-
NF-κB Inhibitor
Bengamide B is a potent inhibitor of NF-κB with an IC50 of 85 nM. This compound effectively reduces LPS-induced expression of pro-inflammatory cytokines, including TNF-α, IL-6, and MCP-1, demonstrating significant anti-inflammatory activity. Additionally, Bengamide B displays antitumor efficacy, with an IC50 of 2 nM against HCT-116 colorectal cancer cells, making it a valuable reagent for research in inflammation and oncology. -
SEAP Inhibitor
Cycloepoxydon is a potent inhibitor of secreted alkaline phosphatase (SEAP) expression, targeting both NF-κB and AP-1 signaling pathways. It effectively reduces PMA-induced SEAP expression with IC50 values ranging from 1-2 μg/mL (4.2-8.4 μM) for NF-κB and 3-5 μg/mL (12.6-21 μM) for AP-1. This compound is valuable for research applications involving inflammation, cancer biology, and signal transduction studies. -
NF-κB Inhibitor
2,4,5-Trimethoxybenzoic acid is an NF-κB inhibitor with notable anti-inflammatory properties. This compound, derived from purple perilla extracts, effectively inhibits LPS-induced inflammatory responses by blocking the activation of NF-κB and STAT signaling pathways. It has been shown to suppress M1 macrophage phenotype-mediated inflammation, making it a valuable tool for research into diabetes and related inflammatory conditions. -
IKKε/TBK-1 Inhibitor
MRT67307 hydrochloride is a selective inhibitor of IKKε and TBK-1, exhibiting IC50 values of 160 nM and 19 nM, respectively. Additionally, it inhibits ULK1 and ULK2 with IC50s of 45 nM and 38 nM, respectively. This compound is employed in research to study autophagy regulation and related cellular processes. It is particularly useful in investigations of inflammatory signaling pathways and cancer biology. -
HDAC Inhibitor
HDAC-IN-37 is a potent inhibitor of histone deacetylases (HDACs), demonstrating IC50 values of 0.0551 μM for HDAC1, 1.24 μM for HDAC3, 0.948 μM for HDAC8, and 34.2 μM for HDAC6. This compound effectively increases histone acetylation through a slow-off binding mechanism. Additionally, HDAC-IN-37 disrupts the transition from the G1 phase to the S phase of the cell cycle and promotes early apoptosis in various cell types, making it a valuable tool for research in cancer biology and therapeutic development. -
c-Met/HDAC Inhibitor
c-Met/HDAC-IN-3 is a dual inhibitor targeting c-Met and histone deacetylase 1 (HDAC1), exhibiting IC50 values of 12.50 nM and 26.97 nM, respectively. This compound demonstrates significant biological activity by inducing apoptosis and causing cell cycle arrest at the G2/M phase. c-Met/HDAC-IN-3 serves as a valuable tool for research in cancer biology and therapeutic development, particularly in studies focused on synergistic inhibition of oncogenic pathways. -
HDAC6 Inhibitor
HDAC6-IN-4 is a potent and selective inhibitor of histone deacetylase 6 (HDAC6), exhibiting an IC50 value of 23 nM. This compound promotes apoptosis in cancer cells and demonstrates significant antitumor efficacy while exhibiting minimal toxicity. HDAC6-IN-4 is valuable for research in cancer biology, particularly in studies focused on epigenetic regulation and therapeutic development. -
HDAC Inhibitor
HDAC-IN-31 is a selective and orally active histone deacetylase (HDAC) inhibitor, exhibiting IC50 values of 84.90 nM for HDAC1, 168.0 nM for HDAC2, 442.7 nM for HDAC3, and greater than 10,000 nM for HDAC8. This compound induces apoptosis and triggers G2/M phase cell cycle arrest, demonstrating significant antitumor efficacy. HDAC-IN-31 is applicable in research focused on diffuse large B-cell lymphoma and other cancer studies. -
Topoisomerase/HDAC Inhibitor
Top/HDAC-IN-1 is a dual inhibitor targeting both topoisomerase and histone deacetylases (HDACs), demonstrating IC50 values of 18 nM for HDAC1, 230 nM for HDAC2, 790 nM for HDAC3, 87 nM for HDAC6, and 5250 nM for HDAC8. This compound exhibits significant antitumor activity against HCT116 cells, with an IC50 of 180 nM, effectively inducing apoptosis and promoting G2 cell cycle arrest. Top/HDAC-IN-1 serves as a valuable tool in cancer research, particularly for studies involving epigenetic modulation and cell proliferation. -
