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Benzoic acid, 4-hydroxy-2-methoxy-3-methyl-, methyl ester is a chemical with a specific purpose. Lookchem provides you with multiple data and supplier information of this chemical.

116386-96-0

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116386-96-0 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 116386-96-0 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 1,1,6,3,8 and 6 respectively; the second part has 2 digits, 9 and 6 respectively.
Calculate Digit Verification of CAS Registry Number 116386-96:
(8*1)+(7*1)+(6*6)+(5*3)+(4*8)+(3*6)+(2*9)+(1*6)=140
140 % 10 = 0
So 116386-96-0 is a valid CAS Registry Number.

116386-96-0Downstream Products

116386-96-0Relevant academic research and scientific papers

Rational drug design of benzothiazole-based derivatives as potent signal transducer and activator of transcription 3 (STAT3) signaling pathway inhibitors

Gao, Dingding,Jin, Nan,Fu, Yixian,Zhu, Yueyue,Wang, Yujie,Wang, Ting,Chen, Yuehong,Zhang, Mingming,Xiao, Qiang,Huang, Min,Li, Yingxia

, (2021/03/14)

The cumulative evidence supports STAT3, a transcriptional mediator of oncogenic signaling, as a therapeutic target in cancer. The development of STAT3 inhibitors remain an active area of research as no inhibitors have yet to be approved for cancer treatment. In a continuing effort to develop more potent STAT3 inhibitors based on our previously identified hit compound 16w, a series of benzothiazole derivatives with unique binding mode in SH2 domain of STAT3 were designed, synthesized and biologically evaluated. Of note, compound B19 demonstrated excellent activity against IL-6/STAT3 signaling pathway with the IC50 value as low as 0.067 μM as determined by a luciferase reporter assay. Moreover, multiple compounds displayed potent antiproliferative activity against MDA-MB-468 and JAK2 mutant HEL cell lines. Further biochemical study using Western blot assay indicated that B19 blocked the phosphorylation of STAT3 at Tyr 705 and Ser 727 and thus suppressed STAT3-mediated gene expression of c-MYC and MCL-1. Simultaneously, it induced cancer cell G2/M phase arrest and apoptosis both in MDA-MB-468 and HEL cell lines. Finally, molecular docking study along with surface plasmon resonance (SPR) and fluorescence polarization (FP) assays disclosed the binding mode of B19 in STAT3 SH2 domain. Taken together, our finding suggests that B19 is a promising therapeutic STAT3 inhibitor for cancer treatment.

Synthesis of Averufin and its Role in Aflatoxin B1 Biosynthesis

Townsend, Craig A.,Christensen, Siegfried B.,Davis, Steven G.

, p. 839 - 862 (2007/10/02)

Described are two total syntheses of (+/-)-averufin (4) proceeding through a common intermediate and predicated on the efficient introduction of isotopic label(s) at side-chain and nuclear sites for the purpose of biosynthetic investigations of aflatoxin B1 (8).Using these methods, (+/-)--and --averufin, (65) and (68) respectively, and a 1:1 mixture of (+/-)-- and --averufin (71) were prepared and incorporated into aflatoxin B1 using mycelial suspensions of Aspergillus parasiticus (SU-1).In each instance efficient and specific utilization of label was observed in the product by (13)C-n.m.r.spectroscopy, demonstrating the intact incorporation of averufin.When compared with earlier observations of acetate incorporation, a complete correlation of the carbon skeleton from the intermediate anthraquinone stage of the four carbons lost in this overall process were unambiguously identified.In the formation of the dihydrobisfuran, the anthraquinone nucleus migrates to C-2' to branch the linear side-chain of averufin.Deuterium bound at C-1' in averufin is carried to C-13 of aflatoxin.Preparation from (+/-)-averufin (68) of (+/-)--averufin (73) and incorporation of the latter into versiconal acetate (5) demonstrated loss of the terminal two carbons of the averufin side-chain, presumably as acetate, by way of a Baeyer-Villiger-like oxidation.

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