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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PROTAC BRD4 Degrader
PROTAC BRD4 Degrader-16 is an effective degrader specifically targeting BRD4, with IC50 values of 34.58 nM for BRD4 (BD1) and 40.23 nM for BRD4 (BD2). This compound is known to significantly reduce Cyclin B1 expression, which is associated with G2/M cell cycle progression. Additionally, PROTAC BRD4 Degrader-16 effectively induces apoptosis in MV-4-11 cells, contributing to its potential utility in cancer research and therapeutic applications. -
JAK2/STAT3 Inhibitor
DPP is a Platinum(IV) complex featuring a pterostilbene-derived axial ligand that specifically targets the JAK2/STAT3 signaling pathway. This compound displays significant antiproliferative activity against breast cancer cells by inducing apoptosis through the activation of caspase-3 and cleavage of poly ADP-ribose polymerase. Additionally, DPP enhances the maturation and antigen presentation capability of dendritic cells, demonstrating favorable safety profiles in in vivo studies, making it a promising candidate for cancer immunotherapy research. -
HDAC Inhibitor
HDAC-IN-60 is a potent inhibitor of histone deacetylases (HDACs). This compound promotes the generation of reactive oxygen species (ROS) within cells, leading to DNA damage and subsequent activation of the mitochondrial apoptotic pathway. Additionally, HDAC-IN-60 can effectively disrupt the cell cycle at the G2/M phase, making it valuable for research in cancer biology and therapeutic interventions targeting HDACs. -
HDAC Inhibitor
MC2590 is a selective histone deacetylase (HDAC) inhibitor that targets class I and IIb HDAC isoforms, including HDAC1-3, -6, -8, and -10, with IC50 values ranging from 0.015 μM to 0.156 μM. It also inhibits other HDAC isoforms, such as HDAC4, HDAC5, HDAC7, HDAC9, and HDAC11, with higher IC50 values between 1.35 μM and 3.98 μM. MC2590 has been shown to induce G2/M cell cycle arrest and influences the expression of pro- and anti-apoptotic microRNAs, leading to the induction of apoptosis. This compound is valuable for research in cancer biology, epigenetics, and cell cycle regulation. -
PARP1/BRD4 Inhibitor
PARP1/BRD4-IN-2 is a selective inhibitor of PARP1 and BRD4, demonstrating IC50 values of 197 nM and 238 nM, respectively. This compound effectively impedes DNA damage repair mechanisms, inhibits the G0/G1 cell cycle transition, and induces apoptotic cell death. PARP1/BRD4-IN-2 has shown significant anti-tumor efficacy in the MDA-MB-468 xenograft mouse model, making it a valuable tool for research in triple-negative breast cancer (TNBC). -
HDAC/CDK Inhibitor
CDK/HDAC-IN-2 is a dual inhibitor of histone deacetylases (HDACs) and cyclin-dependent kinases (CDKs), exhibiting IC50 values of 6.4 nM for HDAC1, 0.25 nM for HDAC2, 45 nM for HDAC3, and >1000 nM for HDAC6,8, as well as 8.63 nM for CDK1, 0.30 nM for CDK2, and >1000 nM for CDK4,6,7. This compound demonstrates significant antiproliferative effects, inducing apoptosis and causing cell cycle arrest in the G2/M phase. CDK/HDAC-IN-2 is particularly valuable in cancer research due to its potent antitumor efficacy. -
HDAC3/6 Inhibitor
HDAC3/6-IN-2 is a selective inhibitor of histone deacetylases HDAC3 and HDAC6, exhibiting IC50 values of 0.368 μM and 0.635 μM, respectively. This compound demonstrates significant antitumor activity by promoting apoptosis in cancer cells. Additionally, HDAC3/6-IN-2 reduces the levels of HDAC3 and HDAC6, leading to the upregulation of acetylated histone H3 and α-tubulin, which may enhance therapeutic outcomes for cancers associated with these targets. -
HDAC Inhibitor
HDAC-IN-71 is a potent histone deacetylase (HDAC) inhibitor that exhibits IC50 values of 12.6 nM for HDAC1, 14.1 nM for HDAC2, 20 nM for HDAC3, 3 nM for HDAC6, and 72 nM for HDAC10. This compound effectively induces apoptosis, making it a valuable tool in cancer research. Its selective inhibition of multiple HDAC isoforms can aid in elucidating the role of histone modification in tumor progression and therapeutic response. -
