Ligand for orphan nuclear receptor Nur77 and uses thereof

10808005 ยท 2020-10-20

Assignee

Inventors

Cpc classification

International classification

Abstract

Provided are use of a compound of Formula I as a ligand of orphan nulear receptor Nur77, and in the prevention or treatment of a orphan nulear receptor Nur77 associated disease, ##STR00001##

Claims

1. A method for treating a triple negative breast cancer, comprising administering to a subject in need thereof an effective amount of a compound selected from (1)-(2), or a tautomer, a stereoisomer or a pharmaceutically acceptable salt or ester thereof: ##STR00083## wherein, in formula (I), X represents NH, N(R), O, CH.sub.2 or halogen; wherein, when X is halogen, R.sub.1 is absent; when the bond between Y and the carbon atom attached thereto is a single bond, Y represents H, halogen, OR, SR or NRR; when the bond between Y and the carbon atom attached thereto is a double bond, Y represents O, S or NR; R.sub.1 is absent or represents H, PO(OR).sub.2, C.sub.1-6alkyl, glycosyl, C.sub.1-6alkoxycarbonyl-C.sub.1-6alkyl, 3- to 8-membered cycloalkyl-aminoacyl, aryl-C.sub.1-6alkyl or aryl, wherein the C.sub.1-6alkyl, glycosyl, C.sub.1-6alkoxycarbonyl-C.sub.1-6alkyl, 3- to 8-membered cycloalkyl-aminoacyl, aryl-C.sub.1-6alkyl and aryl are unsubstituted or substituted with one or more substituents selected from the group consisting of halogen, hydroxy, amino, C.sub.1-6alkyl, C.sub.1-6alkoxy, C.sub.1-6alkylamino and C.sub.1-6alkanoyl; R.sub.2 represents H, D, PO(OR).sub.2, CONH.sub.2, NH.sub.2, NHR, NRR, NHCOR, NRCOR, NHCOOR, NHCONHR, NHCONRR, NRCONHR, NRCONRR, OH, OR, OCONHR, OCONRR, SH, SR, SOR, SOOR, SO.sub.2NHR, nitro, halogen, glycosyl, cyano, trifluoromethyl, C.sub.1-6alkyl, 3- to 8-membered cycloalkyl, 3- to 8-membered heterocycloalkyl, aryl, C.sub.1-6alkyl-substituted aryl, 6- to 15-membered heteroaryl, alkenyl, alkynyl, sulfinyl, sulfonic acid group or sulfonate group; wherein the C.sub.1-6alkyl, 3- to 8-membered cycloalkyl, 3- to 8-membered heterocycloalkyl, aryl, C.sub.1-6alkyl-substituted aryl, 6- to 15-membered heteroaryl, alkenyl and alkynyl are unsubstituted or substituted with one or more substituents selected from the group consisting of amino, halogen, hydroxy, oxy, C.sub.1-6alkyl, C.sub.1-6alkoxy, C.sub.1-6alkylthio, C.sub.1-6alkanoyl, 3- to 8-membered cycloalkyl, 3- to 8-membered oxocycloalkyl, cyano, trifluoromethyl, C.sub.1-6alkoxycarbonyl, C.sub.1-6alkylamido, ureido group, carbamate, carboxyl and aryl; R.sub.3 and R.sub.4 each independently is absent or represents H, C.sub.1-6alkyl, C.sub.1-6alkanoyl, C.sub.1-6alkoxycarbonyl, glycosyl, aryl-C.sub.1-6alkyl or aryl, wherein the C.sub.1-6alkyl, C.sub.1-6alkanoyl, C.sub.1-6alkoxycarbonyl, glycosyl, aryl-C.sub.1-6alkyl and aryl are unsubstituted or substituted with one or more substituents selected from the group consisting of halogen, hydroxy, amino, C.sub.1-6alkyl, C.sub.1-6alkoxy, C.sub.1-6alkylamino and C.sub.1-6alkanoyl; R and R each independently is selected from H, C.sub.1-6alkyl, 3- to 8-membered cycloalkyl, aryl-C.sub.1-6alkyl or aryl, wherein the C.sub.1-6alkyl, 3- to 8-membered cycloalkyl, aryl-C.sub.1-6alkyl and aryl are unsubstituted or substituted with one or more substituents selected from the group consisting of halogen, hydroxy, amino, C.sub.1-6alkyl, C.sub.1-6alkoxy, and C.sub.1-6alkylamino; R represents C.sub.1-6alkyl or aryl; custom character in Formula (I) represents single bond or double bond.

2. The method according to claim 1, wherein, in formula (I), the bond between Y and the carbon atom attached thereto is a double bond, and Y represents O.

3. The method according to claim 1, wherein, in formula (I), X in the compound represents NH, N(R), O, CH.sub.2 or halogen; R represents C.sub.1-6alkyl or 3- to 8-membered cycloalkyl; wherein, when X is halogen, R.sub.1 is absent.

4. The method according to claim 1, wherein, in formula (I), R.sub.1 is absent or represents hydrogen, C.sub.1-4alkyl, PO(OR).sub.2, monoglycosyl, C.sub.1-4alkoxycarbonyl-C.sub.1-4alkyl, 3- to 6-membered cycloalkyl-aminoacyl, aryl-C.sub.1-4alkyl or aryl; wherein the C.sub.1-4alkyl, monoglycosyl, C.sub.1-4alkoxycarbonyl-C.sub.1-4alkyl, 3- to 6-membered cycloalkyl-aminoacyl, aryl-C.sub.1-4alkyl and aryl are unsubstituted or substituted with one or more substituents selected from the group consisting of: halogen, hydroxy, amino, C.sub.1-4alkyl, C.sub.1-4alkoxy, C.sub.1-4alkylamino and C.sub.1-4alkanoyl; R represents C.sub.1-4alkyl.

5. The method according to claim 1, wherein, in formula (I), R.sub.2 represents H, D, OH, PO(OR).sub.2, C.sub.1-6alkyl, 9- to 15-membered fused heteroaryl or sulfonate; wherein the C.sub.1-6alkyl or 6- to 15-membered heteroaryl is unsubstituted or substituted with one or more substituents selected from the group consisting of amino, halogen, hydroxy, oxy, C.sub.1-6alkyl, C.sub.1-6alkoxy, C.sub.1-6alkanoyl, cyano, trifluoromethyl and carboxyl; R represents H, C.sub.1-6alkyl or aryl.

6. The method according to claim 1, wherein, in formula (I), the Carbon 7 and Carbon 8 of the compound are linked with a carbon-carbon double bond.

7. The method according to claim 1, wherein, in formula (I), the bond between Y and the carbon atom attached thereto in the compound is a double bond.

8. The method according to claim 1, wherein, in formula (I), the bond between Y and the carbon atom attached thereto in the compound is a single bond.

9. The method according to claim 1, wherein the compound has the following structure: ##STR00084## wherein R.sub.3 and R.sub.4 each independently represents H, C.sub.1-6alkyl or C.sub.1-6alkanoyl.

10. The method according to claim 1, wherein the compound has the following structure: ##STR00085## wherein R.sub.4 represents H, C.sub.1-6alkanoyl, C.sub.1-6alkoxycarbonyl or monoglycosyl substituted with one or more C.sub.1-6alkanoyl groups.

11. The method according to claim 1, wherein the compound is selected from the following compounds: ##STR00086## ##STR00087## ##STR00088## ##STR00089## ##STR00090## ##STR00091## ##STR00092## ##STR00093## ##STR00094## ##STR00095## ##STR00096## ##STR00097## ##STR00098## ##STR00099##

Description

DRAWINGS

(1) FIG. 1 showed the screening of compounds capable of binding to Nur77 using Biacore T200. The results of the binding of YXY101 to Nur77-LBD detected by Biacore T200 were shown, wherein red dots represented compound YXY101; blue dots represented control compounds. The results showed that compound YXY101 was able to bind to Nur77-LBD.

(2) FIG. 2A showed the chemical structure of Celastrol (compound YXY101).

(3) FIG. 2B showed the results of further experiment on the binding of different concentrations of YXY101 (0.04 M, 0.08 M, 0.16 M, 0.32 M, 0.64 M) to Nur77-LBD. The results showed that the dissociation constant (Kd) of compound YXY101 to Nur77-LBD was 292 nM;

(4) FIG. 2C showed the results of experiment on the binding of YXY101 to Nur77-LBD detected by circular dichroism spectroscopy, wherein the red curve represents YXY101+Nur77-LBD; the blue curve represents Nur77-LBD. The results showed that compound YXY101 was able to change the CD spectrum of Nur77-LBD. It indicated that compound YXY101 was able to bind to Nur77-LBD.

(5) FIG. 2D showed the results of experiment on the binding of YXY101 to Nur77-LBD detected by HPLC, wherein the red curve represented YXY101+Nur77-LBD; the purple curve represented YXY101+RXR-LBD. The results showed that compound YXY101 was able to bind to Nur77-LBD to form a complex, but not to RXR-LBD.

(6) FIG. 2E showed the results of experiment on the binding of YXY101 to Nur77-LBD detected by dual-luciferase reporter assay system. The results showed that compound YXY101 was able to inhibit the transactivation function of Nur77, but had no significant effect on transactivationthat of glucocorticoid receptor (GR). It indicated that compound YXY101 was capable of binding to Nur77-LBD and inhibiting the transcriptional activity of Nur77-LBD; whereas compound YXY101 does not bind to GR.

(7) FIG. 2F showed the molecular docking of YXY101 to Nur77. The results showed that YXY101 binded to known hydrophobic grooves on the surface of Nur77 protein mainly by hydrophobic interaction.

(8) FIGS. 3A-3B showed the results of immunoblotting analysis of IB and phosphorylated IKK/ in cells treated with different concentrations of YXY101 and TNF.

(9) FIG. 3C showed the immunofluorescence staining results of cells treated with YXY101 and TNF (Scale bar: 20 m).

(10) FIG. 3D showed the analysis results of NF-B activity of cells treated with YXY101 and TNF, wherein **P<0.01, ***P<0.001 (T test).

(11) FIG. 3E showed the results of immunoblot analysis of IB and phosphorylated IKK/ in different cancer cell lines treated with different concentrations of YXY101 and TNF.

(12) FIG. 3F showed the results of immunoblot analysis of IB in HepG2 cells stimulated with TNF and treated with different compounds.

(13) FIGS. 4A-4B showed the results of immunoblot analysis of Nur77, RXR and IB in HepG2 cells transfected with different siRNAs and treated with different concentrations of YXY101 and TNF.

(14) FIG. 4C showed the results of immunoblot analysis of IB in MEF cells and Nur77/MEF cells treated with different concentrations of YXY101 and TNF.

(15) FIG. 4D showed the immunofluorescence staining results of MEF cells and Nur77/MEF cells treated with YXY101 and TNF (Scale bar: 10 m).

(16) FIG. 4E showed the results of immunoblot analysis of IB in MEF cells and Nur77/MEF cells treated with different concentrations of XS0284 and TNF.

(17) FIG. 5A showed the proliferation ratio of different breast cancer cells (MDA-MB-231; MDA-MB-468; BT549; SKBR3; T47D and MCF-7) in relation to YXY101 concentration, as well as the IC50 of YXY101; wherein MDA-MB-231, MDA-MB-468, BT549 and SKBR3 are triple negative breast cancer cells, indicated by red curves; T47D and MCF-7 are triple positive breast cancer cells, indicated by blue curves.

(18) FIG. 5B showed the results of immunoblot analysis of parp and ER in MDA-MB-231 and MCF-7 cells treated with different concentrations of YXY101 (0 M, 0.25 M, 0.5 M, 1 M, 2 M, or 4 M).

(19) FIG. 5C showed the results of immunoblot analysis of parp and p-mTOR in MDA-MB-231 treated with different concentrations of YXY101 (0 M, 2 M, or 4 M) for 12 h or 24 h.

(20) FIG. 5D showed the results of immunoblot analysis of parp in MDA-MB-231 cells treated with YXY101 in combination with TNF for different time period (1 h, 6 h or 12 h).

(21) FIG. 5E showed the curves of proliferation ratios of Hela cells in relation to concentrations of YXY101, and the results showed that the IC50 of YXY101 for wild-type Hela cells was 1.189 M, while the IC50 for Nur77 knock-out Hela cells was 58.166 M.

(22) FIGS. 6A-B showed results from testing the anti-tumor effect of YXY101 alone or in combination with TNFa on triple-negative breast cancers via nude mice xenograft experiments. In FIG. 6A, the left panel showed the tumors formed in nude mice from each group; the middle panel showed the RTV values of the tumors formed in nude mice from each group; the right panel showed the weight values of the tumors formed in nude mice from each group. FIG. 6B showed the immunohistochemical staining results of tumor tissues of nude mice from each group.

(23) FIG. 7A showed the general state of MMTV-PYVT mice at 2 weeks, 11 weeks, 13 weeks or 17 weeks after intragastric administration of 2 mg/kg of YXY101.

(24) FIG. 7B showed the results of HE staining and immunohistochemical staining of tumor tissues of MMTV-PYVT mice at 2 weeks, 11 weeks, 13 weeks or 17 weeks after intragastric administration of 2 mg/kg of YXY101.

(25) FIG. 7C showed the analysis results of weight, morphology, HE staining and immunohistochemical staining of lung tissues of MMTV-PYVT mice at 2 weeks, 11 weeks, 13 weeks or 17 weeks after intragastric administration of 2 mg/kg of YXY101.

(26) FIG. 8A showed the survival curves within 60 days of wild-type mmtv-PyMT mice, and Nur77-knocked-out mmtv-PyMT mice.

(27) FIG. 8B showed the statistical results of tumor weight comparison at 11 weeks, 13 weeks, and 17 weeks in wild type mmtv-PyMT mice, Nur77 knockout mmtv-PyMT m ice.

(28) FIG. 8C showed the comparison results of tumor in appearance and morphological size at 11 weeks, 13 weeks, and 17 weeks in wild type mmtv-PyMT mice and Nur77-knocked-out mmtv-PyMT mice.

(29) FIG. 8D showed the effect of YXY101 on the survival rate of mmtv-PyMT mice detected at the animal level.

(30) FIG. 9A showed the results of p-P70S6K levels in MB-MDA-231 breast cancer cells treated with TNF under starvation condition, detected by immunoblotting technology.

(31) FIG. 9B showed the results of p-P70S6K levels in SKBR3 breast cancer cells treated with TNF under starvation condition, detected by immunoblotting technology.

(32) FIG. 9C showed the results of levels of p-mTOR, p-P70S6K, p-S6 in wild-type and Nur77-knocked-out MEF cells treated with TNF for different periods of time (30 min, 2 h) or at different concentrations (20 ng/ml/, 40 ng/ml) under starvation conditions, detected by immunoblotting technology.

(33) FIG. 10A showed the results of levels of p-mTOR, p-P70S6K in MB-MDA-231 breast cancer cells treated with TNF (20 ng/ml), YXY101 (1 M, 2 M, 4 M) under starvation condition, detected by immunoblotting technology.

(34) FIG. 10B showed the results of levels of p-mTOR, p-P70S6K, Nur77 in MB-MDA-231 breast cancer cells, which were transfected with Flag empty plasmid or Flag-Nur77 plasmid and treated with TNF, YXY101 for 3 h, 6 h under starvation condition, detected by immunoblotting technology.

(35) FIG. 10C showed the results of levels of p-P70S6K and Nur77 in MB-MDA-231 cells which were treated to silence Nur77 gene, and then with TNF, YXY101 under starvation condition, detected by immunoblotting technology.

