deacetylation

Exifone (NSC-680919) is a mixed, nonessential activator of HDAC1 that is capable of binding to both free and substrate-bound enzyme, resulting in an increased relative maximal rate of HDAC1-catalyzed deacetylation.

Selisistat (EX-527) is a potent and specific inhibitor of the deacetylase SIRT1 (IC50=38 nM). Selisistat can be used in the study of neurological disorders such as Huntington's chorea.

MDL-811, an allosteric activator of SIRT6, markedly enhances the deacetylation of histone H3 at lysine residues 9, 18, and 56 (H3K9Ac, H3K18Ac, and H3K56Ac), presenting potential utility in colorectal cancer research [1].

YK-3-237 (B-[2-Methoxy-5-[(1E)-3-oxo-3-(3,4,5-trimethoxyphenyl)-1-propen-1-yl]phenyl]boronic acid) reduces acetylation of mtp53 and exhibits anti-proliferative effects toward triple-negative breast cancer (TNBC) cells carrying mtp53.

Sirt1/2-IN-2 (compound hsa55) serves as a dual inhibitor for SIRT1 with an IC50 of 1.8 μM and SIRT2 with an IC50 of 2.4 μM, respectively. It effectively inhibits p53 deacetylation while enhancing the acetylation of p53 and α-tubulin. The compound also promotes apoptosis and exhibits anti-proliferative effects on human leukemia cell lines [1].

Sirt1/2-IN-4 (compound PS3) is a potent triple inhibitor of SIRT1, SIRT2, and SIRT3, exhibiting IC50 values of 1.2 μM (SIRT1), 1.9 μM (SIRT2), and 18.6 μM (SIRT3), respectively. It effectively inhibits p53 deacetylation, indicating potential anticancer properties [1].

Nanatinostat, also known as Tractinostat, CHR-3996 and VRx-3996, is an orally bioavailable, second-generation hydroxamic acid-based inhibitor of histone deacetylase (HDAC) with potential antineoplastic activity. HDAC inhibitor CHR-3996 inhibits HDAC, resulting in an accumulation of highly acetylated histones, the induction of chromatin remodeling, and the selective transcription of tumor suppressor genes; these events may result in the inhibition of tumor cell division and the induction of tumor cell apoptosis. This agent may upregulate HSP70 and downregulate anti-apoptotic Bcl-2 proteins more substantially than some first-generation HDAC inhibitors. HDACs, upregulated in many tumor cell types, are a family of metalloenzymes responsible for the deacetylation of chromatin histone proteins.

CG-200745 is a potent inhibitor of HDAC. CG200745 induces apoptosis and also inhibits the deacetylation of histone H3 and tubulin.

SRTCX1002 is a SIRT1 Activator Suppressing Inflammatory Responses through Promotion of p65 Deacetylation and NF-κB Activity inhibitor.

Herkinorin is an opioid analgesic and an analogue of the natural product Salvinorin A. herkinorin is a μ-opioid agonist with more than 100x higher μ-opioid affinity and 50x lower κ-opioid affinity compared to Salvinorin A. Herkinorin is a semi-synthetic c

HDAC1/6-IN-1 is a potent multi-target inhibitor of GLP (IC50: 1.3 nM), HDAC6 (IC50: 13 nM) and HDAC1 (IC50: 89 nM). HDAC1/6-IN-1 inhibits the methylation and deacetylation of H3K9 at the protein level. HDAC1/6-IN-1 can block the cell cycle of cancer cells in G0/G1 phase, induce apoptosis and prevent cancer cell migration and invasion.

Sirt1/2-IN-3 (compound PS9) serves as a dual inhibitor of SIRT1/2, exhibiting IC50 values of 1.4 μM (SIRT1) and 2.0 μM (SIRT2), respectively. This compound effectively inhibits p53 deacetylation while simultaneously elevating p53 and α-tubulin acetylation levels. Additionally, Sirt1/2-IN-3 promotes apoptosis and exhibits antiproliferative effects on human leukemia cell lines [1].

Ivaltinostat (CG-200745) formic is an oral active panHDAC inhibitor with an isohydroxamic acid component that binds zinc at the bottom of the catalytic pocket. Ivaltinostat formic inhibited the deacetylation of histone H3 and tubulin. Ivaltinostat formic promotes p53 accumulation, induces p53-dependent trans activation, and enhances MDM2 and p21 (Waf1/Cip1) protein expression. Ivaltinostat formic increases the sensitivity of Gemcitabine resistant cells to Gemcitabine and 5-Fluorouracil (5-FU). Ivaltinostat formic induces apoptosis and has antitumor effect.