HDAC6 Inhibitor
C1A is an inhibitor of class I and II histone deacetylases (HDACs) as well as sirtuins, demonstrating an IC50 of 479 nM specifically for HDAC6. This compound promotes sustained acetylation of HDAC6 substrates, including α-tubulin and HSP90, contributing to its potent anticancer properties. C1A has been shown to effectively induce apoptosis in various cancer cell lines, making it a valuable tool for research in cancer biology and therapeutic development. -
LSD1/HDAC Inhibitor
LSD1/HDAC-IN-2 is a potent inhibitor of lysine-specific demethylase 1 (LSD1) and several histone deacetylases (HDAC1, HDAC2, HDAC3, HDAC6, and HDAC8), with IC50 values ranging from 1.0 to 39.0 nM. This compound demonstrates significant biological activity by inhibiting the proliferation of colorectal cancer cells, inducing apoptosis, and causing G2/M cell cycle arrest. Additionally, LSD1/HDAC-IN-2 reduces cell migration and displays antitumor efficacy in mouse models, making it a valuable tool for cancer research and therapeutic development. -
HDAC Inhibitor
HDAC-IN-42 is a potent and selective inhibitor of histone deacetylases (HDACs), displaying IC50 values of 0.19 µM for HDAC1 and 4.98 µM for HDAC6. This compound demonstrates significant anticancer and anti-proliferative effects, inducing apoptosis and causing cell cycle arrest in the G2/M phase. HDAC-IN-42 is valuable for research applications focused on cancer biology and the modulation of gene expression through epigenetic mechanisms. -
PARP1 Inhibitor
PARP1-IN-14 is a potent inhibitor of PARP1, displaying an IC50 of 0.6 ± 0.1 nM. It demonstrates significant antiproliferative effects on MDA-MB-436 (BRCA1−/−) and Capan-1 (BRCA2−/−) cell lines, with IC50 values below 0.3 nM. This compound is valuable for cancer research, particularly in studies focused on DNA repair mechanisms and therapeutic strategies for BRCA-deficient tumors. -
Top/HDAC Dual Inhibitor
Top/HDAC-IN-2 is a dual inhibitor targeting topoisomerase and histone deacetylases (HDACs). This compound demonstrates significant antitumor activity and effectively induces apoptosis in cancer cells. Its ability to concurrently interfere with these critical pathways makes it a valuable tool for researchers investigating cancer therapeutics and cell death mechanisms. -
FLT3/HDAC Inhibitor
HDAC-IN-63 is a dual inhibitor targeting both FLT3 and HDAC, with IC50 values of 0.844 nM for FLT3 and 30.0 nM for HDAC1. It demonstrates potent inhibition of MV4-11 cell proliferation, with an IC50 of 92 nM, and effectively induces apoptosis while arresting the cell cycle in MV4-11 cells. This compound serves as a valuable research tool for the study of acute myeloid leukemia (AML) and the exploration of novel therapeutic strategies. -
PARP-1 Inhibitor
PARP1-IN-46 is a potent PARP-1 inhibitor with an IC50 of 2.4 nM, targeting the PARP-1 enzyme to modulate DNA damage response pathways. It exhibits significant anti-proliferative effects in both rat (C6) and human (U87MG) glioma cell lines by promoting PARP cleavage and inducing reactive oxygen species (ROS), ultimately leading to increased cell apoptosis. Additionally, PARP1-IN-46 effectively inhibits glioma cell migration, invasion, and colony formation, making it a valuable tool for research on glioma biology and potential therapeutic strategies. -
PROTAC HDAC6 Degrader
PROTAC HDAC6 Degrader 1 is a selective compound designed to target and degrade histone deacetylase 6 (HDAC6) through the proteolysis-targeting chimera (PROTAC) mechanism. With a DC50 of 3.5 nM, this degrader exhibits significant antiproliferative effects, particularly by inducing apoptosis in myeloid leukemia cell lines. It serves as a valuable tool for research on cancer therapies and the modulation of histone deacetylation pathways. -
HDAC4 Inhibitor
HDAC4-IN-1 is a selective inhibitor of histone deacetylase 4 (HDAC4), demonstrating an IC50 of 0.077 μM. This compound has been shown to enhance caspase-mediated apoptosis, highlighting its potential in anticancer applications. HDAC4-IN-1 is a valuable tool for research into drug combinations aimed at increasing the efficacy of cancer therapies. -