(36) FIG. 10D showed the results of levels of p-S6, p-mTOR, and p62 in wild-type or Nur77-knocked-out type MEF cells treated with TNF, YXY101 (0.5 Mm, 1 M), detected by immunoblotting technology.

(37) FIG. 11A showed the proliferation ratios of different breast cancer cells (MDA-MB-231 and MCF-7) in relation to concentration of XS0503, as well as the IC50 value of XS0503.

(38) FIG. 11B showed the IC50 analysis results of MDA-MB-231 cells treated with YXY101 derivatives XS0077, XS0335, XS0419, XS0474, or XS0488.

(39) FIG. 11C showed the analysis results of inhibition rate to seven breast cancer cells, BT474, ZR-75-1, BT549, HCC1937, HS578T, MCF-7, and T47D, treated with YXY101 derivatives, XS0284, XS0285, XS0394, XS0418, XS0419, XS0474, XS0486, XS0462, XS0491, XS0492, or XS0488.

(40) FIG. 12A showed the immunoblotting analysis results of PARP in MDA-MB-231 cells treated with YXY101 (4 M) or different YXY101 derivatives (4 M), XS0394, XS0395, XS0419, XS0420, XS0421, XS0284, XS0335, XS0488, XS0491, XS0492, XS0418, XS0502, XS0503, XS0506, XS0507, XS0508, XS0077, as well as TNF (20 ng/ml).

(41) FIG. 12B showed the immunoblotting analysis results of P-mTOR, P-p70S6K, and PS6 in MDA-MB-231 cells under starvation treatment with serum-free medium for 10 h, and treated with YXY101 (2 M) or different YXY101 derivatives (2 M), XS0284, XS0285, XS0335, XS0394, XS0418, XS0419, XS0454, XS0462, XS0473, XS0474, XS0480, XS0486, XS0488, XS0491, or XS0492, as well as TNF (20 ng/ml).

(42) FIG. 13 showed the experimental results for detecting the binding of different compounds (XS0418, XS0419, XS0474, XS0394, XS0492, XS0491, XS0488) to Nur77-LBD by using Biacore T200. The results showed that the dissociation constant (Kd) of the compound XS0418 to Nur77-LBD is 3.67 M; the dissociation constant (Kd) of the compound XS0419 to Nur77-LBD is 404 nM; the dissociation constant (Kd) of the compound XS0474 to Nur77-LBD is 2.60 M; the dissociation constant (Kd) of the compound XS0394 to Nur77-LBD is 1.26 M; the dissociation constant (Kd) of the compound XS0492 to Nur77-LBD is 1.30 M; the dissociation constant (Kd) of the compound XS0491 to Nur77-LBD is 0.336 M; the dissociation constant (Kd) of the compound XS0488 to Nur77-LBD is 1.28 M.

(43) FIG. 14 showed the results of experiment on WT mice and PYVT mice, which were respectively treated with LFD feeding and HFD feeding and intragastric administrated with two compounds, YXY101 and its derivative XS0284. FIG. 14A showed the morphology and appearance of the mice in different experimental groups under different treatment conditions. FIG. 14B showed the comparison of the morphology and size of the tumors of the above mice. FIG. 14C showed the curves of change in body weight of the above mice during the 12-day period of intragastric administration. FIG. 14D showed the statistical significance of the change in body weight of the above mice before and after treatment.

(44) FIG. 15A showed a comparison of morphology and size of tumors after treating with YXY101 or its derivative XS0284 in WT and Nur77-knocked-out mice of PYVT.

(45) FIG. 15B showed the statistical results of tumor tissue weight in the above mice.

(46) FIG. 16 showed the results of tissue morphology and HE staining of the heart, liver, small intestine, white fat and kidney of mice of each group, which were observed after 12 hours of intragastric administration or intraperitoneal injection of YXY101 or XS0284 (200 mg/kg) in acute toxicity model mice induced by single intragastric administration or intraperitoneal injection of 200 mg/kg of YXY101 or its derivative XS0284.

EXAMPLE 1. CHARACTERIZATION OF COMPOUND YXY101

(47) (1) Surface Plasmon Resonance (SPR)

(48) The binding of YXY101 to Nur77 was tested by surface plasmon resonance. Briefly, 50 g purified ligand binding domain of Nur77 (Nur77-LBD) protein was coupled to CM5 of Biacore; the binding of YXY101 (20 m) to Nur77-LBD was subsequently tested by Biacore T200. Unrelated compounds were used as controls. The test results were shown in FIG. 1.

(49) FIG. 1 showed the test results of the binding of YXY101 to Nur77-LBD by Biacore T200, wherein red dots represented the compound YXY101; blue dots represented control compounds. The results showed that the compound YXY101 was able to bind to Nur77-LBD.

(50) (2) Binding Kinetics of YXY101 to Nur77

(51) The dissociation constant (Kd) of YXY101 to Nur77 was tested by surface plasmon resonance. Briefly, Biacore T200 instrument was used to measure the binding of YXY101 in different concentrations (0.04 M, 0.08 M, 0.16 M, 0.32 M, 0.64 M) to Nur77-LBD. The test results were shown in FIG. 2B.

(52) The results showed that the dissociation constant (Kd) of the compound YXY101 to Nur77-LBD was 292 nM.

(53) (3) Circular Dichroism Spectroscopy (CD)

(54) The binding of YXY101 to Nur77-LBD was further analyzed by circular dichroism spectroscopy (CD). Briefly, YXY101 (1 ml, 1 mg/ml) was added to the phosphate buffer (10 m, pH 7.4) of Nur77-LBD protein (1 ml, 1 mg/ml) and incubated at 4 C. for 3 h. 0.7 ml of the incubation buffer was detected with Jasco J-810 spectropolarimeter. The CD spectra was obtained from 190 nm to 260 nm. Nur77-LBD solution (i.e., no YXY101 was added) alone was used as control. The results of the detection were shown in FIG. 2C.

(55) The results showed that the compound YXY101 was able to change the CD spectrum of Nur77-LBD, indicating that the compound YXY101 was able to bind to Nur77-LBD.

(56) (4) High Performance Liquid Chromatography (HPLC) Analysis

(57) The binding of YXY101 to Nur77-LBD was further analyzed by high performance liquid chromatography (HPLC). Briefly, YXY101 (600 uL, 0.1 mg/ml) was incubated with purified Nur77-LBD protein (5 ml, 1 mg/ml). After incubation for 3 h at 4 C., the complex of YXY101 and Nur77-LBD was captured using Ni beads. The complex was then degenerated with chloroform, and YXY101 in the degenerated product was extracted. Then, HPLC spectrometer (Shimadzu L C 20A, Japan) was used to detect YXY101 in the extracted product, wherein ODS column (5 um, 4.6*250 mm) was used, and the mobile phase was 0.2% H.sub.3PO.sub.4 acetonitrile. The detection wavelength was 425 nm. In addition, the above experiment was repeated using YXY101 and RXR-LBD (ligand binding domain of retinoic X receptor ) as control. The results of the detection were shown in FIG. 2D.

(58) The results showed that the compound YXY101 was able to bind to Nur77-LBD to form a complex, but not to RXR-LBD.

(59) (5) Dual Luciferase Reporter Assay

(60) The binding of YXY101 to Nur77-LBD was further analyzed by dual luciferase reporter assay. In addition, the experiment was repeated using YXY101 and glucocorticoid receptor (GR) as control. The results were shown in FIG. 2E.

(61) The results showed that the compound YXY101 was able to inhibit the transactivation of Nur77, but had no significant effect on the transactivation of glucocorticoid receptor (GR). This indicated that the compound YXY101 was capable of binding to Nur77-LBD and inhibiting its transcriptional activity; but not to GR.

(62) (6) Molecular Simulation

(63) The docking of YXY101 to Nur77 (PDB code: 4JGV) was performed using AutoDock V4.2. The conformation of YXY101 was generated by the Lamarckian genetic algorithm. In the crystal structure of Nur77, grid center was chosen aroud the reported coordinates (12.08, 18.29, 4.233) of THPN, and the grid size was set to 40*40*40 (X, Y, Z) grid points with a spacing of 0.375 A between grid points.

(64) In the molecular docking, the standard docking protocol was applied: the number of randomly placed individuals was 150; the maximum number of energy evaluation was 2.5 million; the rate of gene mutations was 0.02; the rate of crossover was 0.8; the probability of performing local evaluation was 0.06; the lower bound on rho was 0.01; PyMOL Version 0.99 was used for molecular visualization. The results were shown in FIG. 2F.

(65) The molecular docking studies showed that YXY101 binded to the known hydrophobic grooves on the surface of Nur77 protein mainly by hydrophobic interaction.

EXAMPLE 2. YXY101 INHIBITS THE BIOLOGICAL EFFECT OF TNF

(66) HepG2 cells were treated with different concentrations of YXY101 (0 M, 0.25 M, 0.5 M, 1 M, 2 M or 4 M) for 1 hour, and then exposed to TNF (0 ng/mL or 20 ng/mL) for 30 minutes. IB and phosphorylated IKK/ in the cells were then detected by WB. The results were shown in FIGS. 3A-3B.

(67) The results of FIGS. 3A-3B showed that TNF was capable of inducing phosphorylation of IKK/ and degradation of IB in cells; whereas YXY101 was capable of inhibiting TNF-induced phosphorylation of IKK/ and degradation of IB.

(68) HepG2 cells were treated with YXY101 (0 or 1 M) for 1 hour, and then exposed to TNF (20 ng/mL) for 30 minutes. The p65 subunit of NF-B in the cells was then detected by immunofluorescence staining method. Untreated cells were used as controls. The results were shown in FIG. 3C.

(69) FIG. 3C showed the immunofluorescence staining results of HepG2 cells treated with YXY101 and TNF (Scale bar: 20 m). The results in FIG. 3C showed that TNF was able to induce nuclear import of the p65 subunit of NF-B in cells; whereas YXY101 was able to inhibit TNF-induced p65 nuclear import.

(70) The NF-B reporter gene was transfected into HEK-293T cells and then treated with YXY101 (0 or 1 M) and TNF (20 ng/mL). NF-B activity in the cells was then analyzed. Untreated cells were used as controls. The results were shown in FIG. 3D.

(71) FIG. 3D showed the analytic results of NF-B activity of cells treated with YXY101 and TNF, wherein **P<0.01, ***P<0.001 (T test). The results in FIG. 4D showed that TNF was able to induce transactivation of NF-B in cells; whereas YXY101 was able to inhibit TNF-induced NF-B transactivation.

(72) A variety of cancer cell lines (LO2, SMMC-7721, QGY-7703, HeLa, H460) were treated with different concentrations of YXY101 (0 M, 1 M or 4 M) for 1 hour, and then exposed to TNF (0 ng/mL or 20 ng/mL) for 30 minutes. IB and phosphorylated IKK/ in the cells were then detected by WB. The results were shown in FIG. 3E.

(73) The results showed that TNF was able to induce phosphorylation of IKK/ and degradation of IB in various cell lines, whereas YXY101 was able to inhibit TNF-induced phosphorylation of IKK/ and degradation of IB.

(74) In addition, HepG2 cells were also applied in the experiment. Briefly, HepG2 cells were treated with various compounds (YXY101, XS0284, and XS0287) in specified concentrations for a specified period of time, and then exposed to TNF (0 ng/mL or 20 ng/mL) for 30 minutes. IB in the cells was then detected by WB. The results were shown in FIG. 3F.

(75) FIG. 3F showed that YXY101 and its derivatives XS0284 and XS0287 were capable of inhibiting TNF-induced degradation of IB in HepG2 cells.

(76) The results of FIGS. 3A-3F indicated that YXY101 and its derivatives XS0284 and XS0287 were capable of inhibiting various biological effects of TNF in cells, including phosphorylation of IKK/, degradation of IB, nuclear import of the p65 subunit of NF-B, and transactivation of NF-B.

EXAMPLE 3. Nur77 MEDIATES THE INHIBITORY EFFECT OF YXY101 ON BIOLOGICAL EFFECTS OF TNF

(77) SiRNA, Nur77 SiRNA or RXR SiRNA as controls were transfected into HepG2 cells. Subsequently, the HepG2 cells were treated with different concentrations of YXY101 (0 M, 1 M or 4 M) for 1 hour, and then exposed to TNF (0 ng/mL or 20 ng/mL) for 30 minutes. Nur77, RXR and IB in the cells were then detected by WB. The results were shown in FIGS. 4A-4B.

(78) FIGS. 4A-4B showed the results of immunoblot analysis of Nur77, RXR and IB in the HepG2 cells transfected with different SiRNAs and treated with different concentrations of YXY101 and TNF. The results showed that Nur77 SiRNA effectively inhibited/knocked out the expression of Nur77 in the cells; and, RXR SiRNA effectively inhibited/knocked out the expression of RXR in the cells; while the control SiRNA did not affect the normal expression of Nur77 and RXR. Further, the results of FIGS. 5A-5B showed that YXY101 was able to inhibit TNF-induced degradation of IB in the cells expressing Nur77; however, when Nur77 expression was knocked out, YXY101 lost its ability to inhibit IB degradation. These results indicated that the inhibitory effect of YXY101 on biological effects of TNF was mediated by Nur77.

(79) The above results were also confirmed by using MEF cells and Nur77/MEF cells (i.e., MEF cells not expressing Nur77). Briefly, MEF cells and Nur77/MEF cells were treated with different concentrations of YXY101 (0 M or 1 M) for 1 hour, and then exposed to TNF (0 ng/mL or 20 ng/mL) for 30 minutes. Subsequently, IB in the cells was detected by WB. The results were shown in FIG. 4C.

(80) The results showed that YXY101 was able to inhibit TNF-induced degradation of IB in the MEF cells expressing Nur77; however, in Nur77/MEF cells, YXY101 lost the ability to inhibit IB degradation. These results indicated that the inhibitory effect of YXY101 on the biological effects of TNF was mediated by Nur77.

(81) In addition, MEF cells and Nur77/MEF cells were treated with YXY101 (0 or 1 M) for 1 hour, and then exposed to TNF (20 ng/mL) for 30 minutes. Subsequently, the p65 subunit of NF-B in the cells was detected by immunofluorescence staining. Untreated cells were used as controls. The results were shown in FIG. 4D.

(82) FIG. 4D showed the results of immunofluorescence staining of the MEF cells and the Nur77/MEF cells treated with YXY101 and TNF (Scale bar: 10 m). The results showed that YXY101 was able to inhibit TNF-induced p65 nuclear import in the MEF cells expressing Nur77; however, in the Nur77/MEF cells, YXY101 lost the ability to inhibit p65 nuclear import. These results indicated that the inhibitory effect of YXY101 on the biological effects of TNF was mediated by Nur77.

(83) FIG. 4E showed the results of immunoblot analysis of IB in MEF cells and Nur77/MEF cells treated with different concentrations of XS0284 and TNF. The results show that XS0284 was able to inhibit TNF-induced degradation of IB in the MEF cells expressing Nur77; however, in the Nur77/MEF cells, XS0284 lost the ability to inhibit IB degradation. These results indicated that the inhibitory effect of XS0284 on the biological effects of TNF was mediated by Nur77.

EXAMPLE 4. YXY101 HAS SIGNIFICANT ANTI-TUMOR ACTIVITY, AND IS PARTICULARLY SENSITIVE TO TRIPLE-NEGATIVE BREAST CANCER, THE BIOLOGICAL FUNCTION IS DEPENDENT ON Nur77

(84) Different breast cancer cells (MDA-MB-231; MDA-MB-468; BT549; SKBR3; T47D and MCF-7) were treated with different concentrations of YXY101 (1 M, 1.3 M, 1.6 M, 1.9 M, 2.2 M, 2.5 M, 2.8 M, 3.1 M, 3.4 M, 3.7 M, 4.0 M) for 72 h, and the proliferation ratio of the breast cancer cells were determined. Curves of the cancer cell proliferation ratio in relation to the concentrations of YXY101 were plotted, and the IC50 of YXY101 was determined. The results were shown in FIG. 5A.

