Epigenetics
Epigenetics research delves into the molecular mechanisms that control gene expression and cellular traits without altering the underlying DNA sequence. One crucial aspect of this field is the role of small molecules, which act as powerful regulators of epigenetic modifications. These small compounds, typically comprising a few dozen to a few hundred atoms, have emerged as essential tools in understanding and manipulating the epigenome.
- DNA Methylation Inhibitors: Small molecules like 5-azacytidine and 5-aza-2'-deoxycytidine are DNA methyltransferase inhibitors. They block the addition of methyl groups to DNA, leading to DNA demethylation. This can reactivate silenced genes, potentially offering therapeutic avenues for conditions like cancer.
- HDAC inhibitors: HDACs remove acetyl groups from histone proteins, contributing to gene repression. Small molecule HDAC inhibitors, such as Vorinostat and Romidepsin, can reverse this process by increasing histone acetylation, allowing genes to be more accessible for transcription. These inhibitors are being explored for cancer therapy and other conditions.
- Histone Methyltransferase Inhibitors: Small molecules like GSK126 inhibit specific histone methyltransferases, affecting histone methylation patterns. This can alter gene expression, making them promising candidates for cancer and other diseases with epigenetic dysregulation.
- RNA Modulators: Small molecules can also target non-coding RNAs involved in epigenetic regulation. For instance, small molecules called small interfering RNAs (siRNAs) can be designed to target and degrade specific long non-coding RNAs, influencing gene expression.
- Epigenetic Reader Domain Inhibitors: These small molecules target proteins that recognize and bind to specific epigenetic marks. Examples include inhibitors of bromodomain-containing proteins (BET inhibitors), which can disrupt gene regulation by interfering with protein-DNA interactions.
Small molecules in epigenetics research not only provide insights into the fundamental biology of gene regulation but also hold immense promise for developing novel therapeutics. Their ability to selectively modulate specific epigenetic marks and pathways has led to ongoing clinical trials and drug development efforts for various diseases, including cancer, neurological disorders, and inflammatory conditions. Understanding and harnessing the power of these small molecules is at the forefront of modern epigenetics research, offering new hope for precision medicine and targeted therapies.
3 key components involved in the regulation of epigenetic modifications
Epigenetics Writer
Epigenetics writers are enzymes responsible for adding chemical marks or modifications to DNA or histone proteins. These marks include DNA methylation (addition of methyl groups to DNA) and histone modifications (such as acetylation, methylation, phosphorylation, etc.).
Epigenetics Reader
Function: Epigenetics readers are proteins that can recognize and bind to specific epigenetic marks on DNA or histones. These reader proteins interpret the epigenetic code and facilitate downstream cellular processes, such as gene activation or repression.
Epigenetics Eraser
Function: Epigenetics erasers are enzymes responsible for removing or reversing epigenetic marks on DNA or histones. This process allows for the dynamic regulation of gene expression and the resetting of epigenetic states during various stages of development and in response to environmental changes.
Catalog No.
