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Combination therapy is often an effective strategy to treat cancer. In this study, we examined the growth-inhibitory effects of Am80 (tamibarotene), a specific retinoic acid receptor (RAR) alpha/beta agonist, in combination with a histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA), or a DNA methyl transferase (DNMT) inhibitor, 5-aza-2?-deoxycytidine, on androgen receptor (AR)-positive and AR-negative prostate cancer cell lines (LNCaP and PC-3, respectively). We found that the combination therapy of SAHA and Am80 showed an enhanced growth-inhibitory effect on LNCaP cells. Further studies with various HDAC isotype-selective inhibitors showed that SAHA and KD5170 (a selective class I and II HDAC inhibitor) each increased the RARalpha protein level in LNCaP cells. Our results indicate that the target of the enhancing effect belongs to the Class IIb HDACs, especially HDAC6. Dual targeting of Class IIb HDAC and RARalpha may be a candidate therapeutic strategy for prostate cancer.

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Reference:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

 

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Additional Sex Combs-Like 1 (ASXL1) is mutated at a high frequency in all forms of myeloid malignancies associated with poor prognosis. We generated a Vav1 promoter-driven Flag- Asxl1Y588X transgenic mouse model, Asxl1Y588XTg, to express a truncated FLAG-ASXL1aa1-587 protein in the hematopoietic system. The Asxl1Y588XTg mice had an enlarged hematopoietic stem cell (HSC) pool, shortened survival, and predisposition to a spectrum of myeloid malignancies, thereby recapitulating the characteristics of myeloid malignancy patients with ASXL1 mutations. ATAC- and RNA-sequencing analyses revealed that the ASXL1aa1-587 truncating protein expression results in more open chromatin in cKit1 cells compared with wild-type cells, accompanied by dysregulated expression of genes critical for HSC self-renewal and differentiation. Liquid chromatography?tandem mass spectrometry and coimmunoprecipitation experiments showed that ASXL1aa1-587 acquired an interaction with BRD4. An epigenetic drug screening demonstrated a hypersensitivity of Asxl1Y588XTg bone marrow cells to BET bromodomain inhibitors. This study demonstrates that ASXL1aa1-587 plays a gain-of-function role in promoting myeloid malignancies. Our model provides a powerful platform to test therapeutic approaches of targeting the ASXL1 truncation mutations in myeloid malignancies. (Blood. 2018;131(3):328-341)

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Reference:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

 

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DNA in the nucleus of eukaryote cells is packaged in the nucleosomes around histone proteins, and this is highly organized and tightly regulated to control gene transcription. This packaging is not static and the histone tails undergo a wide variety of post-translational modifications that regulate gene transcription, and these patterns have been shown to be aberrantly regulated in multiple disease states. The biology behind these histone modifications is being elucidated, and it is now known that multiple proteins control the writing, reading and removal of these covalent histone modifcations. The first agents, vorinostat and romidepsin, which inhibit histone deacetylase enzymes responsible for removing one of these marks have been approved for use in humans. This review focuses on the progress in the development of the second generation of epigenetic modifiers able to modulate histone marks, and restore normal gene transcription.

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Reference:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

 

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INHIBITORS OF HISTONE DEACETYLASE FOR THE TREATMENT OF DISEASE

Disclosed herein are carbonyl compounds of having the structural formula: or a pharmaceutically acceptable salt, ester, or prodrug thereof, Methods and compositions are disclosed for treating disease states including, but not limited to cancers, autoimmune diseases, tissue damage, central nervous system disorders, neurodegenerative disorders, fibrosis, bone disorders, polyglutamine-repeat disorders, anemias, thalassemias, inflammatory conditions, cardiovascular conditions, and disorders in which angiogenesis play a role in pathogenesis, using the compounds of the invention. In addition, methods of modulating the activity of histone deacetylase (HDAC) are also disclosed.