(85) FIG. 5A showed the proliferation ratio of different breast cancer cells (MDA-MB-231; MDA-MB-468; BT549; SKBR3; T47D and MCF-7) in relation to the concentrations of YXY101, as well as the IC50 of YXY101; wherein MDA-MB-231, MDA-MB-468, BT549 and SKBR3 are triple negative breast cancer cells and the results thereof were indicated by red curves; T47D and MCF-7 are three positive breast cancer cells and the results thereof were indicated by blue curves. The results showed that the inhibitory ability of YXY101 for the proliferation of triple-negative breast cancer cells was significantly stronger than that for triple-positive breast cancer cells; wherein, the IC50 of YXY101 for inhibiting the proliferation of MDA-MB-231, MDA-MB-468, BT549 and SKBR3 were 1.204, 0.187, 0.245 and 2.646 M respectively, which were far lower than that for T47D and MCF-7 (74.465 M and 11.498 M, respectively), suggesting that YXY101 can be used particularly advantageously for the treatment of triple negative breast cancers.

(86) FIG. 5E showed that the IC50 of YXY101 was 1.189 M in wild-type Hela cells, while 58.166 M in Nur77 knocked-out Hela cells. The results indicated that the tumor inhibitory effect of YXY101 was dependent on Nur77. Moreover, FIG. 1 and FIG. 2B showed that YXY101 can specifically bind to Nur77, the anti-tumor activity of YXY101 was closely related to Nur77.

(87) Further, MDA-MB-231 and MCF-7 cells were treated with different concentrations of YXY101 (0 M, 0.25 M, 0.5 M, 1 M, 2 M, or 4 M), followed by detection of parp and ER in the cells by WB. The results were shown in FIG. 5B.

(88) FIG. 5B showed the results of immunoblot analysis of parp and ER in the MDA-MB-231 and MCF-7 cells treated with different concentrations of YXY101 (0 M, 0.25 M, 0.5 M, 1 M, 2 M, or 4 M). The results showed that YXY101 can induce parp cleavage, i.e., apoptosis, in the MDA-MB-231.

(89) Further, MDA-MB-231 was treated with different concentrations of YXY101 (0 M, 2 M, or 4 M) for different period of time (12 h or 24 h), followed by detection of parp and p-mTOR in the cells by WB. The results were shown in FIG. 5C.

(90) FIG. 5C showed the results of immunoblot analysis of parp and p-mTOR in the MDA-MB-231 treated with different concentrations of YXY101 (0 M, 2 M, or 4 M) for 12 h or 24 h. The results showed that YXY101 can induce apoptosis in MDA-MB-231 in a time- and concentration-dependent manner.

(91) In addition, MDA-MB-231 cells were also treated with YXY101 in combination with TNF for different period of time (1 h, 6 h or 12 h), followed by detection of parp in the cells by WB. The results were shown in FIG. 5D.

(92) FIG. 5D showed the results of immunoblot analysis of parp in the MDA-MB-231 cells treated with YXY101 in combination with TNF for different period of time (1 h, 6 h or 12 h). The results showed that, in MDA-MB-231, YXY101 in combination with TNF can induce stronger apoptosis.

EXAMPLE 5. INHIBITORY EFFECT OF YXY101 ON THE PROLIFERATION OF BREAST CANCER TUMORS

(93) In this section, we tested the anti-tumor effect of YXY101 alone or in combination with TNF on triple-negative breast cancers via nude mice xenograft experiments.

(94) 1) Laboratory Animals and Reagents

(95) MDA-MB-231 cells; BALB/c (nu/nu) nude mice, weighed 18-20 g, female, raised in SPF animal house, fodder, drinking water, animal cages, litter were all autoclaved, the litter was changed every two days, and strictly aseptic operations were performed. Under sterile conditions, the cells in the logarithmic growth phase for inoculation were collected and washed with serum-free medium, the number of viable cells was counted under inverted microscope and the survival rate >95%, the cell concentration was adjusted to 110.sup.6/ml, and the tumor cells were re-suspended in PBS to prepare the cell suspension. Each nude mouse was inoculated on right subaxillary with 0.2 ml of the above cell suspension, and the tumor growth condition was observed regularly.

(96) 2) Grouping and Administration

(97) The drug-administered groups: when the diameter of the transplanted tumor of nude mice reached about 0.5 cm, the nude mice without hemorrhage, necrosis and infection were selected for experiment. The nude mice were weighed, the tumor diameter of which was measured, and then grouped, 6 nude mice in each group; the mice of the experimental groups were administered with TNF (12010.sup.4 U/kg), YXY101 (2 mg/kg), or the combination thereof, and the mice of the control group were given the same amount of normal saline. TNF was administered by intratumoral injection every other day; YXY101 was administered intragastrically daily. The nude mice were sacrificed 6 hours after the last administration, and the tumor weight was measured.

(98) During the treatment, the food intake and body weight of the nude mice were not significantly reduced, the activity was normal, and no symptoms such as loose hair and diarrhea appeared. At the end of treatment, no death occurred in each group of nude mice. After the nude mice were sacrificed, the autopsy showed tumors had clear boundaries, uneven surface, tough texture, significant local expansion of blood vessels, and necrosis occurred in the central area of some tumors. No metastasis was observed in all groups of nude mice, and no obvious changes in appearance in the heart, liver, spleen, lung, kidney and other organs was observed in the treatment groups of nude mice.

(99) 3) Observation Index

(100) Drawing of Tumor Growth Curves:

(101) The formula for calculating the tumor volume (TV) is: V=abc; wherein a, b and c represent length, width and height, respectively. The tumor volume was calculated based on the measurement results, and the tumor growth curve was plotted with time as abscissa and tumor volume as ordinate.

(102) The anti-tumor activity evaluation index was the relative tumor proliferation rate T/C (%): wherein T represents the RTV of the treatment group; C represents the RTV of the negative control group. The therapeutic effect evaluation criteria were: T/C %>40% for ineffective; T/C %40% and p<0.05 for effective.

(103) The experimental results were shown in FIG. 6. The left panel of FIG. 6A showed the tumors formed in each group of nude mice; the middle panel showed the RTV of the tumors formed in each group of nude mice; the right panel showed the weight of the tumors formed in each group of nude mice. The results of FIG. 6A showed that tumors were developed in nude mice after inoculation with MDA-MB-231 cells; and, YXY101 had good anti-tumor effect; and the combination of YXY101 and TNF induced even stronger anti-tumor effect.

(104) FIG. 6B showed the results of immunohistochemical staining of tumor tissues in nude mice of each group. The results of FIG. 6B show that YXY101 can induce caspase3 cleavage in tumor tissues and promote apoptosis of tumor cells; and the combination of YXY101 and TNF can induce stronger apoptosis of tumor cells.

EXAMPLE 6. INHIBITORY EFFECT OF YXY101 ON PROLIFERATION AND METASTASIS OF BREAST CANCER

(105) 1) Laboratory Animals and Reagents

(106) MMTV-PYVT transgenic mice of breast cancer, 9-week-old, female, were raised in SPF animal house, fodder, drinking water, animal cages, litter were all autoclaved, the litter was changed every two days, strictly aseptic operations were performed.

(107) 2) Grouping and Administration

(108) Female MMTV-PYVT transgenic mice of breast cancer were housed under the conditions of temperature 231 C., humidity: 40-60%, natural light, freely drinking of water, and freely access to chow diet. Thirty-six mice with tumor began to grow in chest were selected and randomly divided into three groups, and each group was subdivided into the control group and the YXY101 group.

(109) The administration was performed as follows:

(110) 11 Wk time point

(111) Control group: 9-week-old mice were given normal saline at 7:00 m every day before the fodder was given;

(112) YXY101 group: 9-week-old mice were intragastrically administered once at a dose of 2 mg/kg at 7:00 m every day.

(113) 13 k time point

(114) Control group: 11-week-old mice were given normal saline at 7:00 m every day before the fodder was given;

(115) YXY101 group: 11-week-old mice were intragastrically administered once at a dose of 2 mg/kg at 7:00 m every day.

(116) 17 k time point

(117) Control group: 15-week-old mice were given normal saline at 7:00 m every day before the fodder was given;

(118) YXY101 group: 15-week-old mice were intragastrically administered once at a dose of 2 mg/kg at 7:00 m every day.

(119) After continuous administration for two weeks according to the above method, each animal was bled from the eye, and the supernatant was taken to determine the serum inflammation index; tumor tissue having clear boundary, uneven surface, and tough texture was routinely treated and embedded for immunostaining.

(120) The experimental results were shown in FIG. 7 and FIG. 8. FIG. 7A showed the general state of MMTV-PYVT mice at 2 weeks, 11 weeks, 13 weeks or 17 weeks after intragastric administration of 2 mg/kg of YXY101. The results in FIG. 7A showed that YXY101 inhibits the progression of breast cancer tumors.

(121) FIG. 7B showed the results of HE staining and immunohistochemical staining of tumor tissues of MMTV-PYVT mice at 11 weeks, 13 weeks or 17 weeks after intragastric administration of 2 mg/kg of YXY101 for two weeks. The results of FIG. 7B showed that YXY101 can inhibit the proliferation of breast cancer tumors.

(122) FIG. 7C showed the analytic results of weight, morphology, HE staining and immunohistochemical staining of lung tissue of MMTV-PYVT mice at 11 weeks, 13 weeks or 17 weeks after intragastric administration of 2 mg/kg of YXY101 for two weeks. The results of FIG. 7C showed that YXY101 can inhibit lung metastasis caused by breast cancer.

(123) The experimental results in FIGS. 7A-7C indicated that YXY101 was capable of inhibiting the proliferation and metastasis of breast cancer tumors.

(124) FIG. 8A showed, at the animal level, the survival curves of wild-type mmtv-PyMT mice and Nur77-knocked-out mmtv-PyMT mice within 60 days, and FIG. 8D showed the effect of YXY101 on the survival rate of mmtv-PyMT mice detected at the animal level. The results showed that the survival rate of mice after knockingout of Nur77 was significantly improved, predicting that Nur77 was significantly associated with the development of breast cancer. FIG. 8B showed the statistical results of the tumor tissue weight of the above two kinds of mice, and the results showed that the weight of breast cancer tissue significantly decreased after knocking out of Nur77, and FIG. 8C also showed the comparison in appearance and morphology of these tumor tissues, clearly indicating the Nur77-knocked-out mice had smaller and smoother tumor tissue. The above results indicated that Nur77 played a crucial role in the development of breast cancer.

(125) In summary, we creatively screened drug targeting at Nur77 by using SPR technology, thereby obtaining the drug molecule YXY101 that specifically binds to Nur77, it showed significant anti-tumor activity, especially sensitive to triple-negative breast cancer, and this therapeutic activity for breast cancer was dependent on Nur77. The compound was a very promising active molecule for the treatment of triple negative breast cancer, and the screening method was an effective way to develop drug molecule that specifically binds to Nur77 and for the target treatment of triple negative breast cancer.

EXAMPLE 7. INFLAMMATION CAN INDUCE TUMORIGENESIS TO A CERTAIN EXTENT, AND THIS PROCESS IS Nur77 RELEVANT

(126) In the previous study, we found that the development of breast cancer, especially triple-negative breast cancer, was also accompanied by inflammatory response and high activation of mTOR signaling pathway. Chronic inflammation was also an important basis for the development of breast cancer, and many non-steroidal anti-inflammatory drugs effective to other tumors had also been used for the prevention and treatment of breast cancer.

(127) FIGS. 9A-9B showed p-P70S6K levels of MB-MDA-231 and SKBR3 breast cancer cells treated with TNF for 1 h, 3 h, and 6 h under starvation conditions, detected by immunoblotting. The results showed that p-P70S6K was up-regulated under the induction of TNF, and this was time-dependent. The results indicated that the mTOR signaling pathway was activated in an inflammatory environment, which might be closely related to tumorigenesis. FIG. 9C showed levels of p-mTOR, p-P70S6K, and p-S6 in wild-type or Nur77-knocked-out MEF cells treated with TNF in gradient concentration or gradient time under starvation conditions, detected by immunoblotting. The results showed that the activation of mTOR signaling pathway caused by TNF can be regulated by time and concentration, and such activation was dependent on Nur77.

(128) In combination with Example 6 and Example 7, Nur77 was not only important for the development of breast cancer, but also can be used as a target for the treatment of breast cancer. Therefore, Nur77 was a valuable biochemical indicator for the detection of development of breast cancer, and can be used to evaluate breast cancer progression and treatment strategies.

EXAMPLE 8. YXY101 WAS ABLE TO SIGNIFICANTLY INHIBIT mTOR ACTIVITY, WHICH IN TURN INHIBITS TUMORS, AND THIS PROCESS RELIES ON Nur77

(129) In this section, the internal environment of tumor was experimentally simulated, that was, TNF, a cytokine that caused acute inflammation, was used to simulate tumorigenesis. This method could provide an experimental basis for screening drugs inhibiting tumors. By this method, Nur77-dependent compounds that inhibited the mTOR signaling pathway were screened to find a drug effective in the targeting treatment of triple-negative breast cancer.

(130) FIG. 10A showed the test results of p-mTOR, p-P70S6K levels in MB-MDA-231 breast cancer cells treated with TNF (20 ng/ml), YXY101 (1 M, 2 M, 4 M) under starvation conditions, detected by immunoblotting. The results showed that YXY101 can significantly down-regulate p-mTOR and p-P70S6K activated by TNF, suggesting that the anti-tumor mechanism of the compound was through its inhibition of mTOR activity. FIG. 10B showed the test results of p-mTOR, p-P70S6K, Nur77 levels in MB-MDA-231 breast cancer cells transfected with Flag empty plasmid or Flag-Nur77 plasmid, and treated with TNF, YXY101 for 3 h, 6 h under starvation conditions, detected by immunoblotting. FIG. 10C showed the test results of p-P70S6K and Nur77 levels in MB-MDA-231 cells, which were treated to silence Nur77 gene, and then with TNF, YXY101 under starvation conditions, detected by immunoblotting. FIG. 10D showed the test results of p-S6, p-mTOR, and p62 levels in wild-type or Nur77-knocked-out type MEF cells treated with TNF, YXY101 (0.5 Mm, 1 M), detected by immunoblotting. It indicated from the results of FIGS. 10B-10D that, through ways of overexpression and knockout of Nur77, the activity of YXY101 of down-regulating mTOR activity was confirmed as depending on Nur77.

(131) In conclusion, the inhibition of mTOR signaling pathway can be used as an effective indicator for screening anticancer drugs. By this method, compounds screened having potent activity of inhibiting mTOR signaling pathway via Nur77 have potential anticancer activity.

EXAMPLE 9. INDUCTION OF APOPTOSIS OF YXY101 DERIVATIVES ON TRIPLE-NEGATIVE BREAST CANCER CELLS

(132) Different breast cancer cells (MDA-MB-231 and MCF-7) were treated with different concentrations of YXY101 derivative XS0503 (0.16 M, 0.31 M, 0.625 M, 1.25 M, 2.5 M, 5 M, 10.0 M) for 24 h, and the proliferation ratio of breast cancer cells were measured. Curves of the cancer cell proliferation ratio in relation to the concentrations of XS0503 were plotted, and the IC50 of YXY101 was determined. The results were shown in FIG. 11A.