mTOR/HDAC6 Inhibitor
mTOR/HDAC6-IN-1 is a potent dual inhibitor targeting mTOR and HDAC6, exhibiting IC50 values of 133.7 nM and 56 nM, respectively. This compound is known to induce significant autophagy and apoptosis while suppressing cell migration. It holds potential for research applications in triple-negative breast cancer (TNBC) studies, offering insights into the interplay between these critical pathways in cancer progression. -
HDAC Inhibitor
HDAC-IN-59 is a potent inhibitor of histone deacetylases (HDACs), demonstrating significant biological activity in cancer research. This compound promotes the generation of reactive oxygen species (ROS), leading to DNA damage and the induction of apoptosis via the mitochondria-related pathway. Additionally, HDAC-IN-59 effectively disrupts the cell cycle at the G2/M phase, making it a valuable tool for studying the mechanisms of cell growth regulation and apoptosis in various cancer models. -
S100P Inhibitor
5-Methyl cromolyn disodium is a selective inhibitor of the S100P protein, targeting its interaction with the receptor for advanced glycation end-products (RAGE). It effectively suppresses NF-κB activity and cell proliferation while enhancing Gemcitabine-induced apoptosis. In preclinical mouse models, 5-Methyl cromolyn disodium demonstrates significant anti-tumor effects by reducing growth and metastasis of pancreatic ductal adenocarcinoma (PDAC), ultimately extending survival. This compound serves as a valuable tool for investigating pancreatic cancer mechanisms and potential therapeutic approaches. -
JAK/HDAC Inhibitor
JAK/HDAC-IN-2 is a dual-target inhibitor of Janus kinase (JAK) and histone deacetylase (HDAC), specifically inhibiting HDAC3/6 and JAK1/2 with nanomolar potency. This compound demonstrates proapoptotic activity by inhibiting histone deacetylation and STAT3 phosphorylation, contributing to its mechanism of action. JAK/HDAC-IN-2 exhibits significant antiproliferative effects in various hematological malignancies and solid tumors, making it a valuable tool for cancer research and therapeutic studies. -
c-Met/HDAC Inhibitor
c-Met/HDAC-IN-2 is a highly potent dual inhibitor targeting c-Met and histone deacetylases (HDACs), exhibiting IC50 values of 18.49 nM for HDAC1 and 5.40 nM for c-Met. This compound demonstrates significant antiproliferative effects against various cancer cell lines, notably inducing G2/M-phase cell cycle arrest and apoptosis in HCT-116 cells. c-Met/HDAC-IN-2 is a valuable tool for investigating mechanisms of anti-cancer resistance and exploring therapeutic strategies in oncology research. -
HDAC inhibitor
HDAC-IN-67 is a potent inhibitor of histone deacetylases HDAC1 and HDAC6, demonstrating IC50 values of 22 nM and 8 nM, respectively. This compound effectively inhibits cell proliferation and induces apoptosis in various cancer cell lines. Its significant antitumor activity makes HDAC-IN-67 a valuable tool for cancer research and a potential candidate for therapeutic development. -
PIM-1/HDAC Inhibitor
PIM-1/HDAC-IN-1 is a selective inhibitor of PIM-1 as well as histone deacetylases HDAC 1 and HDAC 6, exhibiting an IC50 of 343.87 nM for PIM-1 and 63.65 nM and 62.39 nM for HDAC 1 and HDAC 6, respectively. This compound demonstrates significant apoptotic activity in MCF-7 cell lines, inducing pre-G1 apoptosis and causing cell cycle arrest at the G2/M phase. PIM-1/HDAC-IN-1 is a valuable tool for research on cancer biology and the regulation of cell proliferation and apoptosis. -
FGFR/HDAC Inhibitor
HDAC-IN-50 is a potent dual inhibitor targeting FGFR and HDAC with IC50 values of 0.18 nM for FGFR1, 1.2 nM for FGFR2, 0.46 nM for FGFR3, 1.4 nM for FGFR4, and varying inhibitory effects on HDAC isoforms such as HDAC1 (1.3 nM), HDAC2 (1.6 nM), HDAC6 (2.6 nM), and HDAC8 (13 nM). This compound effectively induces apoptosis and causes cell cycle arrest at the G0/G1 phase. Additionally, HDAC-IN-50 decreases the expression of phosphorylated forms of FGFR1, ERK, and STAT3, indicating its potential applications in cancer research and therapy. -