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Reference:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

 

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Identification of KD5170: A novel mercaptoketone-based histone deacetylase inhibitor

We report the identification of KD5170, a potent mercaptoketone-based Class I and II-histone deacetylase inhibitor that demonstrates broad spectrum cytotoxic activity against a range of human tumor-derived cell lines. KD5170 exhibits robust and sustained histone H3 hyperacetylation in HCT-116 xenograft tumors following single oral or iv dose and inhibition of tumor growth following chronic dosing.

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Reference:
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

 

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Use of histone deacetylase inhibitors for the care of Philadephia-negative myeloproliferative syndromes

The use of substances capable of inhibiting one or more enzymes of the histone deacetylase family (histone deacetylase inhibitors) for the therapeutic treatment of Philadelphia-negative myeloproliferative syndromes (polycythemia vera, essential thrombocythemia or idiopathic myelofibrosis) is described. The dosage of the above-mentioned substances is significantly lower than that normally used for the care of other tumor syndromes and may be from 10 to 150 mg/day/patient.

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Reference£º
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

 

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USE OF HISTONE DEACETYLASE INHIBITORS FOR THE CARE OF PHILADELPHIA-NEGATIVE MYELOPROLIFERATIVE SYNDROMES

The use of substances capable of inhibiting one or more enzymes of the histone deacetylase family (histone deacetylase inhibitors) for the therapeutic treatment of Philadelphia-negative myeloproliferative syndromes (polyeythemia vera, essential thrombocythemia or idiopathic myelotibrosis) is described. The dosage of the above-mentioned substances is significantly lower than that normally used for the care of other tumour syndromes and may be from 10 to 150 mg/day/patient.

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Reference£º
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

 

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SALTS OF INHIBITORS OF HISTONE DEACETYLASE FOR THE TREATMENT OF DISEASE

Disclosed herein are salts of carbonyl compounds as inhibitors of histone deacetylase (HDAC), useful in treating disease states including cancers, autoimmune diseases, tissue damage, central nervous system disorders, neurodegenerative disorders, fibrosis, bone disorders, polyglutamine-repeat disorders, anemias, thalassemias, inflammatory conditions, cardiovascular conditions, and disorders in which angiogenesis plays a role in pathogenesis.

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Reference£º
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

 

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Class IIb HDAC inhibition enhances the inhibitory effect of AM80, a synthetic retinoid, in prostate cancer

Combination therapy is often an effective strategy to treat cancer. In this study, we examined the growth-inhibitory effects of Am80 (tamibarotene), a specific retinoic acid receptor (RAR) alpha/beta agonist, in combination with a histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA), or a DNA methyl transferase (DNMT) inhibitor, 5-aza-2?-deoxycytidine, on androgen receptor (AR)-positive and AR-negative prostate cancer cell lines (LNCaP and PC-3, respectively). We found that the combination therapy of SAHA and Am80 showed an enhanced growth-inhibitory effect on LNCaP cells. Further studies with various HDAC isotype-selective inhibitors showed that SAHA and KD5170 (a selective class I and II HDAC inhibitor) each increased the RARalpha protein level in LNCaP cells. Our results indicate that the target of the enhancing effect belongs to the Class IIb HDACs, especially HDAC6. Dual targeting of Class IIb HDAC and RARalpha may be a candidate therapeutic strategy for prostate cancer.

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Reference£º
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem

 

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USE OF HISTONE DEACETYLASE INHIBITORS FOR THE CARE OF PHILADELPHIA-NEGATIVE MYELOPROLIFERATIVE SYNDROMES

The use of substances capable of inhibiting one or more enzymes of the histone deacetylase family (histone deacetylase inhibitors) for the therapeutic treatment of Philadelphia-negative myeloproliferative syndromes (polyeythemia vera, essential thrombocythemia or idiopathic myelotibrosis) is described. The dosage of the above-mentioned substances is significantly lower than that normally used for the care of other tumour syndromes and may be from 10 to 150 mg/day/patient.

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Reference£º
Benzothiophene – Wikipedia,
Benzothiophene | C8H6S – PubChem