HDAC6 Inhibitor
HDAC6-IN-45 is a selective inhibitor of histone deacetylase 6 (HDAC6), demonstrating an IC50 of 15.2 nM. This compound has been shown to promote neurotrophic effects by enhancing the expression of GAP43 and Beta-3 tubulin, while also activating the Nrf2 signaling pathway. Further research applications include its ability to mitigate H2O2-induced reactive oxygen species production, inhibit apoptosis in PC12 cells, and confer neuroprotective effects in SCOP-induced zebrafish models of Alzheimer's disease. Additionally, HDAC6-IN-45 exhibits antioxidant properties and possesses favorable blood-brain barrier permeability. -
Topo II/ HDAC Inhibitor
Topo II/HDAC-IN-2 is a potent dual inhibitor targeting topoisomerase II (Topo II) and histone deacetylases (HDAC). This compound is known to induce apoptosis in various cancer cell lines, making it a valuable tool for investigating the mechanisms of tumorigenesis and potential therapeutic interventions. Research applications include studies on cancer biology, drug development, and the modulation of epigenetic regulators. -
DNMT3A Inhibitor
(4aS,8aR)-NPD-001 is a potent allosteric inhibitor targeting DNMT3A, disrupting critical protein-protein interactions essential for its activity. This compound demonstrates significant biological activity by inducing apoptosis in acute myeloid leukemia (AML) cell lines and promoting differentiation in various AML cell types, including those harboring the R882 mutation in DNMT3A. Its specific modulation of DNMT3A makes (4aS,8aR)-NPD-001 a valuable tool for research on epigenetic regulation in hematological malignancies. -
Dual PLK1/BET Inhibitor
WNY0824 is a dual inhibitor targeting Polo-like kinase 1 (PLK1) and the Bromodomain and Extra-Terminal (BET) protein family. It demonstrates potent inhibitory activity, with IC50 values of 22 nmol/L for PLK1 and varying efficacy against BRD2, BRD3, BRD4, and BRDT. WNY0824 induces cell cycle arrest and apoptosis by disrupting AR- and MYC-mediated transcriptional processes, making it valuable for research in cancer biology. Furthermore, it has shown effectiveness in inhibiting tumor growth in Enzalutamide-resistant castration-resistant prostate cancer (CRPC) xenograft models, highlighting its potential in overcoming treatment resistance. -
FLT3/HDAC Inhibitor
FLT3/HDAC-IN-3 is a dual inhibitor targeting FLT3 and HDAC, with a potent inhibitory effect on FLT3 (IC50 = 14 nM) and HDAC isoforms, including HDAC1 (IC50 = 27 nM) and HDAC6 (IC50 = 20 nM). This compound demonstrates selective inhibition, exhibiting reduced activity against HDAC8 and no activity toward HDAC4. FLT3/HDAC-IN-3 has shown anti-proliferative effects across various hematological malignancy cell lines and demonstrates efficacy in the Jeko-1 xenograft model without significant toxicity. It is suitable for research focused on hematological malignancies and the role of dual inhibition in therapeutic strategies. -
HDAC Inhibitor
HDAC-IN-81 is a potent HDAC1 inhibitor, demonstrating an IC50 value of 4.5 nM. This compound exhibits significant anti-cancer activity by effectively inhibiting cell proliferation and inducing apoptosis in cancer cells. It serves as a valuable tool for research applications in cancer biology and epigenetic regulation. -
HDAC Inhibitor
Valproic acid magnesium is an orally active histone deacetylase (HDAC) inhibitor that exhibits an IC50 range of 0.5 to 2 mM, specifically inhibiting HDAC1 with an IC50 of 400 μM while promoting the proteasomal degradation of HDAC2. This compound activates Notch1 signaling and demonstrates anti-proliferative effects in small cell lung cancer (SCLC) cells. Valproic acid magnesium has diverse therapeutic applications, including the treatment of epilepsy, bipolar disorder, metabolic diseases, HIV infection, and the prevention of migraine headaches. -
HDAC Inhibitor