Tubulin/HDAC Inhibitor
Tubulin/HDAC-IN-1 is a dual inhibitor targeting tubulin and histone deacetylase 8 (HDAC8) through CH/π interaction and hydrogen bonding, respectively. This compound effectively inhibits tubulin polymerization and selectively inhibits HDAC8 with an IC50 value of 150 nM. Tubulin/HDAC-IN-1 demonstrates cytotoxic effects against a range of human cancer cell lines, induces cell cycle arrest in the G2/M phase, and promotes apoptosis. It is a valuable reagent for research involving hematologic malignancies and solid tumors, including neuroblastoma and leukemia. -
HDAC6 Inhibitor
SAHA-OH is a selective inhibitor of histone deacetylase 6 (HDAC6) with an IC50 of 23 nM, demonstrating a 10- to 47-fold selectivity over HDAC isoforms 1, 2, 3, and 8. This compound exhibits notable anti-inflammatory properties and has been shown to reduce macrophage apoptosis. It is a valuable tool for research focused on the modulation of histone acetylation and the investigation of HDAC6's role in various inflammatory pathways. -
VEGFR-2/HDAC Dual Inhibitor
VEGFR2/HDAC1-IN-1 is a potent dual inhibitor of VEGFR-2 and HDAC, demonstrating IC50 values of 57.83 nM and 9.82 nM, respectively. This compound effectively arrests the cell cycle at the S and G2 phases, leading to apoptosis in HeLa cells. Additionally, VEGFR2/HDAC1-IN-1 exhibits significant anti-angiogenic properties, making it a valuable tool for research in cancer biology and targeted therapies. -
HDAC Inhibitor
HDAC-IN-34 is a potent inhibitor of histone deacetylases (HDACs), demonstrating IC50 values of 0.022 μM for HDAC1 and 0.45 μM for HDAC6. This compound binds to DNA, leading to DNA damage and inducing apoptosis through the p53 signaling pathway. Additionally, HDAC-IN-34 exhibits significant anti-proliferative effects against HCT-116 colorectal cancer cells, with an IC50 of 1.41 μM, making it a valuable tool for cancer research and epigenetic studies. -
NF-κB Inhibitor
NF-κB-IN-5 is a potent inhibitor of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) that acts by directly interacting with the NF-κB complex. This compound demonstrates significant antitumor activity across multiple human cancer cell lines, including HCT116, U87-MG, HepG2, BGC823, and PC9, with IC50 values ranging from 2.02 to 5.35 μM. NF-κB-IN-5 also promotes apoptosis in U87-MG cells and induces cell cycle arrest in the G0/G1 phase, positioning it as a valuable tool for cancer research and therapeutic development. -
HDAC/PSMD14 Inhibitor
HDAC/PSMD14-IN-1 is a dual-target inhibitor of HDAC1 and PSMD14, exhibiting IC50 values of 238.7 nM and 141.2 nM, respectively. This compound demonstrates significant cytotoxicity against esophageal squamous cell carcinoma (ESCC) cell lines, with IC50 values ranging from 30 to 250 nM. In addition to its ability to induce apoptosis, HDAC/PSMD14-IN-1 effectively reverses epithelial-mesenchymal transition (EMT) and shows promising anti-tumor activity in KYSE30 mouse xenograft models. It is a valuable tool for advancing research in esophageal cancer. -
HDAC Inhibitor
1-Alaninechlamydocin is a cyclic tetrapeptide that functions as a potent histone deacetylase (HDAC) inhibitor with an IC50 of 6.4 nM. This compound effectively induces G2/M cell cycle arrest and promotes apoptosis in MIA PaCa-2 cells, making it a valuable tool for cancer research. Its activity in modulating epigenetic regulation highlights its potential applications in therapeutic development and studies of cellular differentiation and survival. -
HDAC Class I Inhibitor
HDAC-IN-27 is a selective inhibitor of Class I histone deacetylases (HDAC1-3) with an IC50 range of 0.43 to 3.01 nM. It demonstrates significant anti-proliferative and pro-apoptotic effects against acute myeloid leukemia (AML) cell lines by promoting histone acetylation, specifically AcHH3 and AcHH4. This compound is valuable for research into the mechanisms of AML and potential therapeutic applications in histone modification regulation. -
HDAC6 Inhibitor