Ac-RGK(Ac)-AMC, fluorogenic substrate for assaying histone deacetylase (HDAC) activity in a two-step enzymatic reaction. The assay consists of the initial lysine deacetylation by HDAC followed by the release of the fluorescent group by trypsin.

Salvinorin A carbamate, a potent κ-opioid receptor (KOR) full agonist, exhibits nearly the same potency as salvinorin A, with EC50 values of 6.2 and 4.5 nM, respectively, for activating the human KOR to augment the binding of [35S]GTPγS. Enhancing biological stability, the addition of a carbamate group to salvinorin A reduces deacetylation.

Physalin B is one of the major active compounds from the Solanaceae family of plants and has a wide range of biological activities for the treatment of inflammatory eczema and herpes, among other diseases.Physalin B ameliorates lipopolysaccharide-induced inflammatory response due to acute lung injury by inhibiting NF-κB and NLRP3 through activation of the PI3K/Akt pathway.Physalin B inhibits PDGF-BB-induced VSMC proliferation and migration and phenotypic transformation through activation of the Nrf2 pathway. Physalin B inhibits PDGF-BB-induced VSMC proliferation, migration and phenotypic transformation through activation of the Nrf2 pathway.Physalin B exerts antitumor activity by inhibiting LAP2α-HDAC1-mediated deacetylation of glioma-associated oncogene 1 and hepatic stellate cell activation.

4-Hydroxyestrone, an endogenous estrogen metabolite, can strongly protect neuronal cells against oxidative damage.

S2116 is a powerful inhibitor of lysine-specific demethylase 1 (LSD1), and it is a derivative of N-alkylated tranylcypromine (TCP). S2116 exhibits its inhibitory effects by increasing H3K9 methylation and inducing reciprocal H3K27 deacetylation at super-enhancer regions. In TCP-resistant T-cell acute lymphoblastic leukemia (T-ALL) cells, S2116 triggers apoptosis by repressing the transcription of NOTCH3 and TAL1 genes. Furthermore, S2116 demonstrates significant growth retardation of T-ALL cells when xenotransplanted into mice.

MDL-801 is an activator of SIRT6 deacetylation.

MDL-800 is a SIRT6 modulator with antitumor activity for the study of hepatocellular carcinoma and non-small cell lung cancer.

Bisthianostat, also known as CF367 or CF367;-C, is a novel Orally Efficacious Pan-HDAC Inhibitor. Bisthianostat selectively binds to and inhibits HDACs, which inhibits deacetylation of histone proteins and leads to the accumulation of highly acetylated histones. This may result in an induction of chromatin remodeling, the inhibition of tumor oncogene transcription, and the selective transcription of tumor suppressor genes. This prevents cell division, induces cell cycle arrest and apoptosis. This may inhibit the proliferation of susceptible tumor cells. HDACs, upregulated in many tumor cell types, are a family of enzymes that deacetylate histone proteins.

BMf-BH3 belongs to the Bcl-2 apoptosis mediator family. This peptide belongs to the Bcl-2 apoptosis mediator family. Bmf is a key player in histone deacetylase (HDAC) inhibition, which alters the balance between deacetylation and acetylation.

JAK/HDAC-IN-2, a potent 2-amino-4-phenylaminopyrimidine dual-target inhibitor, effectively suppresses JAK1/2 and HDAC3/6 at nanomolar concentrations. This compound exhibits proapoptotic properties, inhibits histone deacetylation, and impedes STAT3 phosphorylation, demonstrating notable antiproliferative activity against various hematological malignancies and solid tumors [1].

SIRT5 inhibitor 3 (compound 46) is an effective and competitive SIRT5 inhibitor (IC50=5.9 μ M). SIRT5 inhibitor 3 shows inhibitory effect on the deacetylation of SIRT5. SIRT5 inhibitor 3 has research value in cancer and neurodegenerative diseases.

BPK-25 is an active acrylamide compound that enhances the degradation of proteins in the nucleosome remodeling and deacetylation (NuRD) complex through a post-translational mechanism involving covalent protein interaction. Additionally, BPK-25 acts as an inhibitor of TMEM173 activation by the cyclic dinucleotide ligand cGAMP.

CAY10602 is a SIRT1 activator. CAY10602 was derived from high throughput screening for compounds that increase SIRT1-mediated deacetylation of a SIRT1-specific substrate. Functional assays show that CAY10602 dose-dependently suppresses the NF-κB-dependent

SRTCX1003, a SIRT1 activator, suppresses inflammatory responses through promotion of p65 deacetylation and inhibition of NF-κB activity.