Nanatinostat TFA is a potent, orally active inhibitor of class I histone deacetylases (HDACs), with IC50 values of 3 nM, 4 nM, and 7 nM for HDAC1, HDAC2, and HDAC3, respectively. It demonstrates reduced activity against HDAC5 and HDAC6, with IC50 values of 200 nM and 2100 nM, respectively. Nanatinostat TFA effectively induces apoptosis in myeloma cells and exhibits significant anticancer properties against various malignancies, including advanced solid tumors and colorectal cancer. Its selective inhibition of HDACs positions it as a valuable compound for cancer research and therapeutic development. -
PI3K/HDAC Inhibitor
Fimepinostat mesylate is a potent dual inhibitor targeting class I phosphoinositide 3-kinases (PI3Ks) and histone deacetylases (HDACs). It exhibits IC50 values of 19 nM for PI3Kα, 54 nM for PI3Kβ, 39 nM for PI3Kδ, and 1.7 nM for HDAC1, 5.0 nM for HDAC2, 1.8 nM for HDAC3, and 2.8 nM for HDAC10. This compound is valuable for research applications focusing on cancer biology, epigenetic regulation, and cellular signaling pathways. -
FLT3/JAK2 Inhibitor
JAK2/FLT3-IN-3 is a potent dual inhibitor of FLT3 and JAK2, exhibiting IC50 values of 2.01 nM for JAK2, 0.51 nM for FLT3, and 104.40 nM for JAK3. This compound induces apoptosis in cancer cells and demonstrates significant antitumor activity. Its ability to inhibit both FLT3 and JAK2 pathways makes it a valuable tool for research related to hematological malignancies and targeted cancer therapies. -
PARP 2 Inhibitor
PARP-2-IN-2 is a potent inhibitor of PARP-2, exhibiting an IC50 value of 0.057 μM. This compound effectively induces cell cycle arrest and apoptosis in MCF-7 breast cancer cells, highlighting its potential as a therapeutic agent in cancer research. PARP-2-IN-2 is valuable for investigations into cancer biology and therapeutic strategies targeting DNA repair mechanisms. -
HDAC Inhibitor
MC2625 is a potent histone deacetylase (HDAC) inhibitor, specifically targeting HDAC3 and HDAC6 with IC50 values of 80 nM and 11 nM, respectively. This compound effectively increases levels of acetylated histone H3 and acetylated tubulin, promoting apoptosis in cancer stem cells (CSCs) and inhibiting their growth. MC2625 serves as a valuable tool for research focused on cancer therapeutics and the role of epigenetics in tumor biology. -
JAK2/STAT3 Inhibitor
Cernuumolide J is a selective inhibitor of JAK2/STAT3 signaling pathway. It induces G2/M phase arrest and apoptosis in HEL leukemia cells by downregulating the phosphorylation of JAK2, STAT3, and Erk, while promoting the phosphorylation of JNK and p38 MAPK. Cernuumolide J exhibits a concentration-dependent growth inhibition of HEL leukemia cells, with an IC50 value of 1.79 μM, making it a valuable compound for research in anti-cancer therapy. -
Sirtuin Inhibitor
Sirt1/2-IN-4 is a potent triple inhibitor of the sirtuin family, specifically targeting SIRT1 and SIRT2 with IC50 values of 1.2 μM and 1.9 μM, respectively, and showing moderate inhibition of SIRT3 at 18.6 μM. This compound effectively prevents the deacetylation of p53, highlighting its potential role in cancer research. Its ability to modulate sirtuin activity makes it a valuable tool for investigating the biological implications of sirtuin inhibition in various cancer models. -
HDAC Inhibitor, Topoisomerase I Inhibitor
WJ35435 is a dual-target HDAC and topoisomerase I inhibitor that exerts anticancer activity by inducing DNA damage and promoting cell cycle arrest at the G1 and G2 phases, ultimately leading to apoptosis. This compound enhances histone H3 acetylation and phosphorylation, along with α-tubulin acetylation and the formation of γ-H2AX, thereby effectively demonstrating its anti-HDAC properties. WJ35435 holds potential for advancing research in cancer therapeutics. -
PARP1 Inhibitor
KU-0058948 hydrochloride is a highly selective inhibitor of PARP1, exhibiting an IC50 of 3.4 nM. It is demonstrated to induce cell cycle arrest and apoptosis in primary myeloid leukemic cells and various myeloid leukemic cell lines. This reagent is valuable for research into the mechanisms of leukemia and the therapeutic potential of PARP inhibition in hematological malignancies. -