Daphnegiravone D is an inhibitor of HDAC6, targeting histone deacetylation to modulate gene expression. This compound demonstrates significant anti-hepatocellular carcinoma activity by inducing apoptosis and selectively inhibiting the proliferation of liver cancer cells. Its mechanism involves the p38 and JNK MAPK signaling pathways, making it a valuable tool for research in cancer therapeutics and cellular signaling. -
HDAC1/6 Inhibitor
HDAC1/6-IN-1 is a potent inhibitor targeting HDAC1 and HDAC6, exhibiting IC50 values of 1.3 nM and 13 nM, respectively. This compound effectively inhibits the methylation and deacetylation of H3K9, leading to significant biological activity, including the induction of apoptosis in cancer cells, G0/G1 cell cycle arrest, and the inhibition of cell migration and invasion. It serves as a valuable tool in cancer research and the study of epigenetic regulation. -
c-Myc Inhibitor
EP12 is a selective c-Myc inhibitor that stabilizes c-Myc G-quadruplexes. This compound induces apoptosis and causes DNA damage in multiple myeloma cells, effectively inhibiting their growth. Additionally, EP12 disrupts the nuclear translocation of P65/P50 by interfering with the NF-κB signaling pathway, highlighting its potential in cancer research and therapeutic applications. -
IRAK4 Inhibitor
Emavusertib phosphate is a potent inhibitor of IRAK4, exhibiting an IC50 of 57 nM. This compound effectively disrupts NF-κB and MyD88 signaling pathways, leading to a significant reduction in pro-inflammatory cytokines such as IL-6 and IL-10. Emavusertib phosphate demonstrates both anti-inflammatory and anti-proliferative effects on cancer cells, promoting apoptosis and showcasing antitumor activity in preclinical mouse models. Its applications extend to investigating inflammatory diseases and cancer therapies. -
IRAK4 Inhibitor
Emavusertib maleate is a potent inhibitor of IRAK4, demonstrating an IC50 of 57 nM, and FLT3. This orally bioavailable compound inhibits NF-κB and MyD88 signaling pathways, effectively reducing the production of pro-inflammatory cytokines such as IL-6 and IL-10. Its anti-inflammatory and anti-proliferative properties make it a valuable tool for cancer research, promoting apoptosis in cancer cells and demonstrating antitumor activity in preclinical mouse models. -
NF-κB Inhibitor
Amorfrutin A is an NF-κB inhibitor that inhibits TNF-α-induced IκBα degradation, p65 nuclear translocation, and DNA-binding activity of the NF-κB complex. This compound promotes apoptosis in HeLa cells by enhancing the proteolytic activities of caspase-3 and PARP. Its mechanism suggests potential research applications in studying inflammation, cancer biology, and cell death pathways. -
IRAK4 Inhibitor
Emavusertib tosylate is a potent inhibitor of IRAK4, displaying an IC50 of 57 nM. By targeting IRAK4 and FLT3, it effectively disrupts NF-κB and MyD88 signaling pathways, resulting in the reduction of pro-inflammatory cytokines such as IL-6 and IL-10. This compound demonstrates significant anti-inflammatory and anti-proliferative properties against cancer cells, promoting apoptotic mechanisms. Additionally, Emavusertib tosylate has shown noteworthy antitumor activity in preclinical mouse models, making it a valuable reagent for cancer research and inflammation studies. -
TAK1 Inhibitor
Triptriolide is a TAK1 inhibitor that plays a pivotal role in regulating apoptosis in mouse podocytes. It enhances cell survival and protects podocyte function by modulating the Bcl-2 family proteins and inhibiting Caspase-3 activity. Additionally, Triptriolide activates the TAK1-NF-κB signaling pathway, leading to the upregulation of podocin. This reagent is relevant for studies focusing on kidney health and podocyte resilience under stress conditions. -
IRAK4 Inhibitor
Emavusertib mesylate is a potent inhibitor of IRAK4, demonstrating an IC50 of 57 nM. This orally active compound effectively disrupts the NF-κB and MyD88 signaling pathways, leading to a reduction in pro-inflammatory cytokines such as IL-6 and IL-10. Emavusertib mesylate displays anti-inflammatory and anti-proliferative properties against cancer cells, promoting apoptosis. Additionally, it has shown significant antitumor activity in mouse models, making it valuable for cancer research and therapeutic studies targeting inflammatory pathways. -