(133) FIG. 11A showed the curves of the proliferation ratio of different breast cancer cells (MDA-MB-231 and MCF-7) in relation to XS0503 concentrations, as well as the IC50 value of XS0503; wherein MDA-MB-231 was represented by red curves; MCF-7, a three positive breast cancer cell, was represented by blue curves. The results showed that the inhibitory ability of XS0503 on the proliferation of triple-negative breast cancer cells was significantly stronger than that on triple-positive breast cancer cells; wherein, the IC50 of XS0503 for inhibiting the proliferation of MDA-MB-231 was 1.19 M, which was lower than that for MCF-7 (2.65 M). This suggested that YXY101 can be used particularly advantageously for the treatment of triple negative breast cancer.

(134) Further, MDA-MB-231 was treated with different YXY101 derivatives, XS0077, XS0335, XS0419, XS0474, or XS0488 (0.16 M, 0.31 M, 0.625 M, 1.25 M, 2.5 M, 5 M, 10.0 M), followed by measurement of MDA-MB-231 proliferation ratio. The results in FIG. 11B showed that the IC50 for the inhibition of proliferation of MDA-MB-231 treated with XS0077, XS0335, XS0419, XS0474 and XS0488 were 1.84 M, 1.88 M, 1.27 M, 2.93 M, and 1.90 M, respectively.

(135) FIG. 11C showed the inhibition rate analysis results of seven breast cancer cells, BT474, ZR-75-1, BT549, HCC1937, HS578T, MCF-7, and T47D, which have been treated with YXY101 derivatives, XS0284, XS0285, XS0394, XS0418, XS0419, XS0474, XS0486, XS0462, XS0491, XS0492, or XS0488. The results showed that the above derivatives had certain inhibitory effects on different breast cancer cells, wherein XS0284, XS0285, XS0418, XS0419, XS0462 and XS0488 had inhibitory effects on the proliferation of various breast cancer cells, which were close or even stronger than that of YXY101.

(136) Further, YXY101 (4 M) or different YXY101 derivatives (4 M), XS0394, XS0395, XS0419, XS0420, XS0421, XS0284, XS0335, XS0488, XS0491, XS0492, XS0418, XS0502, XS0503, XS0506, XS0507, XS0508, or XS0077, and TNF (20 ng/ml) were used to treat MDA-MB-231 cells and PARP in the cells were subjected to immunoblotting analysis. The results FIG. 12A showed that, in comparison with YXY101, the red font-labeled derivatives including XS0418, XS0419, XS0492, XS0508 and XS0077 can more significantly induce PARP cleavage in triple negative breast cancer of MDA-MB-231 cells.

(137) FIG. 12B showed the results of immunoblotting analysis of P-mTOR, P-p70S6K, and PS6 in MDA-MB-231 cells under starvation treatment with serum-free medium for 10 h, and treated with YXY101 (2 M) and different YXY101 derivatives (2 M), XS0284, XS0285, XS0335, XS0394, XS0418, XS0419, XS0454, XS0462, XS0473, XS0474, XS0480, XS0486, XS0488, XS0491, or XS0492, and TNF (20 ng/ml). In comparison with YXY101, the red font-labeled derivatives including XS0335, XS0394, XS0418, XS0419, XS0474, XS0486, XS0491 and XS0492 can more significantly reduce P-mTOR, P-p70S6K, and PS6.

EXAMPLE 10. CHARACTERIZATION OF OTHER COMPOUNDS BY SURFACE PLASMON RESONANCE (SPR)

(138) According to the methods described in Examples 1 and 2, the binding of various YXY101 derivatives (XS0418, XS0419, XS0474, XS0394, XS0492, XS0491, XS0488) to Nur77-LBD was detected by SPR using Biacore T200 instrument. The results were shown in FIG. 13.

(139) FIG. 13 showed the results of experiment for detecting the binding of various compounds (XS0418, XS0419, XS0474, XS0394, XS0492, XS0491, XS0488) to Nur77-LBD using Biacore T200 instrument. The results showed that the dissociation constant (Kd) of the compound XS0418 to Nur77-LBD is 3.67 M; the dissociation constant (Kd) of the compound XS0419 to Nur77-LBD is 404 nM; the dissociation constant (Kd) of the compound XS0474 to Nur77-LBD is 2.60 M; the dissociation constant (Kd) of the compound XS0394 to Nur77-LBD is 1.26 M; the dissociation constant (Kd) of the compound XS0492 to Nur77-LBD is 1.30 M; the dissociation constant (Kd) of the compound XS0491 to Nur77-LBD is 0.336 M; the dissociation constant (Kd) of the compound XS0488 to Nur77-LBD is 1.28 M.

EXAMPLE 11. XS0284 IS MORE EFFECTIVE IN TREATING HYPERLIPEMIA INDUCED BREAST CANCER THAN YXY101

(140) In order to prove that YXY101 derivatives can also inhibit breast cancer, we selected XS0284 showing strong inhibitory effect on P-mTOR, P-p70S6K and PS6 for confirmation. The results of FIGS. 14A-14D showed that both of YXY101 and XS0284 can significantly inhibit the development of breast cancer, whether under low-fat feeding conditions or high-fat feeding conditions. Under low-fat feeding conditions, the inhibitory effect of XS0284 on breast cancer was close to that of YXY101, while under high-fat feeding conditions, the inhibition effect of XS0284 was stronger than that of YXY101. The above conclusions can be reflected in the size of tumor tissue and the change of body weight of mice.

(141) These results indicated that a series of YXY101 derivatives (such as XS0284) can also inhibit tumor development, and they were even superior to YXY101 in term of tumor inhibition.

EXAMPLE 12. THE TUMOR INHIBITION EFFECTS OF YXY101 AND ITS DERIVATIVES IS DEPENDENT ON Nur77

(142) In order to prove the anti-tumor effect of YXY101 and its derivatives is relied on Nur77, we selected YXY101 and its derivative XS0284, which showed significant inhibitory effect on P-mTOR, P-p70S6K and PS6 for confirmation. FIGS. 15A-15B showed the results of two types of PYVT mice, wild type and Nur77-knocked-out type, which had been intragastrically administered with YXY101 (5 mg/kg) or XS0284 (10 mg/kg) respectively for two weeks. By comparing the tumor tissue size of each experimental group, the results showed that YXY101 and XS0284 were effective in inhibiting tumors in wild-type mice, but neither of the two compounds could exert an inhibitory effect on Nur77-deficient mice.

(143) The above results indicated that YXY101 and its derivatives rely on Nur77 to exert their tumor suppressing effect.

EXAMPLE 13. THE ACUTE TOXIC-SIDE EFFECTS OF XS0284 ARE LOWER THAN YXY101

(144) In this example, acute toxicity model mice were established by single intragastric injection of 200 mg/kg of YXY101 or its derivative XS0284 or by single intraperitoneal injection of 20 mg/kg of YXY101 or its derivative XS0284. In this example, after intragastric administration or intraperitoneal injection of YXY101 or XS0284, the mice were observed for food intake, drinking of water, spontaneous activity, mental state, movement of the limbs, bowel quality, hair gloss, etc., and any possible toxic reactions and time points of oneset as well as offset thereof were recorded in details. The tissue morphologies of the heart, liver, small intestine, white fat and kidney were observed by Histopathological method.

(145) The experimental results were shown in FIG. 16. FIG. 16A showed the intragastric injection group: 1) the cardiomyocytes of the mice from the control group had clear boundaries, with ample and obvious nuclei, the myocardial fibers were arranged neatly and clearly; in the liver tissue, the sinus hepticus was ample and clear, the lobuli hepatis had clear boundary; the intestinal tissue had clear boundaries, the cells were plump, the intestinal villi with obvious boundaries were arranged neatly; the adipose tissue cells had clear boundaries and were arranged neatly. 2) Compared with the control group, the myocardial cells and myocardial fibers of the mice from the YXY101 group were arranged disorderly; the lobuli hepatis boundaries were blurred, the cytoplasm was reduced, and most of the hepatocytes died; the intestinal tissue was swollen apparently, the cell death increases, the inflammatory reaction was obvious, the intestinal villi were arranged disorderly; the adipose tissue cells were arranged disorderly and some of the fibers were broken. 3) Compared with the blank group, the cardiac myocytes of the mice from the XS0284 group had relatively clear boundaries, the myocardial fibers were arranged relatively neatly and had obvious boundaries; the hepatocytes in the liver tissue had obvious boundaries and clear structure; the intestinal tissue had clear boundaries, the cells were plump, the intestinal villi were neatly arranged and had obvious boundaries; the adipose tissue cells had clear boundaries, and were neatly arranged, and the fiber breakage was reduced. It can be concluded that the XS0284 group showed a weaker toxic effect on the liver and small intestine than YXY101.

(146) FIG. 16B showed the intraperitoneal injection group. 1) The cardiomyocytes of the mice from the control group had clear boundaries, with ample and obvious nuclei, the myocardial fibers were arranged neatly and had clear boundaries; in the liver tissue, the sinus hepticus was ample and clear, the lobuli hepatis had clear boundaries; the adipose tissue cells had clear boundaries and were arranged neatly; the glomeruli of the kidney tissue had clear boundaries, the cells were plump and were arranged neatly and had obvious boundaries. 2) Compared with the control group, the myocardial cells and myocardial fibers of the mice from the YXY101 group were arranged disorderly; the lobuli hepatis had substantially obvious boundaries, the hepatocytes were plump and had normal morphology; but the adipose tissue cells were arranged disorderly and had many inflammatory cell infiltration; the kidney tissue had blurred glomerulus boundaries and many inflammatory cell infiltration, and the arrangement was not neat. 3) Compared with the control group, the cardiac cardiomyocytes of the mice from the XS0284 group had relatively clear boundaries, the myocardial fibers were relatively neatly arranged and had obvious boundaries; the hepatocytes in the liver tissue had obvious boundaries and clear structure; the adipose tissue cells had clear boundaries and were arranged neatly, the fiber breakage was reduced; the kidney tissue had clear glomerular boundaries, the cells were full, and there was a small amount of inflammatory cell infiltration. It can be concluded that the XS0284 group of the intraperitoneal injection group showed less toxicity to kidney and adipose than YXY101.

(147) These results indicated that a series of derivatives of YXY101, such as XS0284, had less acute toxicity to animals than YXY101. It further suggested that this series of compounds had stronger targeting and specificity than YXY101, and this series of YXY101 derivatives was possibly to be developed as a safer anticancer drug.

(148) Preparation of Compound XS0077

(149) ##STR00046##

(150) Compound YXY101 (50 mg, 0.11 mmol) was dissolved in 2 mL of DMF with stirring, followed by an addition of sodium hydrogencarbonate (56 mg, 0.66 mmol) and methylene chloride (42 L, 0.66 mmol), then subjected to an reaction with stirring at room temperature for 12 hours. The reaction was quenched with 1 mol/L HCl (1 mL), then the resulting mixture was added with 9 mL of purified water, and extracted with ethyl acetate three times (5 mL each time). The organic layer was collected, dried over anhydrous sodium sulfate, and then subjected to vacuum evaporation to remove organic solvent ethyl acetate, thereby obtaining an orange-red solid of mixed crude product. The orange-red solid product was obtained by column chromatography, n-hexane and ethyl acetate (hexane/ethyl acetate=10:1) was used as eluent, and the column was packed with 300-400 mesh silica gel.

(151) .sup.1H NMR (600 MHz, DMSO-d6) ppm 0.44 (s, 3H), 0.91 (d, J=14.31 Hz, 1H), 1.07 (s, 3H), 1.12 (s, 3H), 1.21 (s, 3H), 1.30-1.35 (m, 1H), 1.38 (s, 3H), 1.41-1.46 (m, 1H), 1.50-1.59 (m, 3H), 1.61-1.72 (m, 4H), 1.78-1.86 (m, 1H), 1.95 (td, J=13.98, 3.76 Hz, 1H), 2.06 (d, J=14.12 Hz, 1H), 2.09 (s, 3H), 2.17-2.22 (m, 1H), 2.31 (d), J=15.77 Hz, 1H), 3.48 (s, 3H), 6.35 (d, J=7.15 Hz, 1H), 6.39 (d, J=1.28 Hz, 1H), 7.07 (dd, J=7.15, 1.10 Hz, 1H), 8.72 (s, 1H).

(152) .sup.13C NMR (151 MHz, DMSO-d6) ppm 10.10, 17.96, 21.41, 28.08, 29.19, 29.42, 30.12, 30.34, 31.34, 32.23, 32.91, 34.39, 36.02, 37.83, 38.8, 39.83, 41.99, 43.64, 44.48, 51.44, 117.26, 118.05, 120.18, 126.89, 133.13, 146.42, 162.94, 167.80, 177.93, 177.96.

EXAMPLE 15. PREPARATION OF COMPOUND XS0284

(153) ##STR00047##

(154) Compound YXY101 (50 mg, 0.11 mmol) was dissolved in methanol (2.5 mL) with stirring under nitrogen atmosphere. Followed by an addition of an aqueous solution of sodium hydrogen sulfite (14 mg, 0.13 mmol, dissolved in 1 mL of water) and allowed to react at room temperature for 3 hours. After the reaction, the reaction system was concentrated by a rotary evaporator to give colorless crystals. The colorless crystals were recrystallized from methanol/water, and the obtained product was dried in vacuo to afford compound XS0284 (56.6 mg) as white solid.

(155) .sup.1H NMR (600 MHz, DMSO-d6) ppm 0.59 (s, 3H) 0.86 (d, J=12.10 Hz, 1H) 1.05 (s, 3H) 1.09 (s, 3H) 1.18 (s, 3H) 1.43-1.60 (m, 6H) 1.62 (s, 3H) 1.78-1.85 (m, 1H) 1.93-2.04 (m, 3H) 2.21 (s, 3H) 2.32 (d, J=15.22 Hz, 1H) 4.48 (d, J=6.24 Hz, 1H) 5.81 (d, J=6.60 Hz, 1H) 6.58 (s, 1H) 7.61 (br.s., 1H) 8.81 (br.s., 1H).

(156) .sup.13C NMR (151 MHz, DMSO-d6) ppm 13.57, 18.46, 21.64, 29.04, 29.98, 30.47, 30.60, 30.64, 31.94, 32.92, 34.80, 35.11, 36.90, 36.96, 37.90, 38.07, 43.95, 44.39, 60.19, 108.96, 118.87, 123.26, 124.39, 140.89, 141.93, 144.02, 150.07, 180.00.

EXAMPLE 16. PREPARATION OF COMPOUND XS0285

(157) ##STR00048##

(158) Compound YXY101 (50 mg, 0.11 mmol) was dissolved in N,N-dimethylformamide (2 mL) with stirring. Sodium hydrogencarbonate (50.4 mg, 0.6 mmol) was added, then benzyl bromide (0.17 mg, 20 L) was added, and the reaction was carried out under stirring at room temperature for 24 hours. The reaction was stopped, and the reaction mixture was added with deionized water (15 mL), and extracted with ethyl acetate for three times. The combined ethyl acetate layer was washed with saturated aqueous solution of NaCl three times, dried over anhydrous Na.sub.2SO.sub.4, concentrated by a rotary evaporator to give a crude product (dark red-brown oily matter). The crude product was separated and purified by a rapid column chromatography (ethyl acetate:n-hexane) and dried in vacuo to afford compound XS-0285 (44 mg) as red solid.

