HETEROCYCLES

Note | Special issue | Vol. 79, No. 1, 2009, pp. 1093-1100
Received, 3rd October, 2008, Accepted, 28th November, 2008, Published online, 4th December, 2008.
DOI: 10.3987/COM-08-S(D)61

■ Syntheses and Evaluation as Glycosidase Inhibitor of 1,5-Dideoxy-1,5-imino-D-glucitol Analogs of Salacinol, a Potent α-Glucosidase Inhibitor Isolated from Ayurvedic Medicine, Salacia reticulata

Genzoh Tanabe, Takanori Hatanaka, Toshie Minematsu, Hisashi Matsuda, Masayuki Yoshikawa, and Osamu Muraoka*

Faculty of Pharmaceutical Sciences, Kinki University, 3-4-1, Kowakae, Higashi-Osaka 577-8502, Japan

Abstract

N-Alkylated deoxynojirimycin (10) bearing the same alkyl chain as salacinol (1), a potent α-glucosidase inhibitor isolated from Ayurvedic traditional medicine, Salacia reticulata, was found to inhibit both rat intestinal maltase and sucrase as strong as 1, while 10 has been reported to be inactive against glucoamylase G2 from Aspergillus niger. Its O-desulfate (12) was also found active against these enzymes, and characteristic sulfate anion moiety of 1 was found not essential for the α-glucosidase inhibitory activity.

INTRODUCTION
In 1997 the authors isolated a potent α-glucosidase inhibitor salacinol (1) from Ayurvedic traditional medicine, Salacia reticulata1,2 which has been used for the treatment of diabetes in Sri Lanka and India. The structure of 1 established by the X-ray crystallographic analysis was quite unique, the ring sulfonium ion being stabilized by the sulfate counter anion by forming a spirobicyclic-like configuration comprised of 1-deoxy-4-thio-D-arabinofranosyl cation and 1-deoxy-L-erythrosyl-3-sulfate anion. Several related sulfonium sulfates, kotalanol (2), ponkolanol (3) and salaprinol (4) have been subsequently isolated from the same Salacia species of plant.3–5 The α-glucosidase inhibitory activities of 1-3 are potent, and have been revealed to be as strong as those of voglibose and acarbose, which are widely used clinically these days.1-4 Owing to both the high inhibitory activity and the intriguing structure, much attention has been focused on such sulfonium sulfate inner salts, intensive studies on the structure-activity relationships (SAR) based on their structure having been reported.6-16 On the other hand, a large number of glycosidase inhibitors are based on azasugar derivatives with either five- or six-membered ring structures.17,18 Among them, an azasugar (5) and deoxynojirimycin (6) were the representatives, and two derivatives of deoxynojirimycin namely miglitol (7) and N-butyldeoxynojirimycin (8) are currently in use as drugs for the treatment of Type II diabetes and Gaucher’s disease, respectively.17,18 On the basis of these background, the activity of N-alkylated analog of 5 with the same L-erythritol-type side chain (9) as salacinol had been tested independently by the authors6,7 and by Ghavami and co-workers,8,9,10 but 9 and related compounds were revealed inactive against α-glucosidases. By the intensive SAR studies by Szczepina and co-workers,13 deoxynojirimycin N-alkylate (10) was also found inactive against glucoamylase G2 from Aspergillus niger.
In this paper, we present our own results on the inhibitory activity of 10 against rat intestinal α-glucosidases. As the O-sulfate anion moiety of 1 has been found not essential for the inhibitory activity by our recent findings on salacinol de-O-sulfate11 (11), the activity of its de-O-sulfate (12) was also examined. Against the rat intestinal maltase and sucrase, both 10 and 12 showed almost nearly equal inhibitory activity to salacinol (1).