HDAC Inhibitor
HDAC-IN-39 is a potent inhibitor of histone deacetylases (HDACs), exhibiting IC50 values of 1.07 μM for HDAC1, 1.47 μM for HDAC2, and 2.27 μM for HDAC3. This compound also significantly disrupts microtubule polymerization and induces cell cycle arrest at the G2/M phase, highlighting its potential for modulating cell cycle dynamics. Furthermore, HDAC-IN-39 demonstrates promising anticancer activity, particularly against resistant cancer cell lines, making it a valuable tool for cancer research and therapeutic exploration. -
Topoisomerase/HDAC Inhibitor
Top/HDAC-IN-3 is an orally active dual inhibitor targeting topoisomerase and histone deacetylase (HDAC). This compound enhances intracellular levels of reactive oxygen species (ROS), leading to DNA damage and subsequently inhibiting cancer cell colony formation and migration. Additionally, Top/HDAC-IN-3 induces apoptosis and cell cycle arrest in cancer cells. In non-small cell lung cancer (NSCLC) models, it demonstrates significant antitumor activity, achieving a tumor growth inhibition (TGI) of 77.5% at a dosage of 100 mg/kg. -
HDAC6 Inhibitor
TNI-97 is a highly selective and orally active inhibitor of histone deacetylase 6 (HDAC6), exhibiting an IC50 of 0.2 nM. This compound effectively suppresses the growth and clonogenicity of triple-negative breast cancer (TNBC) cells, specifically MDA-MB-453. TNI-97 induces PANoptosis, encompassing apoptosis, necroptosis, and pyroptosis in these cells. Additionally, TNI-97 demonstrates significant antitumor activity in mouse models, including xenografts and allografts of TNBC, making it a valuable tool for research focused on triple-negative breast cancer. -
HDAC6 Inhibitor
PTG-0861 is a selective inhibitor of histone deacetylase 6 (HDAC6) with an IC50 value of 5.92 nM. This compound effectively induces apoptosis, making it a valuable tool for research in acute myeloid leukemia, multiple myeloma, and other hematological malignancies. Its specificity towards HDAC6 positions it as a promising candidate for studies aimed at understanding epigenetic regulation in cancer. -
HDAC/ Topo II α Inhibitor
KT32 is a potent dual inhibitor targeting histone deacetylases (HDAC) and topoisomerase II alpha (Topo II α). This compound promotes cell death through the activation of apoptotic pathways, making it valuable for research in cancer biology and therapeutic studies. KT32's ability to modulate chromatin structure and DNA topology renders it an essential tool for exploring the mechanisms of tumor progression and treatment resistance. -
HDAC Inhibitor
(E/Z)-Dacinostat is a potent histone deacetylase (HDAC) inhibitor that plays a critical role in inducing apoptosis in cancer cells, particularly leukemia. By promoting the generation of reactive oxygen species (ROS) and instigating DNA damage, (E/Z)-Dacinostat enhances the cytotoxic efficacy of fludarabine against leukemia cells. Its mechanism involves modulation of DNA repair pathways and intracellular signaling, making it a valuable tool for cancer research and therapeutic investigations. -
HDAC Inhibitor
SK-7041 is a histone deacetylase (HDAC) inhibitor with an IC50 value of 172 nM. This compound promotes hyperacetylation of histones H3 and H4, leading to the inhibition of tumor cell growth both in vitro and in vivo. Additionally, SK-7041 induces apoptosis and causes cell cycle arrest at the G1 phase, making it a valuable tool for cancer research and therapeutic exploration. -
HDAC8 Inhibitor
HDAC8-IN-3 is a potent inhibitor of Histone Deacetylase 8 (HDAC8), exhibiting an IC50 value of 9.3 μM. This compound induces thermal stabilization and demonstrates cytotoxic effects, leading to apoptosis in leukemic cell lines. HDAC8-IN-3 is valuable for research applications focused on cancer metabolism, epigenetic regulation, and therapeutic development for hematological malignancies. -
Hsp90/HDAC6 Inhibitor