LSD1 Inhibitor
LSD1-IN-25 is a potent and selective inhibitor of lysine-specific demethylase 1 (LSD1), demonstrating an IC50 of 46 nM and a Ki of 30.3 nM. This compound effectively induces apoptosis in cancer cells, making it a valuable tool for investigating the role of LSD1 in cancer biology and therapeutic applications. Its oral bioavailability further supports its use in preclinical studies aimed at targeting epigenetic regulation in malignancies. -
HDAC Inhibitor
HDAC-IN-46 is a potent inhibitor of histone deacetylases (HDACs), demonstrating IC50 values of 0.21 μM for HDAC1 and 0.021 μM for HDAC6. In MDA-MB-231 cells, HDAC-IN-46 promotes the upregulation of phosphorylated p38 while downregulating Bcl-xL and cyclin D1, leading to significant G2 phase cell cycle arrest and apoptosis. This compound is valuable for research focused on triple-negative breast cancer (TNBC). -
PARP1/NAMPT Inhibitor
PARP1/NAMPT-IN-1 is a potent dual inhibitor of PARP1 and NAMPT, exhibiting IC50 values of 1.2 nM and 6.7 nM, respectively. This compound disrupts the homologous recombination repair pathway, leading to the accumulation of DNA double-strand breaks, which induces cell cycle arrest and apoptosis. Additionally, PARP1/NAMPT-IN-1 demonstrates antimigratory effects and has shown significant antitumor activity in a breast cancer xenograft model. It is a valuable tool for research on triple-negative breast cancer (TNBC). -
JAK3-Inhibitor
JAK3 covalent inhibitor-2 is a selective covalent inhibitor targeting Janus kinase 3 (JAK3), exhibiting an IC50 of 7.2 nM. This compound demonstrates anti-inflammatory activity, low toxicity, and favorable bioavailability, making it suitable for research applications involving autoimmune diseases and inflammatory disorders. Its specificity for JAK3 supports investigations into therapeutic strategies aimed at modulating immune responses. -
HDAC Inhibitor
HDAC-IN-57 is a potent orally active inhibitor of histone deacetylases (HDACs), exhibiting IC50 values of 2.07 nM for HDAC1, 4.71 nM for HDAC2, 2.4 nM for HDAC6, and 107 nM for HDAC8. In addition, HDAC-IN-57 inhibits lysine-specific demethylase 1 (LSD1) with an IC50 of 1.34 µM. This compound induces apoptosis and demonstrates significant anti-tumor activity, making it a valuable tool for cancer research and therapeutic development targeting epigenetic regulation. -
PARP1/c-Met Inhibitor
PARP1/c-Met-IN-1 is a selective dual inhibitor targeting PARP1 and c-Met, demonstrating IC50 values of 3.3 nM and 32.2 nM, respectively. This compound effectively induces apoptosis and causes cell cycle arrest in the G2/M phase in MDA-MB-231 cells. Additionally, PARP1/c-Met-IN-1 has shown significant antitumor activity in murine models, making it a valuable tool for cancer research and therapeutic development. -
PARP1 Inhibitor
PARP1-IN-10 is a potent inhibitor of PARP1, exhibiting an IC50 value of 50.62 nM in vitro without inducing cytotoxic effects. This compound induces cell cycle arrest at the G2/M phase and promotes apoptosis, thereby enhancing the cytotoxic efficacy of temozolomide (TMZ). PARP1-IN-10 is valuable for research in cancer biology and therapeutics, particularly in understanding the interplay between DNA repair mechanisms and chemotherapeutic sensitivity. -
PARP1 Inhibitor
PARP1-IN-55 is a selective inhibitor of PARP1, demonstrating potent activity with an IC50 of 0.019 μM. It exhibits considerable anti-proliferative effects on MCF-7 breast cancer cells, with an IC50 of 3.6 μM. By inhibiting the PARP1-mediated DNA damage repair pathway, PARP1-IN-55 induces reactive oxygen species accumulation, disrupts mitochondrial membrane potential, and promotes apoptosis while inhibiting cancer cell migration, invasion, and colony formation. This compound serves as a valuable tool for investigating breast cancer biology and therapeutic strategies. -
PROTAC KDM4 Degrader