Product Name
Application
Product Information
Citations
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JAK2 Inhibitor
Fedratinib hydrochloride hydrate is a selective, ATP-competitive inhibitor targeting the JAK2 kinase. With an IC50 of 3 nM for both JAK2 and the mutant JAK2V617F, it demonstrates significant potency. This compound exhibits 35-fold selectivity over JAK1 and 334-fold selectivity over JAK3. Fedratinib hydrochloride hydrate effectively induces apoptosis in cancer cells, making it a valuable tool for research in myeloproliferative disorders. -
Tip60 HAT Inhibitor
TH1834 is a selective inhibitor of the Tip60 (KAT5) histone acetyltransferase (HAT). This compound has demonstrated the ability to induce apoptosis and enhance DNA damage in breast cancer cells. Notably, TH1834 does not interfere with the activity of the related MOF HAT, making it a valuable tool for investigating the role of Tip60 in cancer biology and exploring potential therapeutic applications. -
KDM3B Inhibitor
PFI-90 is a selective inhibitor of the histone demethylase KDM3B, effectively inhibiting the action of PAX3-FOXO1. This compound induces apoptosis and promotes myogenic differentiation, leading to increased cell death. PFI-90 exhibits potential antitumor activity, making it a valuable tool for cellular and cancer research studies. -
STAT3/JAK Inhibitor
Brevilin A is a potent inhibitor of the STAT3/JAK signaling pathway, with an IC50 value of approximately 10.6 μM for STAT3. It exhibits anti-tumor properties and effectively inhibits the proliferation of cancer cells. Additionally, Brevilin A has been shown to induce both apoptosis and autophagy, making it a valuable tool for cancer research and therapeutic investigations. -
METTL3 Inhibitor
UZH1a is a selective inhibitor of METTL3, demonstrating an IC50 of 280 nM. This compound has shown potential for epitranscriptomic modulation, influencing various cellular processes. Additionally, UZH1a exhibits antitumor activity and serves as a valuable chemical probe for investigating the biological functions of METTL3 in research applications. -
LSD1 Inhibitor
Bomedemstat ditosylate is a potent and irreversible inhibitor of lysine-specific demethylase 1 (LSD1). By inhibiting LSD1, Bomedemstat ditosylate increases methylation levels of H3K4 and H3K9, leading to significant alterations in gene expression. This compound demonstrates notable anti-cancer properties, effectively inhibiting cancer cell proliferation and inducing apoptosis, making it a valuable tool for cancer research and therapeutic development. -
PKD/PIM2 Inhibitor
CRT0066101 is a potent and orally active inhibitor of Protein Kinase D (PKD) with IC50 values of 1 nM, 2.5 nM, and 2 nM for PKD1, PKD2, and PKD3, respectively. Additionally, it serves as an effective PIM2 inhibitor with an IC50 of approximately 135.7 nM. This compound exhibits notable anti-inflammatory activity demonstrated in LPS-induced lung injury models in mice, as well as anticancer effects, making it a valuable tool for research in cancer and inflammation-related studies. -
SIRT2/Hsp70 Inhibitor
YM-08 is a selective inhibitor of SIRT2 and Hsp70, exhibiting an IC50 of 19.9 μM for SIRT2. This compound effectively penetrates the blood-brain barrier, making it a valuable tool for studying neurodegenerative diseases and cellular stress responses. Its dual inhibitory activity allows for investigation into SIRT2 and Hsp70's roles in various biological processes and potential therapeutic applications. -
HSP70/SIRT2 Inhibitor
HSP70/SIRT2-IN-2 is a dual inhibitor targeting SIRT2 and HSP70, demonstrating an IC50 of 45.1±5.0 μM for SIRT2. This compound exhibits significant antitumor activity, making it a valuable tool for cancer research. Its ability to simultaneously inhibit these two proteins positions HSP70/SIRT2-IN-2 as a useful candidate for studies focused on tumor progression and potential therapeutic strategies. -
HDAC1/HDAC2 Inhibitor
MRLB-223 is a selective inhibitor of HDAC1 and HDAC2, demonstrating potent activity against tumor cells. It induces histone hyperacetylation and activates the intrinsic apoptotic pathway, leading to tumor cell apoptosis and degradation of Bcr-Abl in a caspase-dependent manner. Notably, MRLB-223 mediates p53-independent cell death in Bcr-Abl-expressing myeloid cells and shows efficacy in animal models of Eμ-myc lymphoma. This compound is valuable for research focusing on the mechanisms of lymphomagenesis and therapeutic strategies for Eμ-myc lymphoma. -