(159) .sup.1H NMR (600 MHz, CHLOROFORM-d) ppm 0.50 (s, 3H) 0.97 (d, J=13.75 Hz, 1H) 1.09 (s, 3H) 1.21 (s, 3H) 1.22-1.25 (m, 3H) 1.25-1.28 (m, 1H) 1.41 (s, 3H) 1.47-1.58 (m, 3H) 1.58-1.72 (m, 5H) 1.87 (d, J=6.05 Hz, 1H) 1.99-2.11 (m, 3H) 2.21 (d, J=1.65 Hz, 3H) 2.24 (d, J=14.12 Hz, 1H) 2.44 (d, J=15.77 Hz, 1H) 4.93 (d, J=12.29 Hz, 1H) 5.02 (d, J=12.47 Hz, 1H) 6.32 (d, J=7.15 Hz, 1H) 6.49 (s, 1H) 7.01 (d, J=6.97 Hz, 1H) 7.27-7.30 (m, 2H) 7.30-7.36 (m, 3H).

(160) .sup.13C NMR (151 MHz, CHLOROFORM-d) ppm 10.29, 18.53, 21.58, 28.61, 29.53, 29.90, 30.55, 30.76, 31.57, 32.76, 33.27, 34.69, 36.35, 38.25, 39.43, 40.44, 42.93, 44.25, 45.03, 66.32, 117.36, 118.12, 119.62, 127.38, 128.24, 128.32, 128.64, 134.24, 135.68, 146.06, 164.79, 170.27, 177.95, 178.36.

EXAMPLE 17. PREPARATION OF COMPOUND XS0335

(161) ##STR00049##

(162) Compound YXY101 (50 mg, 0.11 mmol) was dissolved in dichloromethane (1 mL) with stirring. Palladium carbon (5 mg) was added, then dichloromethane (1 mL) was added, and hydrogen was continuously introduced, and reacted at room temperature for 24 hrs. The reaction was stopped. The reaction mixture was added with deionized water (15 mL), extracted with ethyl acetate three times. The ethyl acetate layers were combined, then washed three times with saturated NaCl, dried over anhydrous Na.sub.2SO.sub.4, concentrated by a rotary evaporator to give a crude product (colorless oily matter). The crude product was separated and purified by a rapid column chromatography (ethyl acetate:n-hexane) and dried in vacuo to afford compound XS-0335 (46 mg) as white solid.

(163) .sup.1H NMR (600 MHz, METHANOL-d.sub.4) ppm 0.93-1.00 (m, 2H) 1.03 (s, 3H) 1.11 (s, 3H) 1.19 (t, J=3.48 Hz, 4H) 1.26 (s, 3H) 1.41-1.45 (m, 6H) 1.47-1.55 (m, 2H) 1.57 (d, J=8.25 Hz, 1H) 1.59-1.68 (m, 2H) 1.83-1.98 (m, 3H) 2.06-2.11 (m, 4H) 2.11-2.20 (m, 4H) 2.43 (d, J=15.77 Hz, 1H) 2.68 (d, J=14.67 Hz, 1H) 6.67 (s, 1H).

(164) .sup.13C NMR (151 MHz, METHANOL-d.sub.4) ppm 11.94, 18.51, 20.54, 26.82, 28.66, 30.74, 31.15, 31.57, 31.61, 32.02, 32.09, 32.32, 33.63, 34.65, 37.09, 37.56, 38.53, 39.45, 39.85, 41.69, 58.12, 58.48, 112.24, 121.74, 129.36, 141.47, 142.39, 144.19, 182.95.

EXAMPLE 18. PREPARATION OF COMPOUNDS XS0366, XS0434-XS0438, XS0440, XS0441, XS0443, XS0463 AND XS0464

(165) ##STR00050##

(166) Taking the preparation of XS0366 for example, compound YXY101 (100 mg, 0.22 mmol) was dissolved in dichloromethane (4 mL) under stirring. Indole (52 mg, 0.44 mmol) was added, followed by an addition of aluminum trichloride hexahydrate (5.3 mg, 0.022 mmol), and the reaction was conducted under stirring at room temperature for 5 hours. The reaction was stopped, and the reaction system was added with deionized water (15 mL), then extracted three times with ethyl acetate. The combined ethyl acetate layer was washed with saturated NaCl three times, dried over anhydrous Na.sub.2SO.sub.4, and concentrated by a rotary evaporator to obtain a crude product (brown oily matter). The crude product was separated and purified by rapid column chromatography (ethyl acetate:n-hexane), dried in vacuo to afford compound XS0366 (122.2 mg) as purple red solid.

(167) .sup.1H NMR (600 MHz, CHLOROFORM-d) ppm 0.73 (br. s., 3H) 0.87-0.90 (m, 1H) 0.95-1.00 (m, 3H) 1.01 (br. s., 3H) 1.14 (br. s., 3H) 1.19 (t, J=7.06 Hz, 1H) 1.25-1.27 (m, 1H) 1.34 (br. s., 3H) 1.42-1.57 (m, 4H) 1.57-1.76 (m, 4H) 1.90 (s, 3H) 1.99-2.07 (m, 2H) 2.10-2.17 (m, 1H) 2.40 (d, J=15.04 Hz, 1H) 4.90 (d, J=5.69 Hz, 1H) 6.21 (d, J=6.24 Hz, 1H) 6.23 (br. s., 1H) 6.79 (br. s., 1H) 7.11 (t, J=7.43 Hz, 1H) 7.16 (t, J=7.43 Hz, 1H) 7.28 (d, J=7.89 Hz, 1H) 7.75 (d, J=7.70 Hz, 1H) 7.88 (br. s., 1H).

(168) .sup.13C NMR (151 MHz, CHLOROFORM-d) ppm 11.53, 18.84, 21.93, 28.89, 29.63, 29.75, 30.40, 30.54, 30.72, 31.55, 32.84, 34.62, 35.50, 36.74, 36.94, 37.76, 40.35, 43.62, 44.28, 108.93, 111.30, 119.09, 119.28, 120.23, 121.55, 121.58, 121.67, 127.10, 127.84, 136.49, 139.92, 142.17, 142.83, 147.48, 184.30.

(169) According to the above method, the following compounds were also synthesized in the present invention:

(170) ##STR00051## ##STR00052## ##STR00053## ##STR00054##

EXAMPLE 19. PREPARATION OF COMPOUND XS0395

(171) ##STR00055##

(172) Compound YXY101 (50 mg, 0.11 mmol) was weighed in a 25 ml reaction flask, and 4 ml of acetone was added thereto and dissolved under stirring, and then a drop of concentrated hydrochloric acid was added as catalyst, and the reaction was carried out at room temperature for 12 hours. The reaction was stopped, and the reaction mixture was directly concentrated to remove solvent. The residue was purified by silica gel column chromatography with ethyl acetate:n-hexane=4:1, affording a white solid in a yield of 51%.

(173) .sup.1H NMR (600 MHz, DMSO-d6) ppm 0.62 (s, 3H), 0.82-1.86 (m, 1H), 1.04 (s, 3H), 1.09 (s, 3H), 1.15 (s, 3H), 1.25-1.38 (m, 4H), 1.39 (s, 3H), 1.42-1.50 (m, 2H), 1.55-1.71 (m, 4H), 1.77 (td, J=13.9, 6.1 Hz, 1H), 1.93-2.02 (m, 2H), 2.03 (s, 3H), 2.09 (s, 3H), 2.27-2.36 (m, 2H), 2.67 (dd, J=16.2, 2.7 Hz, 1H), 3.71-3.78 (m, 1H), 5.72 (d, J=6.4 Hz, 1H), 6.63 (s, 1H), 7.91 (s, 1H), 8.94 (s, 1H), 12.06 (br.s., 1H).

(174) .sup.13C NMR (151 MHz, DMSO-d6) ppm 11.64, 18.43, 22.63, 29.01, 29.90, 30.36, 30.47, 30.62, 30.77, 31.44, 31.87, 32.88, 32.92, 34.94, 35.60, 36.79, 36.85, 36.98, 37.74, 39.87, 43.74, 44.36, 51.72, 109.06, 120.00, 122.04, 126.53, 140.46, 141.62, 143.85, 149.91, 179.96.208.01.

EXAMPLE 20. PREPARATION OF COMPOUND XS0419

(175) ##STR00056##

(176) Compound YXY101 (50 mg, 0.11 mmol) was dissolved under stirring in 2 mL of deuterated methanol, then sodium borohydride (44 mg, 1.1 mmol) was added, the reaction was carried out at room temperature for 30 min. The reaction was quenched with 1 mol/L HCl (1 mL), and then 9 mL of pure water was added, and extracted with dichloromethane (5 mL each time) three times. The organic layers were combined, dried over anhydrous sodium sulfate, and then the organic solvent dichloromethane was rapidly removed by vacuum distillation to obtain compound XS0419 (50.1 mg) as a white solid.

(177) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.66 (s, 3H) 0.85 (d, J=13.9 Hz, 1H) 1.05 (s, 3H) 1.11 (s, 3H) 1.17 (s, 3H) 1.22 (s, 3H) 1.29 (ddd, J=13.7, 4.4 Hz, 1H) 1.36-1.41 (m, 1H) 1.43-1.51 (m, 3H) 1.53-1.59 (m, 1H) 1.59-1.63 (m, 1H) 1.63-1.69 (m, 1H) 1.79 (ddd, J=13.8, 6.5 Hz, 1H) 1.86 (ddd, J=13.8, 5.0 Hz, 1H) 1.94-2.00 (m, 2H) 2.01 (s, 3H) 2.04 (d, J=13.6 Hz, 1H) 2.34 (d, J=15.6 Hz, 1H) 2.91 (dd, J=20.0, 1.5 Hz, 1H) 3.18 (dd, J=20.5, 6.2 Hz, 1H) 5.72 (dd, J=6.1, 1.8 Hz, 1H) 6.61 (s, 1H) 7.82 (s, 1H) 8.80 (s, 1H) 12.05 (br. s., 1H).

(178) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 11.53, 18.10, 22.70, 27.30, 28.45, 29.46, 29.77, 30.08, 30.19, 31.39, 32.44, 34.06, 34.09, 34.40, 36.07, 36.56, 37.14, 39.44, 43.25, 43.83, 108.17, 117.67, 120.10, 123.10, 139.35, 140.56, 143.11, 149.22, 179.51.

EXAMPLE 21. PREPARATION OF COMPOUND XS0462

(179) ##STR00057##

(180) First, Celastrol (135.2 mg, 0.3 mmol) was dissolved in 2 mL of DMF under stirring, followed by an addition of sodium hydrogencarbonate (138.6 mg, 1.65 mmol) and ethyl bromide (234 L, 0.15 mmol), the reaction was carried out under stirring at room temperature for 12 hours. The reaction was quenched with 1 mol/L HCl (1 mL), 9 mL of pure water was added. The resulting mixture was extracted three times with ethyl acetate (15 mL each time). The organic layers were combined, dried over anhydrous sodium sulfate, and then the organic solvent ethyl acetate was removed by vacuum evaporation to afford a crude product as orange-red mixture solid. The crude product was separated by column chromatography with n-hexane and ethyl acetate (hexane/ethyl acetate=10:1) as eluent, using 300-400 mesh silica gel packed column, affording an orange-red solid product.

(181) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.47 (s, 3H), 0.91 (d, J=14.1 Hz, 1H), 1.07 (s, 3H), 1.11 (s, 3H), 1.12-1.15 (m, 3H), 1.21 (s, 3H), 1.31-1.36 (m, 1H), 1.38 (s, 3H), 1.41-1.46 (m, 1H), 1.52-1.58 (m, 3H), 1.61-1.71 (m, 4H), 1.78-1.87 (m, 1H), 1.90-1.99 (m, 1H), 2.03-2.08 (m, 1H), 2.09 (s, 3H), 2.21 (d, J=11.2 Hz, 1H), 2.34 (d, J=15.6 Hz, 1H), 3.91 (m, 2H), 6.35 (d, J=7.2 Hz, 1H), 6.39 (s, 1H), 7.05-7.10 (m, 1H), 8.73 (s, 1H).

(182) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 10.53, 14.28, 18.50, 21.84, 28.55, 29.57, 29.75, 30.58, 31.76, 32.76, 33.32, 34.78, 36.43, 38.20, 39.27, 40.13, 40.44, 42.43, 44.04, 44.93, 60.33, 117.74, 118.51, 120.56, 127.29, 133.67, 146.86, 163.40, 168.31, 177.83, 178.41.

EXAMPLE 22. PREPARATION OF COMPOUND XS0474

(183) ##STR00058##

(184) Compound YXY101 (50 mg, 0.11 mmol) was dissolved under stirring in 2 mL of deuterated methanol, then sodium borodeuteride (48.4 mg, 1.1 mmol) was added, the reaction was carried out at room temperature for 30 min. The reaction was quenched with 1 mol/L HCl (1 mL), and then 9 mL of pure water was added. The resulting mixture was extracted three times with dichloromethane (5 mL each time). The organic layers were combined, dried over anhydrous sodium sulfate, and then the organic solvent dichloromethane was rapidly removed by vacuum distillation to obtain compound XS0474 (50.2 mg) as a white solid.

(185) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.66 (s, 3H) 0.85 (d, J=12.84 Hz, 1H) 1.04 (s, 3H) 1.10 (s, 3H) 1.17 (s, 3H) 1.22 (s, 3H) 1.29 (td, J=13.66, 4.40 Hz, 1H) 1.35-1.41 (m, 1H) 1.43-1.52 (m, 3H) 1.53-1.58 (m, 1H) 1.58-1.63 (m, 1H) 1.63-1.69 (m, 1H) 1.79 (td, J=13.66, 6.60 Hz, 1H) 1.86 (td, J=13.71, 5.04 Hz, 1H) 1.94-1.99 (m, 2H) 2.01 (s, 3H) 2.04 (d, J=12.10 Hz, 1H) 2.34 (d, J=15.59 Hz, 1H) 3.16 (d, J=6.05 Hz, 1H) 5.71 (d, J=6.24 Hz, 1H) 6.61 (s, 1H) 7.82 (s, 1H) 8.83 (s, 1H) 12.03 (br. s., 1H).

(186) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 11.60, 18.15, 22.74, 26.98, 28.52, 29.51, 29.83, 30.14, 30.25, 31.45, 32.50, 34.15, 34.21, 34.46, 36.14, 36.62, 37.21, 39.49, 43.31, 43.89, 108.23, 117.68, 120.20, 123.11, 139.45, 140.60, 143.18, 149.32, 179.59.

EXAMPLE 23. PREPARATION OF COMPOUND XS0503

(187) ##STR00059##

(188) First, pristimerin (250 mg, 0.54 mmol) was dissolved in 20 mL of tetrahydrofuran, followed by an addition of LiAlH.sub.4 (1.2 mL, 1.1 mmol), and the reaction was carried out under stirring at room temperature for 2 h. The reaction was quenched with 10 mL of deionized water, and then acidified with 1 mol/L HCl (5 mL). The resulting mixture was performed three times with ethyl acetate (15 mL each time). The organic layers were combined, dried over anhydrous sodium sulfate, and the organic solvent ethyl acetate was removed by vacuum distillation to afford a crude product as orange-yellow mixture solid. The crude product was separated by chromatography column with n-hexane and ethyl acetate (hexane/ethyl acetate=2:1) as eluent, using 300-400 mesh silica gel packed column, affording an orange-yellow solid product.

(189) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.76 (s, 3H) 0.83-0.87 (m, 1H) 0.89 (s, 3H) 1.11 (s, 3H) 1.21 (s, 3H) 1.23-1.25 (m, 1H) 1.26 (s, 3H) 1.27-1.34 (m, 2H) 1.48 (dd, J=6.7, 3.9 Hz, 1H) 1.50-1.54 (m, 1H) 1.55-1.59 (m, 1H) 1.60 (d, J=5.0 Hz, 1H) 1.64 (dd, J=9.2, 4.6 Hz, 2H) 1.65-1.69 (m, 2H) 1.69-1.72 (m, 1H) 1.91 (d, J=5.3 Hz, 1H) 1.93-1.97 (m, 1H) 2.02 (s, 3H) 2.92 (d, J=19.4 Hz, 1H) 2.96 (dd, J=10.3, 4.8 Hz, 1H) 3.15-3.20 (m, 1H) 3.21 (t, J=6.0 Hz, 1H) 4.44 (t, J=5.0 Hz, 1H) 5.73 (dd, J=6.1, 1.7 Hz, 1H) 6.61 (s, 1H) 7.80 (s, 1H) 8.78 (s, 1H).