PROTAC KDM4 Degrader-1 is a potent proteolysis targeting chimera (PROTAC) designed to selectively degrade KDM4A-C while sparing KDM4D. This compound demonstrates significant antiproliferative effects in esophageal cancer cells, inducing apoptosis and cell cycle arrest. Additionally, PROTAC KDM4 Degrader-1 effectively inhibits histone H3 lysine demethylation, making it a valuable tool for research into cancer biology and epigenetic regulation. -
SIRT6 Activator
MDL-811 is a selective allosteric activator of SIRT6, exhibiting an EC50 of 5.7 μM. This compound demonstrates significant anti-inflammatory, antitumor, and neuroprotective properties, making it a valuable tool for research. MDL-811 is particularly relevant for studies related to colorectal cancer and ischemic stroke, providing insights into potential therapeutic strategies targeting SIRT6 modulation. -
Aurora/VEGF/PDGF Inhibitor
Ilorasertib hydrochloride is a potent, orally active inhibitor targeting Aurora kinases, with IC50 values of 116 nM, 5 nM, and 1 nM for Aurora A, B, and C, respectively. Additionally, it exhibits significant inhibition of VEGF and PDGF pathways. This compound is valuable for research related to acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS), facilitating studies into the mechanisms of these hematologic malignancies. -
PROTAC Aurora-A/Aurora-B Degrader
dAurAB5 is a dual PROTAC degrader targeting Aurora-A (DC50 = 8.8 nM) and Aurora-B (DC50 = 6.1 nM). It effectively induces the degradation of these kinases, leading to reduced N-Myc levels and decreased viability in IMR32 neuroblastoma cells. dAurAB5 also downregulates AAK1, PTK2, GAK, and TTK, making it a valuable tool for investigating the molecular mechanisms in neuroblastoma and related cancers. -
FAK/Aurora Kinase Inhibitor
FAK/Aurora kinase-IN-1 is a dual inhibitor targeting focal adhesion kinase (FAK) and Aurora kinase, exhibiting IC50 values of 6.61 nM and 0.91 nM, respectively. This compound demonstrates significant anticancer activity, making it a valuable tool for research applications focused on cancer biology and therapeutic development. Its efficacy in inhibiting both kinases positions it as a promising candidate for further studies in tumor proliferation and treatment strategies. -
Aurora kinase Inhibitor
Aurora kinase-IN-10 is a selective inhibitor of Aurora kinases, demonstrating IC50 values of 5.94 nM for Aurora A and 86.06 nM for Aurora B. This compound exhibits significant anti-tumor activity, making it a valuable tool for research into various cancers, particularly triple-negative breast cancer. Its targeted inhibition of Aurora kinases positions it as a candidate for studies focused on cell cycle regulation and cancer treatment strategies. -
Aurora B inhibitor
Ceftriaxone is a third-generation cephalosporin antibiotic that primarily targets the Aurora B kinase, exhibiting notable inhibitory activity. This compound is also recognized for its broad-spectrum antibacterial efficacy against various Gram-negative and Gram-positive bacteria. Additionally, Ceftriaxone displays anti-inflammatory, antitumor, and antioxidant properties, making it valuable in research applications related to bacterial infections and conditions such as meningitis. -
GRK6/Aurora A Dual Inhibitor
GRK6/Aurora A-IN-1 is a potent dual inhibitor targeting G protein-coupled receptor kinase 6 (GRK6) and Aurora A, exhibiting IC50 values of 120 nM and 11 nM, respectively. GRK6 plays a critical role in the survival of multiple myeloma (MM) cells, making this compound valuable for research in MM studies. This inhibitor can facilitate investigations into the mechanisms of MM cell proliferation and the potential for targeted therapies. -
Aurora A Inhibitor
TAS-119 is a highly selective and orally bioavailable inhibitor of Aurora A with an IC50 of 1.0 nM. It demonstrates significant selectivity for Aurora A compared to other kinases, such as Aurora B, which has an IC50 of 95 nM. TAS-119 exhibits strong antitumor activity, making it a valuable reagent for cancer research focusing on targeted therapies and the exploration of cell cycle regulation.