Polθ/PARP Inhibitor
Polθ/PARP-IN-1 is a potent dual inhibitor targeting DNA polymerase theta (Polθ) and poly (ADP-ribose) polymerase (PARP), exhibiting IC50 values of 45.6 nM and 5.4 nM, respectively. This compound demonstrates significant antiproliferative activity by inducing apoptosis and cell cycle arrest at the G2/M phase, leading to DNA damage. Polθ/PARP-IN-1 is applicable in cancer research and may contribute to therapeutic strategies targeting tumorigenesis. -
CK2/PIM1 Inhibitor
CK2/PIM1-IN-1 is a selective inhibitor targeting casein kinase 2 (CK2) and PIM1, demonstrating IC50 values of 3.787 μM and 4.327 μM, respectively. This compound is designed for research into proliferative disorders, particularly cancer, and has potential applications in studying kinase-related conditions such as inflammation, pain, vascular disorders, pathogenic infections, and certain immunological disorders. -
CBP/β-catenin Antagonist
C-82 is a selective antagonist of CBP/β-catenin interaction, designed to inhibit the binding of β-catenin to CBP while promoting its association with p300. This compound effectively modulates the Wnt signaling pathway, making it a valuable tool for research in cancer biology and developmental processes. C-82 serves as an important reagent for studies investigating the role of β-catenin in transcriptional regulation and related disease mechanisms. -
LSD Derivative
ALD-52 (1-Acetyl-LSD) serves as a prodrug for LSD, primarily targeting serotonin receptors 5-HT1A, 5-HT2A, and 5-HT2C, with binding affinities of 1054, 174, and 10.2 nM, respectively. Upon conversion to LSD, ALD-52 elicits a head-twitch response (HTR) in vivo, demonstrating its psychoactive properties. This compound is valuable in hallucinogen research, providing insights into its pharmacological effects and the underlying mechanisms of serotonergic activity. -
PARP10/PARP15 Inhibitor
PARP10/15-IN-3 is a dual inhibitor targeting PARP10 and PARP15, exhibiting IC50 values of 0.14 µM and 0.40 µM, respectively. This compound effectively penetrates cellular membranes and has demonstrated the ability to rescue cells from apoptosis. PARP10/15-IN-3 serves as a valuable tool for investigating the roles of PARP10 and PARP15 in cellular processes and offers potential applications in studies related to cancer therapy and cell survival mechanisms. -
JAK2/FLT3 Inhibitor
Flonoltinib TFA is a potent and orally bioavailable inhibitor that targets both JAK2 and FLT3, exhibiting IC50 values of 0.7 nM and 4 nM, respectively, alongside 26 nM and 39 nM for JAK1 and JAK3. This compound possesses significant anti-cancer activity, making it a valuable tool for research in oncology and therapeutic development against malignancies driven by these pathways. Its dual inhibition profile highlights its potential in addressing cancers associated with aberrant JAK2 and FLT3 signaling. -
Pim-1 Kinase Inhibitor
Pim-1 kinase inhibitor 2 specifically targets and inhibits Pim-1 kinase activity, a critical regulator of cell survival and proliferation. This compound has been demonstrated to induce apoptosis in various cell types, making it a valuable tool for cancer research. Its potent inhibitory effects on Pim-1 kinase provide insights into the molecular mechanisms of tumorigenesis and underscore its potential in therapeutic applications for cancer treatment. -
SIRT6 PROTAC Degrader
SZU-B6 is a SIRT6-protein-targeting chimeric degrader that achieves a DC50 of 45 nM and 154 nM in SK-HEP-1 and Huh-7 cell lines, respectively. It effectively inhibits the proliferation of SK-HEP-1 cells with an IC50 of 1.51 μM and suppresses colony formation in both SK-HEP-1 and Huh-7 cells. Additionally, SZU-B6 induces apoptosis and causes a cell cycle arrest in the G2/M phase in SK-HEP-1 cells, demonstrating notable antitumor efficacy in mouse models. This compound serves as a valuable tool for studying the functional roles of SIRT6 in cancer research. -
GSPT1/BRD4 Degrader