RESULTS AND DISCUSSION
Syntheses of Ammonium Analogs (10 and 12)
Deoxynojirimycin (6) was prepared starting from a bis-epoxide, 1,2:5,6-dianhydro-3,4-di-O-benzyl-L- iditol (13) according to the literature.19,20 Thus, treatment of 13 with benzyl amine gave N-benzyl-3,4- di-O-benzyl-1,5-dideoxy-1,5-imino-D-glucitol19 (14) and N-benzyl-3,4-di-O-benzyl-1,6-dideoxy-1,6- imino-D-iditol19 (15) in 43% and 36% yield, respectively. Hydrogenolysis of 14 on Pd-C in acetic acid gave deoxynojirimycine19,21-26 (6) quantitatively. Without protection of the hydroxy groups, selective N-alkylation of 6 proceeded successfully by the treatment with a cyclic sulfate11 16 to give 1,5-dideoxy- 1,5-{N-[(2S,3S)-2,4-O-isopropylidene-3-(sulfooxy)butyl]iminoonium}-D-glucitol inner salt (17) in 75% yield. Compound 17 showed quasi-molecular ion peaks at m/z 388 and 386 due to [M+H]+ and [M–H]–, respectively, in its FAB mass spectrum. Its IR spectrum showed absorptions at 3359 cm-1 (-OH), 2527 cm-1 (-N+H) and also at 1261 and 1223 cm-1 (-OSO3– ). The relative stereochemistry of the side chain was determined to be α-orientation in the present study on the basis of NOE studies, correlations between one of the methylene protons on C-1’ and the methine proton on C-5 being detected. Acetal moiety of 17 was then removed using 0.5% hydrochloric acid at room temperature to give the desired ammonium sulfate, 1,5-dideoxy-1,5-{N-[(2S,3S)-2,4-dihydroxy-3-(sulfooxy)butyl]iminoonium}-D-glucitol inner salt (10). Finally, de-O-sulfation of 10 by action of methanolic hydrogen chloride gave 1,5-dideoxy-1,5- {N-[(2S,3S)-2,4-dihydroxybutyl]imino}-D-glucitol hydrogen chloride (12) in 84% yield. Reasonable upfield-shift of the signal due to 3’-methine carbon was observed in its 13C NMR spectrum upon the hydrolysis. The α-orientation of the N-alkyl chain in 12 was also confirmed by the NOE correlations as depicted in Scheme 1.

α-Glucosidase Inhibitory Activity
The glucosidase inhibitory activities of 10 and 12 were tested for rat intestinal α-glucosidases in vitro, and compared with those of salacinol (1) and its de-O-sulfate (11), as shown in Table 1. To these enzymes, the inhibitory activities of 10 were still potent, and IC50 values against maltase and sucrase were 8.8 μM and 2.5 μM, respectively. It is noteworthy that 10 exhibit such selectivity toward enzymes, because 10 was reported to be inactive against glucoamylase G2 from Aspergillus niger.13 Although de-O-sulfation of 10 resulted in slight decrease in inhibition against maltase, 12 still maintained the activity against sucrase to the same extent as 10. Thus, present result revealed that N-alkylated ammonium salts with 6-membered ring structure (10 and 12) also function as sugar mimics against rat intestinal α-glucosidases. The sulfate anion moiety, which is characteristic of a series of salacinol and related analogs (1–4), seems to be not essential for the potent inhibitory activity on the basis of both our present and previous findings. Further investigations on the origin of both the strong α-glucosidase inhibitory activity and enzyme-selectivity of 1 and related compounds are in progress.

EXPERIMENTAL
Mps were determined on a Yanagimoto MP-3S micromelting point apparatus, and mps and bps are uncorrected. IR spectra were measured on either a Shimadzu IR-435 grating spectrophotometer or a Shimadzu FTIR-8600PC spectrophotometer. NMR spectra were recorded on a JEOL JNM-ECA 500 (500 MHz 1H, 125 MHz 13C) or a JEOL JNM-ECA 700 (700 MHz 1H, 175 MHz 13C) spectrometer. Chemical shifts (δ) and coupling constants (J) are given in ppm and Hz, respectively. Low-resolution and high-resolution mass spectra were recorded on a JEOL JMS-HX 100 spectrometer. Optical rotations were determined with a JASCODIP-370 digital polarimeter. Column chromatography was effected over Fuji Silysia Chemical silica gel BW-200. All the organic extracts were dried over anhydrous sodium sulfate prior to evaporation.