(190) .sup.13C NMR (151 MHz, CHLOROFORM-d) ppm 11.49, 19.35, 25.65, 27.80, 28.10, 28.75, 29.36, 30.31, 30.45, 30.57, 32.27, 32.89, 33.58, 34.24, 36.55, 36.82, 36.95, 37.68, 42.91, 43.15, 71.82, 108.42, 118.15, 120.42, 125.27, 139.96, 141.09, 141.87, 151.04.

EXAMPLE 24. PREPARATION OF COMPOUND XS0508

(191) ##STR00060##

(192) XS0077 (50 mg, 0.11 mmol) was weighed and placed in a 50 ml round bottom bottle and added with 3 ml of methanol for dissolution, the air was replaced with nitrogen for protection, then sodium bisulfite solution (28 mg NaHSO.sub.3-1 ml H.sub.2O, 0.26 mmol) was added, and the reaction was carried out at room temperature for 3 h under protection of nitrogen. The reaction was stopped, the solvent was removed via concentration by distillation under reduced pressure. The residual solid was added with pyridine for dissolution, then filtered and concentrated in vacuo to give a white solid in a yield of 90%.

(193) .sup.1H NMR (600 MHz, DMSO-d6) ppm 0.57 (s, 3H) 1.07 (s, 3H) 1.12-1.14 (m, 1H) 1.14-1.16 (m, 1H) 1.17 (s, 3H) 1.21 (s, 3H) 1.22-1.23 (m, 2H) 1.24-1.28 (m, 4H) 1.28-1.32 (m, 2H) 1.38 (s, 3H) 1.40-1.46 (m, 2H) 1.47-1.52 (m, 2H) 1.57 (d, J=6.79 Hz, 1H) 1.59-1.63 (m, 4H) 1.64-1.72 (m, 6H) 1.75-1.83 (m, 4H) 1.92-1.96 (m, 1H) 1.97-2.01 (m, 1H) 2.03-2.07 (m, 1H) 2.09 (s, 3H) 2.18 (d, J=10.82 Hz, 2H) 2.73 (d, J=15.04 Hz, 1H) 3.40-3.49 (m, 1H) 3.80-3.89 (m, 1H) 6.36 (d, J=7.34 Hz, 1H) 6.40 (d, J=0.92 Hz, 1H) 7.07 (dd, J=6.97, 0.92 Hz, 1H) 7.73 (d, J=8.07 Hz, 1H) 8.71 (s, 1H).

(194) .sup.13C NMR (151 MHz, DMSO-d6) ppm 10.08, 18.32, 21.83, 24.68, 24.75, 25.13, 25.29, 25.63, 25.67, 28.38, 28.59, 29.91, 30.13, 31.02, 31.08, 31.39, 31.82, 31.91, 31.93, 32.36, 33.10, 36.02, 36.13, 37.67, 38.99, 42.16, 42.81, 44.45, 44.49, 50.05, 54.77, 117.23, 117.93, 120.04, 126.75, 133.25, 146.43, 153.97, 163.09, 168.74, 175.44, 177.83.

EXAMPLE 25. PREPARATION OF COMPOUND XS0536

(195) ##STR00061##

(196) XS0077 (150 mg, 0.32 mmol) was weighed and placed in a heavy wall pressure vessel, added with potassium carbonate (220 mg, 1.6 mmol), and 4 ml of acetone with stirring to dissolve the sample at room temperature, then added with 100 L of dimethyl sulfate solution; the reaction mixture was transferred to 70 C. oil bath and heated for 8 h. The reaction was quenched with 1 mol/L HCl, followed by an addition of water, then extracted with ethyl acetate three times, dried over anhydrous sodium sulfate, and the solvent was concentrated by a rotary evaporator. The residue was purified by silica gel column chromatography with ethyl acetate:n-hexane=1:20 to afford a pure product as white solid, yield 21%.

(197) .sup.1H NMR (600 MHz, CHLOROFORM-d) ppm 0.61 (s, 3H) 0.94 (d, J=13.75 Hz, 1H) 1.08 (s, 3H) 1.17 (s, 3H) 1.22 (s, 3H) 1.34 (s, 3H) 1.40 (dd, J=14.12, 4.22 Hz, 1H) 1.44 (dd, J=14.40, 2.84 Hz, 1H) 1.51-1.57 (m, 2H) 1.57-1.63 (m, 1H) 1.63-1.69 (m, 2H) 1.73 (d, J=11.37 Hz, 1H) 1.85 (td, J=13.71, 6.33 Hz, 1H) 2.01-2.07 (m, 1H) 2.07-2.13 (m, 2H) 2.17 (s, 3H) 2.18-2.23 (m, 1H) 2.44 (d, J=15.59 Hz, 1H) 3.02 (d, J=19.99 Hz, 1H) 3.28 (dd, J=20.00, 5.87 Hz, 1H) 3.54 (s, 3H) 3.77 (s, 3H) 3.87 (s, 3H) 5.77 (d, J=4.58 Hz, 1H) 6.78 (s, 1H).

(198) .sup.13C NMR (151 MHz, CHLOROFORM-d) ppm 11.77, 18.28, 22.73, 27.85, 28.85, 29.87, 30.29, 30.50, 30.85, 31.55, 32.88, 34.16, 34.51, 34.79, 36.83, 37.15, 37.52, 40.45, 43.69, 44.33, 51.47, 55.88, 60.30, 106.30, 117.63, 125.49, 127.80, 144.62, 144.80, 149.13, 150.89, 179.05.

EXAMPLE 26. PREPARATION OF COMPOUND XS0286

(199) ##STR00062##

(200) Compound YXY101 (50 mg, 0.11 mmol) was dissolved in N,N-dimethylformamide (2 mL) under stirring. Catalysts EDCl (85.4 mg, 0.55 mmol) and HOBT (74.3 mg, 0.55 mmol) were added and stirred for dissolution; p-tert-butylaniline (49.2 mg, 0.33 mmol) was added, and the reaction was carried out under stirring at room temperature for 36 hours. The reaction was stopped, and the reaction system was added with deionized water (15 mL) and extracted three times with ethyl acetate. The combined ethyl acetate layer was washed with saturated NaCl three times, dried over anhydrous Na.sub.2SO.sub.4, concentrated by a rotary evaporator to obtain a crude product (dark-red oily matter). The crude product was purified by rapid column chromatography (ethyl acetate:n-hexane), dried in vacuo to afford compound XS0286 (10 mg) as dark-red solid.

(201) .sup.1H NMR (600 MHz, CHLOROFORM-d) ppm 0.64 (s, 3H) 1.08 (d, J=13.20 Hz, 1H) 1.15 (s, 3H) 1.24-1.27 (m, 6H) 1.40-1.42 (m, 4H) 1.48-1.57 (m, 3H) 1.63 (m, 5H) 1.65-1.79 (m, 5H) 1.85 (d, J=11.92 Hz, 1H) 1.91 (d, J=6.24 Hz, 1H) 1.98-2.06 (m, 3H) 2.08 (d, J=12.10 Hz, 2H) 2.18 (d, J=1.65 Hz, 3H) 2.54 (d, J=15.77 Hz, 1H) 6.29 (d, J=6.79 Hz, 1H) 6.45 (s, 1H) 6.92-7.00 (m, 2H) 7.30-7.34 (m, 2H) 7.34-7.37 (m, 2H) 7.37-7.41 (m, 1H).

(202) .sup.13C NMR (151 MHz, CHLOROFORM-d) ppm 10.21, 18.49, 21.75, 28.58, 29.63, 29.69, 30.41, 30.83, 31.33, 33.24, 33.73, 34.35, 34.98, 36.32, 38.06, 39.38, 41.10, 42.96, 44.47, 45.11, 76.81, 77.02, 77.23, 116.99, 117.95, 119.53, 119.81, 125.89, 127.38, 133.95, 135.11, 146.01, 147.26, 164.68, 170.02, 175.83, 178.38.

EXAMPLE 27. PREPARATION OF COMPOUND XS0287

(203) ##STR00063##

(204) Compound YXY101 (50 mg, 0.11 mmol) was dissolved in N,N-dimethylformamide (2 mL) under stirring. Catalysts EDCl (85.4 mg, 0.55 mmol) and HOBT (74.3 mg, 0.55 mmol) were added and stirred for dissolution; p-methoxyaniline (40.6 mg, 0.33 mmol) was added, and the reaction was carried out under stirring at room temperature for 36 hours. The reaction was stopped. The reaction system was added with deionized water (15 mL) and extracted three times with ethyl acetate. The combined ethyl acetate layer was washed with saturated NaCl three times, dried over anhydrous Na.sub.2SO.sub.4, concentrated by a rotary evaporator to obtain a crude product (dark-red oily matter). The crude product was purified by rapid column chromatography (ethyl acetate:n-hexane), dried in vacuo to afford compound XS0287 (20 mg) as dark-red solid.

(205) .sup.1H NMR (600 MHz, CHLOROFORM-d) ppm 0.53 (s, 3H) 1.05 (d, J=13.94 Hz, 1H) 1.13 (s, 3H) 1.21 (s, 3H) 1.24 (s, 3H) 1.26 (s, 3H) 1.35 (s, 3H) 1.48-1.54 (m, 2H) 1.58 (d, J=7.34 Hz, 2H) 1.64-1.72 (m, 2H) 1.78-1.89 (m, 3H) 2.03-2.11 (m, 2H) 2.18 (s, 3H) 2.55 (d, J=15.77 Hz, 1H) 3.79 (s, 3H) 6.25 (d, J=7.15 Hz, 1H) 6.34 (s, 1H) 6.91 (m, J=8.99 Hz, 2H) 6.96 (d, J=7.15 Hz, 1H) 7.40 (m, J=8.80 Hz, 2H) 7.48 (s, 1H).

(206) .sup.13C NMR (151 MHz, CHLOROFORM-d) ppm 10.23, 18.30, 21.75, 28.46, 29.39, 29.70, 30.30, 30.79, 31.52, 32.86, 33.81, 34.89, 36.21, 37.99, 39.28, 40.96, 42.96, 44.43, 45.12, 55.48, 114.21, 117.18, 117.82, 119.38, 121.99, 127.34, 130.98, 134.06, 146.06, 156.41, 164.80, 170.23, 175.88, 178.42.

EXAMPLE 28. PREPARATION OF COMPOUND XS0394

(207) ##STR00064##

(208) Compound YXY101 (50 mg, 0.11 mmol) and triethylamine (37 L) were dissolved in re-distilled tetrahydrofuran (3.0 mL, 0.26 mmol) under stirring, then cooled to 30 C. Ethyl chloroformate (22 L, 0.23 mmol) was added dropwise to the reaction liquor 10 minutes later. After being conducted at 30 C. for 12 hours under stirring, the reaction was stopped. The insoluble material was filtered off by a Buchner funnel with a fritted glass disc and washed with tetrahydrofuran to give a yellow filtrate. The yellow filtrate was added with 10 mL of pure water, and extracted with ethyl acetate three times (15 mL each time). The organic layer was combined, washed three times with saturated brine (30 mL each time), and dried over anhydrous sodium sulfate. The organic solvent was removed by distillation under reduced pressure to give a crude product as oily mixture. The product as yellow solid was obtained by column chromatography separation with n-hexane and ethyl acetate (hexane/ethyl acetate=10:1) as eluent, and using 300-400 mesh silica gel packed column.

(209) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 1.05-1.07 (m, 1H) 1.08 (s, 3H) 1.09-1.12 (m, 1H) 1.18 (s, 3H) 1.23 (s, 3H) 1.27 (t, J=7.06 Hz, 3H) 1.28-1.31 (m, 1H) 1.41 (s, 3H) 1.43-1.50 (m, 4H) 1.53 (dd, J=12.10, 5.69 Hz, 1H) 1.59 (d, J=7.89 Hz, 1H) 1.65 (d, J=10.64 Hz, 2H) 1.70-1.78 (m, 2H) 1.79-1.85 (m, 1H) 1.90 (td, J=13.98, 3.39 Hz, 1 H) 1.95-2.01 (m, 1H) 2.01-2.06 (m, 1H) 2.15 (s, 3H) 2.26 (d, J=15.22 Hz, 1H) 4.21 (q, J=1.00 Hz, 2H) 6.30 (d, J=7.15 Hz, 1H) 6.40 (d, J=0.73 Hz, 1H) 7.29 (dd, J=7.52, 0.73 Hz, 1H) 12.07 (br. s, 1H).

(210) .sup.13C NMR (151 MHz, CHLOROFORM-d) ppm 11.17, 14.09, 19.00, 21.96, 28.60, 29.35, 29.36, 30.47, 30.67, 31.49, 32.67, 33.38, 34.53, 36.20, 38.24, 39.13, 40.16, 42.88, 44.05, 45.34, 65.05, 117.76, 117.78, 122.70, 126.08, 133.37, 142.54, 152.62, 163.30, 172.96, 183.86, 183.90.

EXAMPLE 29. PREPARATION OF COMPOUND XS0418

(211) ##STR00065##

(212) First, compound YXY101 (50 mg, 0.11 mmol) was stirred and dissolved in 2 mL of tetrahydrofuran, followed by an addition of potassium carbonate (15.2 mg, 0.11 mmol). Ethyl bromoacetate (18.37 mg, 0.11 mmol) was dissolved in 1 mL of tetrahydrofuran, and then added dropwise to the reaction solution. The reaction was carried out under stirring at room temperature for 4 hours, then quenched with 1 mol/L HCl (1 mL), 9 mL of pure water was added. The resulting mixture was extracted three times with ethyl acetate (15 mL each time). The collected organic layer was dried over anhydrous sodium sulfate, and the organic solvent ethyl acetate was removed by distillation in vacuo to afford a crude product as orange-red mixture solid. The product as orange-red solid was obtained by column chromatography separation with n-hexane and ethyl acetate (hexane/ethyl acetate=10:1) as eluent, using 300-400 mesh silica gel packed column.

