Abcam, ab120377, Rottlerin, Kinase inhibitor

Size: 10mg / 50mg
MW 516.5 Da, Purity >95%. Originally reported to inhibit PKC isoforms, especially PKCδ and CAM-KIII. Also inhibits MAPKAP-K2 and PRAK (IC 50 values are 5.4 and 1.9 μM, respectively), CHK2, PLK1, PIM3 and SRPK1.
Key facts
CAS number:82-08-6,
Purity:>95%,
Form:SolidSee storage information,
Molecular weight:516.5 Da,
Molecular formula:C30H28O8,
PubChem:5281847,
Nature:Synthetic,
Solubility:Soluble in DMSO to 100 mM,
Biochemical name:Rottlerin,
Biological description:Originally reported to inhibit PKC isoforms, especially PKCδ and CAM-KIII. Also inhibits MAPKAP-K2 and PRAK (IC50 values are 5.4 and 1.9 μM, respectively), CHK2, PLK1, PIM3 and SRPK1.,
Canonical smiles:CC1=C(C(=C(C(=C1O)C(=O)C)O)CC2=C(C(=C3C(=C2O)C=CC(O3)(C)C)C(=O)C=CC4=CC=CC=C4)O)O,
Isomeric smiles:CC1=C(C(=C(C(=C1O)C(=O)C)O)CC2=C(C(=C3C(=C2O)C=CC(O3)(C)C)C(=O)/C=C/C4=CC=CC=C4)O)O,
InChi:InChI=1S/C30H28O8/c1-15-24(33)19(27(36)22(16(2)31)25(15)34)14-20-26(35)18-12-13-30(3,4)38-29(18)23(28(20)37)21(32)11-10-17-8-6-5-7-9-17/h5-13,33-37H,14H2,1-4H3/b11-10+,
InChiKey:DEZFNHCVIZBHBI-ZHACJKMWSA-N,
IUPAC Name:(E)-1-[6-[(3-acetyl-2,4,6-trihydroxy-5-methylphenyl)methyl]-5,7-dihydroxy-2,2-dimethylchromen-8-yl]-3-phenylprop-2-en-1-one

Properties and Storage Information:
Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C, Storage information-Store under desiccating conditions, The product can be stored for up to 12 months

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
ATM also known as Ataxia-Telangiectasia Mutated has a mass of approximately 370 kDa and plays a vital role in the cellular response to DNA damage. It is largely expressed in the nucleus of eukaryotic cells. CHK2 (Checkpoint Kinase 2) which is 61 kDa acts downstream of ATM and similarly contributes to DNA damage checkpoint control. Protein Kinase C delta (PKCδ) with a mass of 78 kDa regulates various cell signaling pathways and its expression can be found in numerous tissues including the brain and heart. PLK1 (Polo-like kinase 1) weighing around 68 kDa is an important regulator during mitosis. MK2 (MAPKAPK2) Aurora B PAK4 and Myosin Light Chain Kinase (MLCK) DYRK3 SRPK1 PRAK/MK5 PIM3 and CAMKK2 further contribute diverse roles within cellular signaling and are essential throughout the cell cycle and in stress response.
Biological function summary
These proteins interact in complex networks to ensure cell cycle progression and stability. ATM primarily functions in the DNA damage response activating other kinases such as CHK2. PKCδ as a part of the PKC family influences apoptosis cell growth and differentiation. PLK1 associates with various components like the centrosome to control mitosis onset. Aurora B part of the chromosomal passenger complex ensures chromosomal alignment and cytokinesis. MK2 a MAPKAPK along with PAK4 MLCK PRAK/MK5 and others integrates signals from stress pathways to mediate cellular responses.
Pathways
These proteins align with key biological processes such as DNA damage repair and cell division regulation. The ATM-CHK2 pathway is a part of the broader DNA repair machinery working with proteins like BRCA1 and p53 to maintain genomic integrity. PLK1 and Aurora B are essential in the mitotic and cytokinesis pathways coordinating with cyclins and CDKs to regulate cell cycle transitions. These proteins interact in cross-linked pathways laying the groundwork for cellular homeostasis and adaptation.
Defects in these proteins can lead to significant health implications. ATM mutations are closely linked to Ataxia-Telangiectasia affecting neurotransmission and increasing cancer predisposition. CHK2 mutations can result in heightened cancer risks especially breast cancer interacting with proteins such as BRCA2. Disruptions in PLK1 or Aurora B function can contribute to uncontrolled cell proliferation implicated in various cancers. Dysregulation of PKCδ may involve in cardiac hypertrophy and related cardiac disorders. These links highlight the clinical importance of understanding these proteins in therapeutic developments.