISSN	2666-6677
ISSN (online)	2666-6677
DOI	10.1016/j.ajpc.2022.100372
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Article ; Online: Inhibition of epigenetic reader proteins by apabetalone counters inflammation in activated innate immune cells from Fabry disease patients receiving enzyme replacement therapy.

Fu, Li / Wasiak, Sylwia / Tsujikawa, Laura M / Rakai, Brooke D / Stotz, Stephanie C / Wong, Norman C W / Johansson, Jan O / Sweeney, Michael / Mohan, Connie M / Khan, Aneal / Kulikowski, Ewelina

Pharmacology research & perspectives

2022 Volume 10, Issue 3, Page(s) e00949

Abstract: Fabry disease (FD) is a rare X-linked disorder of lipid metabolism, characterized by the accumulation of globotriaosylceramide (Gb3) due to defective the lysosomal enzyme, α-galactosidase. Gb3 deposits activate immune-mediated systemic inflammation, ... ...

Abstract	Fabry disease (FD) is a rare X-linked disorder of lipid metabolism, characterized by the accumulation of globotriaosylceramide (Gb3) due to defective the lysosomal enzyme, α-galactosidase. Gb3 deposits activate immune-mediated systemic inflammation, ultimately leading to life-threatening consequences in multiple organs such as the heart and kidneys. Enzyme replacement therapy (ERT), the standard of care, is less effective with advanced tissue injury and inflammation in patients with FD. Here, we showed that MCP-1 and TNF-α cytokine levels were almost doubled in plasma from ERT-treated FD patients. Chemokine receptor CCR2 surface expression was increased by twofold on monocytes from patients with low eGFR. We also observed an increase in IL12B transcripts in unstimulated peripheral blood mononuclear cells (PBMCs) over a 2-year period of continuous ERT. Apabetalone is a clinical-stage oral bromodomain and extra terminal protein inhibitor (BETi), which has beneficial effects on cardiovascular and kidney disease related pathways including inflammation. Here, we demonstrate that apabetalone, a BD2-selective BETi, dose dependently reduced the production of MCP-1 and IL-12 in stimulated PBMCs through transcriptional regulation of their encoding genes. Reactive oxygen species production was diminished by up to 80% in stimulated neutrophils following apabetalone treatment, corresponding with inhibition of NOX2 transcription. This study elucidates that inhibition of BET proteins by BD2-selective apabetalone alleviates inflammatory processes and oxidative stress in innate immune cells in general and in FD. These results suggest potential benefit of BD2-selective apabetalone in controlling inflammation and oxidative stress in FD, which will be further investigated in clinical trials.
MeSH term(s)	Cytokines/metabolism ; Enzyme Replacement Therapy ; Epigenesis, Genetic ; Fabry Disease/drug therapy ; Fabry Disease/genetics ; Fabry Disease/metabolism ; Humans ; Immunity, Innate ; Inflammation/drug therapy ; Inflammation/genetics ; Leukocytes, Mononuclear/metabolism ; Quinazolinones
Chemical Substances	Cytokines ; Quinazolinones ; apabetalone (8R4A7GDZ1D)
Language	English
Publishing date	2022-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2740389-0
ISSN	2052-1707 ; 2052-1707
ISSN (online)	2052-1707
ISSN	2052-1707
DOI	10.1002/prp2.949
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Article ; Online: BET Protein Inhibition for Pulmonary Arterial Hypertension: A Pilot Clinical Trial.

Provencher, Steeve / Potus, François / Blais-Lecours, Pascale / Bernard, Sarah / Martineau, Sandra / Breuils-Bonnet, Sandra / Weatherald, Jason / Sweeney, Mike / Kulikowski, Ewelina / Boucherat, Olivier / Bonnet, Sebastien

American journal of respiratory and critical care medicine

2022 Volume 205, Issue 11, Page(s) 1357–1360

MeSH term(s)	Humans ; Nuclear Proteins ; Pulmonary Arterial Hypertension
Chemical Substances	Nuclear Proteins
Language	English
Publishing date	2022-03-26
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	1180953-x
ISSN	1535-4970 ; 0003-0805 ; 1073-449X
ISSN (online)	1535-4970
ISSN	0003-0805 ; 1073-449X
DOI	10.1164/rccm.202109-2182LE
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Article ; Online: Breaking boundaries: Pan BETi disrupt 3D chromatin structure, BD2-selective BETi are strictly epigenetic transcriptional regulators.

Tsujikawa, Laura M / Kharenko, Olesya A / Stotz, Stephanie C / Rakai, Brooke D / Sarsons, Christopher D / Gilham, Dean / Wasiak, Sylwia / Fu, Li / Sweeney, Michael / Johansson, Jan O / Wong, Norman C W / Kulikowski, Ewelina

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2022 Volume 152, Page(s) 113230

Abstract: Background: Bromodomain and extraterminal proteins (BETs) are more than just epigenetic regulators of transcription. Here we highlight a new role for the BET protein BRD4 in the maintenance of higher order chromatin structure at Topologically ... ...

Abstract	Background: Bromodomain and extraterminal proteins (BETs) are more than just epigenetic regulators of transcription. Here we highlight a new role for the BET protein BRD4 in the maintenance of higher order chromatin structure at Topologically Associating Domain Boundaries (TADBs). BD2-selective and pan (non-selective) BET inhibitors (BETi) differentially support chromatin structure, selectively affecting transcription and cell viability. Methods: Using RNA-seq and BRD4 ChIP-seq, the differential effect of BETi treatment on the transcriptome and BRD4 chromatin occupancy of human aortic endothelial cells from diabetic patients (dHAECs) stimulated with TNFα was evaluated. Chromatin decondensation and DNA fragmentation was assessed by immunofluorescence imaging and quantification. Key dHAEC findings were verified in proliferating monocyte-like THP-1 cells using real time-PCR, BRD4 co-immunoprecipitation studies, western blots, proliferation and apoptosis assays. Findings: We discovered that 1) BRD4 co-localizes with Ying-Yang 1 (YY1) at TADBs, critical chromatin structure complexes proximal to many DNA repair genes. 2) BD2-selective BETi enrich BRD4/YY1 associations, while pan-BETi do not. 3) Failure to support chromatin structures through BRD4/YY1 enrichment inhibits DNA repair gene transcription, which induces DNA damage responses, and causes widespread chromatin decondensation, DNA fragmentation, and apoptosis. 4) BD2-selective BETi maintain high order chromatin structure and cell viability, while reducing deleterious pro-inflammatory transcription. Interpretation: BRD4 plays a previously unrecognized role at TADBs. BETi differentially impact TADB stability. Our results provide translational insight for the development of BETi as therapeutics for a range of diseases including CVD, chronic kidney disease, cancer, and COVID-19.
MeSH term(s)	COVID-19 ; Cell Cycle Proteins/metabolism ; Chromatin ; Endothelial Cells/metabolism ; Epigenesis, Genetic ; Humans ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Transcription Factors/metabolism
Chemical Substances	BRD4 protein, human ; Cell Cycle Proteins ; Chromatin ; Nuclear Proteins ; Transcription Factors
Language	English
Publishing date	2022-06-07
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2022.113230
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