(213) .sup.1H NMR (600 MHz, CHLOROFORM-d) ppm 0.53 (s, 3H) 0.99 (d, J=14.31 Hz, 1H) 1.11 (s, 3H) 1.25 (t, J=7.20 Hz, 3H) 1.27 (s, 3H) 1.28 (s, 3H) 1.39-1.44 (m, 1H) 1.45 (s, 3H) 1.51 (dd, J=14.95, 4.13 Hz, 1H) 1.54-1.58 (m, 1H) 1.60 (d, J=7.89 Hz, 1H) 1.63-1.67 (m, 1H) 1.67-1.71 (m, 1H) 1.75 (dd, J=15.96, 8.07 Hz, 1H) 1.80-1.82 (m, 1H) 1.83-1.85 (m, 1H) 1.85-1.92 (m, 1H) 2.06 (td, J=14.12, 3.85 Hz, 1H) 2.13-2.18 (m, 1H) 2.21 (s, 3H) 2.25 (d, J=14.31 Hz, 1H) 2.48 (d, J=15.96 Hz, 1H) 4.19 (q, J=7.15 Hz, 2H) 4.41 (d, J=15.77 Hz, 1H) 4.54 (d, J=15.96 Hz, 1H) 6.35 (d, J=7.15 Hz, 1H) 6.53 (d, J=1.10 Hz, 1H) 7.02 (dd, J=7.06, 1.19 Hz, 1H)

(214) .sup.13C NMR (151 MHz, CHLOROFORM-d) ppm 10.23, 14.04, 18.57, 21.61, 28.59, 29.57, 29.74, 30.47, 30.63, 31.55, 32.56, 33.50, 34.67, 36.31, 38.24, 39.39, 40.40, 42.91, 44.19, 45.01, 60.52, 61.28, 117.15, 118.13, 119.52, 127.37, 134.09, 145.98, 164.74, 167.70, 170.03, 177.53, 178.31

EXAMPLE 30. PREPARATION OF COMPOUNDS XS0421, XS0457, XS0473 AND XS0493

(215) ##STR00066##

(216) Taking the synthesis of XS0421 as an example: Compound YXY101 (50 mg, 0.11 mmol) was weighed in a 50 ml sealed tube, then dimethyl phosphite (123 mg, 1.1 mmol) and 2.7 mg of aluminum chloride hexahydrate (0.1 eq) were added, and 2 mL of DCM was added for dissolution. The tube was sealed, and the reaction was performed at room temperature for 6 h. The reaction was stopped and quenched with saturated NaCl. The resulting mixture was extracted with ethyl acetate three times, the organic phases were combined and dried with anhydrous Na.sub.2SO.sub.4, and concentrated under reduced pressure to remove the solvent. The residue was purified by silica gel column chromatography with ethyl acetate:n-hexane=1:2 to gave a white solid, yield 55%.

(217) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.61 (3H, s) 0.86 (1H, d, J=12.84 Hz) 1.06 (3H, s) 1.10 (3H, s) 1.19 (3H, s) 1.22-1.27 (1H, m) 1.27-1.32 (1H, m) 1.40 (1H, d, J=4.95 Hz) 1.43 (1H, d, J=5.32 Hz) 1.49 (1H, d, J=8.07 Hz) 1.51-1.55 (1H, m) 1.57 (3H, s) 1.59-1.60 (1H, m) 1.60-1.64 (1H, m) 1.76-1.85 (1H, m) 1.93-1.97 (1H, m) 1.99 (1H, d, J=2.20 Hz) 2.00-2.02 (1H, m) 2.02-2.06 (1H, m) 2.13 (3H, s) 2.32 (1H, d, J=15.59 Hz) 3.49 (3H, d, J=8.80 Hz) 3.51 (3H, d, J=8.99 Hz) 4.19 (1H, dd, J=23.66, 6.24 Hz) 5.64 (1H, dd, J=6.33, 3.21 Hz) 6.66 (1H, s) 7.97 (1H, s) 9.04 (1H, br. s.) 12.04 (1H, s).

(218) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 12.60, 14.00 (1 C, s) 18.04, 21.58 (1 C, d, J=6.60 Hz) 22.11, 28.78, 29.48, 30.02 (1 C, d, J=13.20 Hz) 30.18, 31.00, 31.45, 32.42, 33.49, 33.57, 34.57, 36.42, 37.43, 37.89, 38.79, 43.88, 52.31 (1 C, d, J=6.60 Hz) 52.81 (1 C, d, J=6.60 Hz) 109.32, 114.64 (1 C, d, J=12.10 Hz) 117.90 (1 C, d, J=7.70 Hz) 121.35 (1 C, d, J=4.40 Hz) 140.50 (1 C, d, J=6.60 Hz) 141.05 (1 C, d, J=3.30 Hz) 144.08 (1 C, d, J=3.30 Hz) 150.62 (1 C, d, J=12.10 Hz) 179.51.

(219) According to the above preparation method, the following compounds were also synthesized in the present invention:

(220) ##STR00067##

EXAMPLE 31. PREPARATION OF COMPOUNDS XS0439, XS0442, XS0444-XS0449, XS0478-XS0480, XS0487 AND XS0490

(221) ##STR00068## ##STR00069## ##STR00070## ##STR00071## ##STR00072##

(222) The preparation method is exemplified by XS0439: Compound YXY101 (100 mg, 0.22 mmol) was dissolved in dichloromethane (4 mL) under stirring. 7-Methoxy-substituted indole (65.3 mg, 0.44 mmol) was added, then aluminum trichloride hexahydrate (5.3 mg, 0.022 mmol). The reaction was carried out under stirring at room temperature for 5 hours. The reaction was stopped, the reaction mixture was added with deionized water (15 mL) and extracted three times with ethyl acetate. The ethyl acetate layers were combined, washed with saturated NaCL three times, dried over anhydrous Na.sub.2SO.sub.4, concentrated by a rotary evaporator to obtain a crude product (brown oily matter). The crude product was separated and purified by rapid column chromatography (ethyl acetate:n-hexane=1:4), dried in vacuo to afford a product as purple red solid.

(223) .sup.1H-NMR (DMSO-d.sub.6) ppm 0.71 (s, 3H), 0.86 (d, J=9.9 Hz, 1H), 0.96 (s, 3H), 1.01 (s, 3H), 1.10 (s, 3H), 1.22-1.29 (m, 2H), 1.32 (s, 3H), 1.34-1.40 (m, 2H), 1.45 (d, J=8.1 Hz, 1H), 1.50-1.61 (m, 3H), 1.62-1.75 (m, 2H), 1.79 (s, 3H), 1.96-2.08 (m, 3H), 2.34 (d, J=15.4 Hz, 1H), 3.88 (s, 3H), 4.79 (d, J=5.9 Hz, 1H), 6.12 (d, J=6.2 Hz, 1H), 6.18 (s, 1H), 6.62 (d, J=7.7 Hz, 1H), 6.73 (s, 1H), 6.90 (t, J=7.9 Hz, 1H), 7.22 (d, J=7.9 Hz, 1H), 7.88 (br. s., 1H), 8.99 (br. s., 1H), 10.69 (s, 1H), 12.04 (br. s., 1H).

(224) .sup.13C-NMR (DMSO-d.sub.6) ppm 11.9, 18.5, 22.3, 29.1, 29.9, 30.4, 30.5, 30.6, 31.8, 32.9, 34.9, 35.4, 35.5, 35.6, 36.8, 36.9, 37.8, 43.5, 44.3, 55.4, 101.8, 108.8, 112.2, 119.2, 119.8, 121.1, 121.6, 122.6, 126.3, 126.7, 128.5, 140.8, 141.4, 144.0, 146.6, 147.0, 180.0.

EXAMPLE 32. PREPARATION OF COMPOUNDS XS0486, XS0491 AND XS0492

(225) ##STR00073##

(226) Taking the preparation of compound XS0486 as an example: First, Compound YXY101 (50 mg, 0.11 mmol) was dissolved in dioxane (600 L), triethylamine (150 L, 0.33 mmol) was added, and then dioxane (100 L) was added to wash the residue on the wall of the reaction bottle, and the reaction solution was cooled to 0 C. Dimethyl phosphite (110 mg, 1.1 mmol) was dissolved in 50 L of carbon tetrachloride, then the dissolved dimethyl phosphite was slowly added dropwise into the reaction solution dissolved with Celastrol, the reaction was carried out under stirring at 0 C. for 12 h, then 10 mL of ice-cold deionized water was added, and 10 mL of saturated ammonium chloride solution was added for quenching the reaction. The resulting mixture was extracted with ethyl acetate three times (15 mL each time), and the organic layer was collected and dried over anhydrous sodium sulfate. The organic solvent ethyl acetate was then removed by distillation under reduced pressure to give a crude product as red mixture solid. The crude product was separated by rapid column chromatography with 300-400 mesh silica gel packed column using n-hexane and ethyl acetate (hexane/ethyl acetate=1:1) as eluent to give a red solid product.

(227) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.60 (s, 3H) 0.96 (d, J=13.57 Hz, 1H) 1.08 (s, 3H) 1.23 (s, 3H) 1.24 (s, 3H) 1.38 (s, 3H) 1.41-1.48 (m, 2H) 1.55-1.60 (m, 3H) 1.61-1.67 (m, 2H) 1.69-1.74 (m, 1H) 1.78 (dd, J=16.14, 7.89 Hz, 1H) 1.81-1.88 (m, 1H) 1.95 (td, J=14.12, 3.85 Hz, 1H) 2.02 (d, J=13.94 Hz, 1H) 2.09 (s, 3H) 2.21-2.24 (m, 1H) 2.27 (d, J=15.96 Hz, 1H) 3.74 (dd, J=11.55, 5.14 Hz, 6H) 6.36 (d, J=7.15 Hz, 1H) 6.39 (d, J=1.28 Hz, 1H) 7.08 (dd, J=6.97, 1.10 Hz, 1H) 8.75 (s, 1H).

(228) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 10.07, 18.53, 21.43, 28.03, 29.09, 29.24, 29.71, 30.07, 31.21, 31.46, 32.76, 33.92, 35.85, 37.71, 38.78, 41.23 (d, J=5.50 Hz,) 41.97, 43.37, 44.45, 55.15 (dd, J=17.61, 5.50 Hz, 2 C) 117.24, 118.13, 120.12, 126.89, 133.12, 146.44, 162.82, 167.43, 172.21 (d, J=11.00 Hz) 177.98.

EXAMPLE 33. PREPARATION OF COMPOUND XS0488

(229) ##STR00074##

(230) First, compound XS0077 (80 mg, 0.17 mmol) was dissolved in tetrahydrofuran (4 mL), triethylamine (370 L, 2.5 mmol) was added, then 4-DMAP (24.7 mg, 0.22 mmol) was added, stirred evenly, and n-butyryl chloride (113 L, 1.1 mmol) was added. The reaction was carried out under stirring at room temperature for 30 min, then quenched with 10 mL of saturated ammonium chloride solution. The resulting mixture was extracted with ethyl acetate three times (15 mL each time). The organic layer was collected and dried over anhydrous sodium sulfate, the organic solvent ethyl acetate was removed by distillation under reduced pressure to give a crude product as red mixture solid. Separation was performed by column chromatography with 300-400 mesh silica gel packed column, using n-hexane and ethyl acetate (hexane/ethyl acetate=4:1) as eluent to give a product as bright yellow solid.

(231) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.46-0.51 (m, 3H) 0.91 (d, J=1.00 Hz, 1H) 0.95-1.01 (m, 3H) 1.08 (s, 3H) 1.12 (s, 3H) 1.23 (s, 3H) 1.36 (ddd, J=13.80, 4.20 Hz, 1H) 1.42 (s, 3H) 1.44-1.48 (m, 1H) 1.54-1.60 (m, 3H) 1.63 (s, 2H) 1.66-1.68 (m, 2H) 1.70 (d, J=9.17 Hz, 2H) 1.83 (dd, J=13.57, 7.70 Hz, 1H) 1.93-1.99 (m, 1H) 2.06 (d, J=13.94 Hz, 1H) 2.10 (s, 3H) 2.22 (d, J=7.34 Hz, 1H) 2.32 (d, J=15.59 Hz, 1H) 2.55 (t, J=7.15 Hz, 2H) 3.49 (s, 3H) 6.38 (s, 1H) 6.41 (d, J=7.15 Hz, 1H) 7.31 (d, J=6.97 Hz, 1H).

(232) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 13.41, 18.05, 21.59, 28.06, 29.11, 29.42, 30.11, 30.16, 30.32, 31.32, 32.21, 32.31, 33.06, 34.36, 34.91, 36.00, 37.90, 38.77, 39.83, 42.22, 43.64, 44.85, 51.48, 117.99, 122.13, 125.21, 133.52, 136.69, 142.26, 162.81, 170.65, 171.21, 176.21, 177.91.

EXAMPLE 34. PREPARATION OF COMPOUND XS0506

(233) ##STR00075##

(234) Compound YXY101 (50 mg, 0.11 mmol) was weighed in a 50 ml round bottom flask, dicyclohexylcarbodiimide (23 mg, 0.11 mmol) and glucose (24 mg, 0.11 mmol) were added, then 2 ml of DCM was added for dissolution. The reaction was carried out at room temperature for 12 h, quenched with a large amount of water, extracted with ethyl acetate three times. The organic phases were combined and dried over anhydrous Na.sub.2SO.sub.4, and concentrated under reduced pressure to remove solvent. Separation and purification were performed by silica gel column with ethyl acetate:n-hexane=1:4 to afford an orange-red solid, yield 42%.

(235) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.57 (s, 3H) 1.07 (s, 3H) 1.12-1.14 (m, 1H) 1.14-1.16 (m, 1H) 1.17 (s, 3H) 1.21 (s, 3H) 1.22-1.23 (m, 2H) 1.24-1.28 (m, 4H) 1.28-1.32 (m, 2H) 1.38 (s, 3H) 1.40-1.46 (m, 2H) 1.47-1.52 (m, 2H) 1.57 (d, J=6.79 Hz, 1H) 1.59-1.63 (m, 4H) 1.64-1.72 (m, 6H) 1.75-1.83 (m, 4H) 1.92-1.96 (m, 1H) 1.97-2.01 (m, 1H) 2.03-2.07 (m, 1H) 2.09 (s, 3H) 2.18 (d, J=10.82 Hz, 2H) 2.73 (d, J=15.04 Hz, 1H) 3.40-3.49 (m, 1H) 3.80-3.89 (m, 1H) 6.36 (d, J=7.34 Hz, 1H) 6.40 (d, J=0.92 Hz, 1H) 7.07 (dd, J=6.97, 0.92 Hz, 1H) 7.73 (d, J=8.07 Hz, 1H) 8.71 (s, 1H).

(236) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 10.08, 18.32, 21.83, 24.68, 24.75, 25.13, 25.29, 25.63, 25.67, 28.38, 28.59, 29.91, 30.13, 31.02, 31.08, 31.39, 31.82, 31.91, 31.93, 32.36, 33.10, 36.02, 36.13, 37.67, 38.99, 42.16, 42.81, 44.45, 44.49, 50.05, 54.77, 117.23, 117.93, 120.04, 126.75, 133.25, 146.43, 153.97, 163.09, 168.74, 175.44, 177.83.

EXAMPLE 35. PREPARATION OF COMPOUND XS0507

(237) ##STR00076##

(238) Compound YXY101 (50 mg, 0.11 mmol) was weighed in a 50 ml round bottom flask, added with 2 ml of DCM for dissolution, then transferred to 78 C. and stirred. DAST (150 ul, 10 eq) was added and reacted at 78 C. for 1 h. The reaction solution was directly poured into a large amount of ice to quench the reaction. The aqueous phase was extracted three times with DCM. The organic phases were combined and dried over anhydrous Na.sub.2SO.sub.4. The organic phase was concentrated under reduced pressure to remove solvent. Separation and purification were performed by column chromatography with ethyl acetate:n-hexane=1:4 system to gave an orange-red solid, yield 58%.

(239) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.56 (s, 3H) 0.98 (d, J=11.92 Hz, 1H) 1.08 (s, 3H) 1.22 (s, 3H) 1.29 (s, 3H) 1.38 (s, 3H) 1.43-1.47 (m, 1H) 1.48-1.52 (m, 1H) 1.55-1.59 (m, 2H) 1.60-1.64 (m, 1H) 1.67 (d, J=4.03 Hz, 1H) 1.71 (d, J=3.85 Hz, 1H) 1.80 (dd, J=16.41, 8.16 Hz, 1H) 1.83-1.87 (m, 1H) 1.88-1.92 (m, 1H) 1.96 (d, J=17.61 Hz, 1H) 1.95-1.95 (m, 1H) 2.09 (s, 3H) 2.20 (d, J=1.83 Hz, 2H) 6.35 (d, J=7.34 Hz, 1H) 6.38 (d, J=1.28 Hz, 1H) 7.06 (dd, J=6.97, 1.28 Hz, 1H) 8.73 (s, 1H).