DP-15 is a targeted degrader for GSPT1 and BRD4, demonstrating DC50 values of 5.25 nM and 0.48 nM, respectively. This compound exhibits potent anti-proliferative effects against acute myeloid leukemia (AML) and non-Hodgkin lymphoma (NHL) cells, with IC50 values in the nanomolar range. Additionally, DP-15 induces G1 phase cell cycle arrest and promotes apoptosis in MOLM13 cells. In vivo studies have shown its effective anti-leukemia activity in MOLM-13 xenograft mouse models, supporting its potential application in cancer research. -
JAK2 Inhibitor
ZT55 is a potent and selective inhibitor of JAK2, exhibiting an IC50 value of 0.031 μM. This compound effectively inhibits the proliferation of JAK2V617F-expressing HEL cell lines, inducing apoptosis and cell cycle arrest. In vivo, ZT55 demonstrates significant efficacy in inhibiting the growth of HEL xenograft tumors in mouse models. It serves as a valuable tool for research in myeloproliferative neoplasms, including polycythemia vera and primary thrombocythemia. -
STAT3/5 Inhibitor
UC-514321 is a potent inhibitor of STAT3 and STAT5, effectively repressing TET1 expression without affecting TET2 or TET3. This compound demonstrates significant promise for the treatment of acute myeloid leukemia (AML) in both in vitro and in vivo settings. Its selective action and low toxicity profile make it a valuable tool for research in cancer therapeutics. -
CDK6/PIM1 Inhibitor
CDK6/PIM1-IN-1 hydrochloride is a potent dual inhibitor targeting CDK6 and PIM1, exhibiting IC50 values of 39 nM and 88 nM, respectively, along with significant inhibition of CDK4 (IC50=3.6 nM). This compound effectively inhibits the proliferation of acute myeloid leukemia (AML) cells, induces G1 phase cell cycle arrest, and promotes apoptosis. CDK6/PIM1-IN-1 hydrochloride is a valuable tool for research investigating the role of CDK6 and PIM1 in cancer biology, particularly in the context of AML. -
HDAC Class I Inhibitor
HDAC-IN-27 dihydrochloride is a potent inhibitor of class I histone deacetylases (HDAC1-3) with IC50 values ranging from 0.43 to 3.01 nM. This compound displays significant antitumor activity both in vitro and in vivo, particularly against acute myeloid leukemia (AML) cell lines, through mechanisms that include apoptosis induction and increased histone acetylation (AcHH3 and AcHH4). HDAC-IN-27 dihydrochloride is an important tool for investigating the roles of HDACs in cancer biology, specifically within the context of AML research. -
SIRT1 Inhibitor
JGB1741 is a potent and selective inhibitor of SIRT1, exhibiting an IC50 of approximately 15 μM. It displays weak inhibitory effects on SIRT2 and SIRT3, with IC50 values greater than 100 μM. JGB1741 enhances the levels of acetylated p53, promoting p53-mediated apoptosis through modulation of the Bax/Bcl2 ratio, cytochrome c release, and PARP cleavage. This compound is valuable for research applications focusing on breast cancer. -
JAK2 Inhibitor
ON044580 is a potent non-ATP-competitive inhibitor of the JAK2 kinase, demonstrating IC50 values of 1.23 μM and 1.09 μM for wild-type and V617F mutant JAK2, respectively. This compound functions by either binding to the STAT-5 binding domain or an allosteric site of JAK2, leading to the suppression of JAK2 kinase activity. ON044580 effectively induces apoptosis in chronic myelogenous leukemia cells that exhibit resistance to Imatinib, and it also inhibits both wild-type and T315I mutant forms of the BCR-ABL kinase. This reagent holds promise for therapeutic applications in myeloproliferative disorders characterized by dysregulated JAK/STAT signaling. -
LSD1 Inhibitor
LSD1-IN-14 is a potent and selective inhibitor of Lysine-specific demethylase 1 (LSD1), exhibiting an IC50 of 0.89 μM. This compound effectively inhibits the proliferation of A549 lung cancer cells and THP-1 monocytic cells, while also inducing apoptosis in tumor cell lines. LSD1-IN-14 is valuable for research applications focused on understanding the role of LSD1 in cancer biology and developing potential therapeutic strategies targeting epigenetic regulation. -
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. -
PARP-1/2/TNKS1/2 Inhibitor