HDAC6/HSP90-IN-2 is a dual inhibitor targeting both HDAC6 and Hsp90, exhibiting IC50 values of 105.7 nM and 61 nM, respectively. This compound demonstrates significant potential in cancer research, enabling the study of mechanisms involved in tumorigenesis and the development of novel therapeutic strategies. Its ability to modulate key cellular pathways associated with cancer progression makes it a valuable tool for investigating the role of HDAC6 and Hsp90 in various malignancies. -
Wee1/HDAC Inhibitor
Wee1/HDAC-IN-1 is a dual inhibitor targeting Wee1 and histone deacetylases (HDACs). It demonstrates potent activity with an IC50 of 1.2 nM for Wee1 and varying IC50 values of 196 nM for HDAC1, 156 nM for HDAC3, and 55 nM for HDAC6. This compound displays significant antiproliferative effects in MV4-11 cells, with an IC50 of 0.076 μM, by disrupting DNA damage repair mechanisms and promoting apoptosis. Wee1/HDAC-IN-1 is suited for research on acute myeloid leukemia (AML). -
HDAC/DNMT Inhibitor
J208 is a dual inhibitor targeting histone deacetylase (HDAC) and DNA methyltransferase (DNMT). This compound effectively inhibits the proliferation of cancer cells and reduces the migration and invasion of triple-negative breast cancer (TNBC) cells. J208 also induces apoptosis and halts the cell cycle at the G0/G1 phase, while activating innate immune signaling pathways by promoting the expression of endogenous retroviruses (ERVs) in TNBC. It serves as a valuable tool for investigating epigenetic regulation and cancer therapy. -
ARP-1/HDAC-1 Inhibitor
DLC-50 is a dual inhibitor of PARP-1 and HDAC-1, exhibiting IC50 values of 1.2 nM and 31 nM, respectively. This compound effectively inhibits the proliferation of various breast cancer cell lines, including MDA-MB-436, MDA-MB-231, and MCF-7, with IC50 values of 0.3, 2.7, and 2.41 μM. Additionally, DLC-50 induces apoptosis specifically in MDA-MB-231 cells and causes cell cycle arrest at the G2 phase, making it a valuable tool for cancer research and therapeutic development. -
CDK9/HDAC Dual Inhibitor
CDK9/HDAC1/HDAC3-IN-1 is a dual inhibitor targeting CDK9 and HDACs. With IC50 values of 0.17 μM for CDK9, 1.73 μM for HDAC1, and 1.11 μM for HDAC3, this compound effectively disrupts the activity of these proteins. It induces cancer cell apoptosis and causes cell cycle arrest at the G2/M phase. Additionally, CDK9/HDAC1/HDAC3-IN-1 exhibits broad-spectrum anti-cancer effects, demonstrating efficacy against various malignancies, including breast, cervical, and liver cancers, as evidenced in murine TNBC MDA-MB-231 xenograft models. -
HDAC1/2 Inhibitor
ZWZH-21 is a selective inhibitor of histone deacetylases HDAC1 and HDAC2, demonstrating IC50 values of 34 nM and 41 nM, respectively. This dual-action compound exhibits potent anti-proliferative effects on colorectal cancer cell lines HCT116 and SW480, with IC50 values of 0.524 μM and 1.063 μM, respectively. Additionally, ZWZH-21 effectively inhibits cell migration and prompts apoptosis in multiple colorectal cancer models, making it a valuable tool for cancer research, particularly in the study of colorectal cancer. -
NF-κB/MAPK/FAK/Akt Inhibitor
Ephemeranthol A is an inhibitor of NF-κB, MAPK, FAK, and Akt signaling pathways. This phenanthrene compound demonstrates notable anti-inflammatory effects through the inhibition of NF-κB and MAPK pathways in macrophages. Additionally, Ephemeranthol A induces apoptosis and inhibits metastasis in non-small cell lung cancer by suppressing FAK/Akt signaling and epithelial-mesenchymal transition (EMT) processes. It is applicable for research into acute and chronic inflammatory diseases as well as non-small cell lung cancer. -
HDAC1/HDAC2 Inhibitor
ST13 is a selective inhibitor of HDAC1 and HDAC2, exhibiting IC50 values of 23 nM and 49 nM, respectively. It offers weak inhibition of HDAC3 and HDAC6, with IC50 values of 4.30 μM and >10 μM, respectively. The binding mechanism of ST13 involves an initial rapid formation of a collision complex followed by a slow conversion to a stable complex. This compound has demonstrated the ability to induce apoptosis in cancer cells and is useful for research on melanoma and triple-negative breast cancer.