(240) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 10.07, 18.85, 21.41, 27.89, 29.26, 29.33, 29.46, 29.94, 31.16, 32.71, 33.79, 35.78, 37.87, 38.74, 40.04, 40.22, 41.89, 43.26, 44.33, 117.21, 118.14, 120.15, 126.99, 132.88, 146.41, 162.78, 167.39 (d, J=418.15 Hz, 1 C), 166.71, 177.97.

EXAMPLE 36. PREPARATION OF COMPOUND XS0509

(241) ##STR00077##

(242) Compound YXY101 (50 mg, 0.11 mmol) was weighed in a 25 ml heavy wall pressure vessel, added with tetrabutylammonium bromide (TBAB, 17.5 mg, 0.05 mmol), and 2 ml of dichloromethane (DCM) was added for dissolution, and then 5% NaOH (180 l) was add dropwise. The reaction was carried out at room temperature for 30 min, then transferred to 50 C. oil bath, and added dropwise with dichloromethane solution of 2,3,4,6-tetraacetoxy--D-glucopyranose bromide (57 mg-1 ml, 0.138 mmol), and reacted at 50 C. for 12 h. The reaction was stopped, and a large amount of water and saturated brine were added. The resulting mixture was extracted with DCM for 3 times. The organic phases were combined and dried over anhydrous Na.sub.2SO.sub.4. The organic phase was concentrated under reduced pressure, and purified by silica gel column chromatography with ethyl acetate:n-hexane=4:1 system to obtain a yellow solid, yield 25%.

(243) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.51 (s, 3H) 0.95 (d, J=13.57 Hz, 1H) 1.08 (d, J=6.24 Hz, 6H) 1.22 (s, 3H) 1.23 (br. s., 1H) 1.38 (s, 3H) 1.41 (d, J=4.22 Hz, 1H) 1.46 (d, J=11.92 Hz, 1H) 1.56 (d, J=7.52 Hz, 2H) 1.58 (s, 3H) 1.60-1.63 (m, 1H) 1.64 (d, J=4.95 Hz, 2H) 1.66-1.69 (m, 1H) 1.81-1.87 (m, 1H) 1.91 (s, 3H) 1.94 (d, J=3.67 Hz, 1H) 1.97 (s, 3H) 2.00-2.04 (m, 1H) 2.08 (s, 3H) 2.12 (s, 3H) 2.19 (d, J=8.80 Hz, 1H) 2.31 (d, J=15.59 Hz, 1H) 3.85-3.90 (m, 1H) 3.92-3.96 (m, 1H) 4.30 (dd, J=8.16, 4.13 Hz, 1H) 5.05 (dd, J=10.09, 8.44 Hz, 1H) 5.23 (d, J=3.48 Hz, 1H) 5.29 (dd, J=10.45, 3.67 Hz, 1H) 5.83 (d, J=8.25 Hz, 1H) 6.36 (d, J=7.15 Hz, 1H) 6.37 (d, J=0.92 Hz, 1H) 7.06 (d, J=6.97 Hz, 1H) 8.71 (s, 1H).

(244) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 10.06, 18.63, 19.97, 20.31, 20.42, 21.57, 28.11, 28.59, 29.22, 29.97, 30.07, 31.31, 32.62, 32.84, 34.57, 35.93, 37.76, 38.52, 40.05, 40.24, 41.97, 43.46, 44.54, 61.76, 67.35, 67.85, 69.78, 71.21, 91.64, 117.29, 118.08, 120.11, 126.93, 133.07, 146.36, 162.86, 167.78, 169.24, 169.41, 169.57, 169.97, 176.51, 177.93.

EXAMPLE 37. PREPARATION OF COMPOUND XS0514, XS0515

(245) ##STR00078##

(246) Taking the synthesis of XS0514 as an example: XS0419 (50 mg, 0.11 mmol) was weighed in a 50 ml round bottom flask, added with 2 ml DCM for dissolution, then transferred to 78 C. and stirred, followed by an addition of diethylaminosulfurtrifluoride (DAST, 150 ul, 10 eq), and reacted at 78 C. for 1 h. The reaction solution was poured into a large amount of ice to quench the reaction. The aqueous phase was extracted three times with DCM. The organic phase was combined, washed with saturated NaHCO.sub.3, dried with anhydrous Na.sub.2SO.sub.4, and concentrated under reduced pressure. Separation and purification were performed by silica gel column chromatography with ethyl acetate:n-hexane=1:8 system to give an orange-red solid, yield 58%.

(247) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.61 (s, 3H) 0.95 (d, J=14.49 Hz, 1H) 1.06 (s, 3H) 1.18 (s, 3H) 1.23 (s, 3H) 1.28 (s, 3H) 1.41 (d, J=14.86 Hz, 2H) 1.47 (dd, J=13.85, 4.31 Hz, 2H) 1.54 (d, J=7.70 Hz, 1H) 1.58-1.63 (m, 2H) 1.74-1.84 (m, 2H) 1.88 (d, J=6.05 Hz, 1H) 1.94 (d, J=10.64 Hz, 1H) 1.98 (d, J=10.09 Hz, 1H) 2.01 (s, 3H) 2.07 (d, J=17.97 Hz, 1H) 2.24 (d, J=15.96 Hz, 1H) 2.89-2.94 (m, 1H) 3.16-3.21 (m, 1H) 5.74 (d, J=4.77 Hz, 1H) 6.61 (s, 1H) 7.81 (br. s., 1H) 8.78 (br. s., 1H).

(248) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 11.56, 18.66, 22.57, 27.30, 28.27, 29.21, 29.54, 29.98, 30.02, 30.08, 31.18, 33.69, 33.99, 34.13, 36.05, 36.27, 37.14, 40.25, 43.12, 43.42, 108.21, 118.07, 120.13, 123.02, 139.23, 140.61, 143.17, 148.76, 167.64 (d, J=380.73 Hz, 1 C).

EXAMPLE 38. PREPARATION OF COMPOUND XS0516

(249) ##STR00079##

(250) XS0077 (50 mg, 0.11 mmol) was weighed in a 25 ml heavy wall pressure vessel, added with tetrabutylammonium bromide (TBAB, 17.5 mg, 0.05 mmol), and 2 ml of dichloromethane (DCM) was added for dissolution, then 5% NaOH (180 L) was added dropwise. The mixture were reacted at room temperature for 30 min, subsequently transferred to 50 C. oil bath, added dropwise with 2,3,4,6-tetraacetoxy--D-glucopyranose bromide-dichloromethane solution (57 mg-1 ml, 0.138 mmol) and reacted at 50 C. for 12 h. The reaction was stopped, a large amount of water and saturated brine were added, and the mixture was extracted with DCM for 3 times. The organic phases were combined, dried over anhydrous Na.sub.2SO.sub.4 concentrated under reduced pressure, and purified by silica gel column chromatography with ethyl acetate:n-hexane=4:1 to afford a yellow solid, yield 25%.

(251) .sup.1H NMR (600 MHz, CHLOROFORM-d) ppm 0.53 (s, 3H) 0.97 (d, J=14.31 Hz, 1H) 1.10 (s, 3H) 1.18 (s, 3H) 1.26 (s, 3H) 1.38 (td, J=14.03, 4.58 Hz, 1H) 1.47 (s, 3H) 1.50 (dd, J=15.59, 4.58 Hz, 1H) 1.53-1.56 (m, 1H) 1.58 (d, J=8.25 Hz, 1H) 1.62-1.65 (m, 2H) 1.66 (d, J=5.32 Hz, 1H) 1.67-1.72 (m, 2H) 1.76-1.80 (m, 1H) 1.82-1.87 (m, 1H) 1.87-1.91 (m, 1H) 1.98 (s, 3H) 2.01 (s, 3H) 2.10-2.14 (m, 1H) 2.15 (s, 3H) 2.18 (s, 3H) 2.23 (s, 3H) 2.42 (d, J=15.77 Hz, 1H) 3.55 (s, 3H) 3.86 (t, J=7.34 Hz, 1H) 4.06 (dd, J=11.10, 7.61 Hz, 1H) 4.16 (dd, J=11.10, 6.14 Hz, 1H) 5.11 (dd, J=10.36, 3.58 Hz, 1H) 5.31 (d, J=7.89 Hz, 1H) 5.38-5.43 (m, 2H) 6.31 (d, J=7.15 Hz, 1H) 6.39 (d, J=1.10 Hz, 1H) 7.02 (dd, J=7.06, 1.01 Hz, 1H).

(252) .sup.13C NMR (151 MHz, CHLOROFORM-d) ppm 11.54, 18.33, 20.61, 20.70, 21.02, 21.86, 28.57, 29.57, 29.85, 30.52, 30.82, 31.55, 32.65, 33.67, 34.70, 36.34, 38.20, 39.24, 40.37, 42.30, 44.27, 45.07, 51.54, 60.81, 66.90, 69.09, 70.49, 70.84, 100.37, 117.93, 123.33, 126.92, 134.32, 134.96, 145.71, 162.50, 170.07, 170.33, 170.35, 170.37, 170.61, 178.68, 179.14.

EXAMPLE 39. PREPARATION OF COMPOUND XS0534

(253) ##STR00080##

(254) XS0077 (150 mg, 0.32 mmol) was weighed and dissolved in 4 mL of acetone with stirring, anhydrous potassium carbonate (180 mg, 1.3 mmol) and dimethyl sulfate (95 L, 0.96 mmol) were added under stirring, the mixture was reacted under oil bath at 70 C. for 12 h. The reaction was quenched with 1 mol/L HCl, then adjusted to pH=7, and extracted with ethyl acetate three times. The organic phases were combined, dried over Na.sub.2SO.sub.4, concentrated to remove solvent under reduced pressure, and separated and purified by silica gel column chromatography with ethyl acetate:n-hexane=1:10 system to afford a white solid, yield 24.3%.

(255) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.51 (s, 3H) 0.87-0.92 (m, 1H) 1.06 (s, 3H) 1.12 (s, 3H) 1.18 (s, 3H) 1.27 (s, 3H) 1.32-1.37 (m, 1H) 1.37-1.42 (m, 1H) 1.47-1.52 (m, 3H) 1.55-1.61 (m, 2H) 1.65 (dd, J=15.68, 8.16 Hz, 1H) 1.80 (td, J=13.43, 7.24 Hz, 1H) 1.84-1.90 (m, 1H) 1.97 (td, J=13.75, 4.03 Hz, 1H) 2.02 (s, 3H) 2.06 (d, J=13.57 Hz, 1H) 2.12-2.18 (m, 1H) 2.33 (d, J=15.77 Hz, 1H) 2.95 (dd, J=20.17, 1.40 Hz, 1H) 3.21 (dd, J=20.72, 6.24 Hz, 1H) 3.46-3.50 (m, 3H) 3.77 (s, 3H) 5.72 (dd, J=6.42, 1.28 Hz, 1H) 6.72 (s, 1H) 8.10 (s, 1H).

(256) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 11.35, 17.69, 22.41, 27.31, 28.41, 29.42, 29.90, 30.13, 30.25, 31.36, 32.37, 34.01, 34.21, 34.36, 36.41, 36.49, 37.11, 39.85, 43.23, 43.80, 51.37, 55.82, 105.29, 117.48, 119.79, 124.58, 139.03, 141.52, 145.83, 148.73, 178.04.

EXAMPLE 41. PREPARATION OF COMPOUND XS0420

(257) ##STR00081##

(258) Compound YXY101 (50 mg, 0.11 mmol) was weighed in a 50 ml round bottom flask, PTSA (100 mg, excess) and 2 mL of toluene were added, and the mixture was stirred at room temperature for 6 h quenched by saturated NaHCO.sub.3 solution, and extracted with ethyl acetate three times. The organic phases were combined, dried with anhydrous Na.sub.2SO.sub.4, concentrated under reduced pressure to remove solvent, and separated and purified by silica gel column chromatography with ethyl acetate:n-hexane=1:4 system to afford an off-white solid in 70% yield.

(259) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 1.03 (s, 3H) 1.06 (s, 3H) 1.07-1.11 (m, 1H) 1.15 (s, 3H) 1.18 (s, 3H) 1.21-1.24 (m, 1H) 1.28-1.32 (m, 1H) 1.37 (td, J=13.75, 5.32 Hz, 1H) 1.46 (dd, J=8.62, 4.03 Hz, 2H) 1.48-1.50 (m, 2H) 1.51-1.55 (m, 1H) 1.58 (dd, J=12.93, 1.93 Hz, 1H) 1.83-1.90 (m, 3H) 2.33 (t, J=1.00 Hz, 1H) 2.36 (s, 3H) 2.38 (s, 3H) 2.80-2.92 (m, 2H) 2.80-2.92 (m, 2H) 7.06 (d, J=8.62 Hz, 1H) 7.18 (s, 1H) 7.49 (d, J=8.44 Hz, 1H) 8.48 (br. s., 1H) 9.92 (s, 1H).

(260) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 10.96, 19.45, 21.73, 21.95, 23.51, 24.03, 25.45, 30.89, 30.96, 34.59, 35.08, 36.41, 37.98, 38.30, 40.71, 41.70, 43.50, 99.01, 102.91, 115.74, 120.73, 126.07, 127.17, 127.30, 129.03, 132.36, 143.60, 146.12, 175.68.

EXAMPLE 42. PREPARATION OF COMPOUND XS0502

(261) ##STR00082##

(262) Compound XS0077 (50 mg, 0.11 mmol) was weighed in a 50 ml round bottom flask, SeO.sub.2 (200 mg, excess) and 2 mL of dioxane were added, and the mixture was stirred at 55 C. for 12 hours. The reaction was quenched by the addition of deionized water, extracted with ethyl acetate for 3 times. The organic phases were dried over Na.sub.2SO.sub.4, concentrated to remove solvent under reduced pressure, and separated and purified by silica gel column chromatography with ethyl acetate:n-hexane=1:10 system to give an off-white solid, yield 16.8%.

(263) .sup.1H NMR (600 MHz, DMSO-d.sub.6) ppm 0.75 (s, 3H) 0.93-0.97 (m, 1H) 1.10 (s, 3H) 1.21 (s, 3H) 1.22 (s, 3H) 1.40 (td, J=14.08, 4.13 Hz, 1H) 1.49 (dt, J=14.53, 4.65 Hz, 1H) 1.71-1.79 (m, 2H) 1.79-1.82 (m, 1H) 1.82-1.88 (m, 1H) 2.07-2.10 (m, 1H) 2.10-2.12 (m, 1H) 2.13 (s, 3H) 2.29 (d, J=14.31 Hz, 1H) 2.46 (t, J=4.77 Hz, 1H) 2.54 (s, 3H) 3.50 (s, 3H) 6.20 (d, J=9.54 Hz, 1H) 6.45 (d, J=9.54 Hz, 1H) 7.11 (s, 1H) 9.44 (s, 1H).

(264) .sup.13C NMR (151 MHz, DMSO-d.sub.6) ppm 11.88, 17.45, 19.70, 21.88, 26.78, 29.04, 30.34, 30.42, 30.47, 31.02, 34.19, 36.47, 40.05, 40.43, 41.84, 46.15, 51.58, 122.97, 125.72, 125.78, 129.24, 136.20, 139.22, 142.11, 142.43, 144.61, 146.30, 176.92, 178.25, 181.38.

(265) Although the embodiments of the present invention have been described in detail, according to the disclosed teaching, various modifications and alternations can be made to the details of the embodiments of the present invention, which are within the scope of the present invention. The scope of the invention is defined by the appended claims and any equivalents thereof.