PARP1/2/TNKS1/2-IN-1 is an inhibitor targeting PARP-1, PARP-2, TNKS1, and TNKS2, with IC50 values of 0.25 nM, 1.2 nM, 13.5 nM, and 4.15 nM, respectively. This compound demonstrates significant antitumor activity and promotes apoptosis, making it a valuable tool for research focused on cancer biology and therapeutic strategies. Its dual inhibitory action can facilitate the exploration of cellular repair mechanisms and enhance the understanding of poly(ADP-ribose) polymerases in cancer treatment. -
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. -
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. -
VEGFR/PARP Inhibitor
VEGFR/PARP-IN-1 is a dual inhibitor targeting Vascular Endothelial Growth Factor Receptor (VEGFR) and Poly(ADP-ribose) Polymerase (PARP), with IC50 values of 191 nM and 60.9 nM, respectively. This compound inhibits DNA damage repair mechanisms, induces apoptosis, and causes G2/M phase cell cycle arrest. It demonstrates significant antiproliferative activity against BRCA wild-type breast cancer cell lines, specifically MDA-MB-231 and MCF-7, with IC50 values of 4.1 μM and 3.5 μM, respectively. VEGFR/PARP-IN-1 is an effective antitumor and anti-metastatic agent, making it valuable for cancer research applications. -
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. -
METTL Inhibitor
ZINC13000658 is an inhibitor of METTL, a family of methyltransferases. This compound demonstrates substantial antiproliferative effects across various cell lines, effectively inducing G1 phase cell cycle arrest and apoptosis in HepG2 (IC50 = 5.632 µM) and SNU-449 (IC50 = 6.184 µM) cells. ZINC13000658's mechanism may involve the inhibition of multiple methyltransferases, including METTL1, METTL3, METTL6, METTL16, and METTL18. This reagent is valuable for investigating various cancer research applications. -
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. -
BD2-selective BET Inhibitor
BET-IN-23 is a BD2-selective BET inhibitor with a reported IC50 of 2.9 nM. This compound exhibits anticancer properties, effectively inhibiting the proliferation of acute myeloid leukemia (AML) cell lines by inducing G0/G1 cell cycle arrest and apoptosis in vitro. BET-IN-23 serves as a valuable tool for research in cancer biology, specifically in the study of leukemia and other malignancies involving BET protein dysregulation. -
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. -
TOPOI/PARP Dual Inhibitor
TOPOI/PARP-1-IN-1 is a dual inhibitor targeting topoisomerase I and PARP-1, demonstrating an IC50 value of 0.09 μM for PARP-1. This compound exhibits significant anti-proliferative and anti-migratory effects on cancer cells, leading to G0/G1 phase cell cycle arrest and apoptosis. In preclinical studies, TOPOI/PARP-1-IN-1 achieved a tumor growth inhibition rate of 75.4% in mice, highlighting its potential for cancer therapy research applications. -
LSD1/KDM1A Inhibitor
TPC-144 is an inhibitor of LSD1/KDM1A, targeting the demethylation process by reducing DNMT1 protein levels, resulting in decreased methylation of LINE-1 elements. This compound has shown promising synergistic effects with Decitabine, enhancing DNA demethylation, which promotes differentiation and apoptosis in leukemia cells. Furthermore, TPC-144 has demonstrated anti-tumor activity in acute myeloid leukemia (AML) models, making it a valuable tool for AML research and therapeutic studies. -
SIRT6 Inhibitor
SIRT6-IN-4 is a selective inhibitor of SIRT6, demonstrating an IC50 of 5.68 μM. This compound effectively inhibits the proliferation of MCF-7 cells with an IC50 of 8.30 μM, leading to cell cycle arrest at the G2/M phase. Additionally, SIRT6-IN-4 reduces cell migration and invasion while inducing apoptosis. Its antitumor efficacy has been confirmed in mouse models, making it a valuable tool for cancer research and therapeutic development. -
JAK2/Bcr-Abl/FLT3 Inhibitor
LS-104 is a non-ATP-competitive inhibitor targeting JAK2, Bcr-Abl, and FLT3. It effectively induces apoptosis in JAK2V617F-positive cells while inhibiting JAK2 autophosphorylation and downstream signaling pathways. Additionally, LS-104 demonstrates significant cytotoxic effects and inhibits the proliferation of FLT3-expressing leukemic cells. This hydroxystyryl-acrylonitrile compound holds potential for research into myeloproliferative disorders and refractory or relapsed hematologic malignancies.