Aminocyclization of Bis-epoxide 13
According to the literature,19 a mixture of bis-epoxide 13 (4.02 g, 12.3 mmol), BnNH2 (6.8 mL, 62.3
mmol), and CHCl3 (60 mL) was heated under reflux for 42 h. Work-up gave a pale yellow oil (11.2 g), which on column chromatography (n-hexane–AcOEt, 3:1) gave N-benzyl-3,4-di-O-benzyl-1,5- dideoxy-1,5-imino-D-glucitol (14, 2.3 g, 43%) and N-benzyl-3,4-di-O-benzyl-1,6-dideoxy-1,6-imino-L- iditol (15, 1.9 g, 36%).
14: colorless needles (from n-hexane–AcOEt). Mp 107.5–109 °C (lit.,19 109 °C). [α]D24 +6.0 (c 1.06, CHCl3) [lit.,19 +4 (c 1.1, CHCl3)]. 1H NMR (500 MHz, CDCl3) δ: 1.82 (1H, br s, OH), 2.17 (dd, J = 11.5, 9.8, H-1ax), 2.35 (1H, br, s, OH), 2.47 (ddd J = 8.6, 3.2, 1.5, H-5), 3.06 (dd, J = 11.5, 4.5, H-1eq), 3.39/4.07 (each d, J = 13.5 Hz, PhCH2N), 3.40 (dd, J = 8.6, 8.6, H-3), 3.64 (ddd, J = 9.8, 8.6, 4.5, H-2), 3.71 (dd, J = 8.6, 8.6, H-4), 3.88 (dd, J = 12.0, 1.5, H-6a), 4.02 (dd, J = 12.0, 3.2, H-6b), 4.72/4.90 (each 1H, d, J = 11.1 Hz, PhCH2O), 4.73/4.92 (each 1H, d, J = 11.8 Hz, PhCH2O), 7.25–7.38 (15H, m, arom.).
Assignments for the H-1ax and H-1ex, and those for one of the methylene protons in the N-benzyl moiety and H-6a in the literature19 were interchanged, and revised in the present study on the basis of 500 MHz 1H-NMR measurements.
15: colorless needles (from n-hexane–AcOEt). Mp 74.5–75.4 °C (lit.,19 77 °C). [α]D24 +14.8 (c 1.13, CHCl3) [lit.,19 +15 (c 1.6, CHCl3)]. 1H and 13C NMR spectroscopic properties of 15 were in good accordance with those reported.19

Deoxynojirimycin (6)
A suspension of 10% palladium-on-carbon (1.0g) in AcOH (6 mL) was pre-equilibrated with hydrogen. To the suspension was added 14 (1.74 g, 4.0 mmol), and the mixture was hydrogenated at rt for 19 h. The catalyst was filtered off, and the filtrate was evaporated. The remaining AcOH was then co-evaporated with benzene to give a pale yellow oil (1.01 g). The aqueous solution (15 mL) of the oil was treated with ion exchange resin IR120B. After filtration of the resulting mixture, the resin was washed with MeOH, and rinsed out with 5% aqueous ammonia. The rinsing was evaporated to give the title compound19,21–26 6 (641 mg, 98%) as a colorless solid, mp 194–195 °C (lit.,19 194–196 °C; lit.,21 199–199.5 °C; lit.,23 199–201 °C). [α]D22 +41.6 (c 1.29, H2O) [lit.,19 +46 (c 0.9, H2O); lit.,21 +40.3 (c 1.47, H2O); lit.,23 +42.0 (c 0.1, H2O)]. 1H NMR (500 MHz, D2O) δ: 2.43 (1H, dd, J = 12.3, 10.6 Hz, H-1ax), 2.51 (ddd, J = 9.6, 6.3, 3.2 Hz, H-5), 3.08 (dd, J = 12.3, 5.2 Hz, H-1eq), 3.20 (dd, J = 9.6, 9.2 Hz, H-4), 3.28 (dd, J = 9.2, 9.2 Hz, H-3), 3.46 (ddd, J = 10.6, 9.2, 5.2 Hz, H-5), 3.59 (dd, J = 11.8, 6.3 Hz, H-6a), 3.79 (dd, J = 11.8, 3.2 Hz, H-6b). 13C NMR (125 MHz, CDCl3) δ: 51.3 (C-1), 63.1 (C-5), 63.9 (C-6), 73.5 (C-2), 74.1 (C-4), 81.0 (C-3).
Coupling Reaction between the Cyclic Sulfates (16) and Deoxynojirimycin (6)
A mixture of deoxynojirimycin (6, 500 mg, 3.06 mmol), cyclic sulfate11 (16, 824 mg, 3.67 mmol), Na2CO3 (705 mg, 6.65 mmol), and DMF (1 mL) was stirred at 45 °C for 24 h. After dilution of the reaction mixture with MeOH, the resulting mixture was filtered, and the filtrate was concentrated at reduced pressure to give a pale yellow oil (1.16 g), which on column chromatography (CHCl3–MeOH–H2O, 9:5:1) gave 1,5-dideoxy-1,5-{N-[(2S,3S)-2,4-O-isopropylidene-3-(sulfooxy)butyl]- iminoonium}-D-glucitol inner salt (17, 890 mg, 75%) as a colorless oil, [α]D24 +52.5 (c 0.5, MeOH). IR (neat): 3359, 2527, 1651, 1384, 1261, 1223, 1070, 1015 cm-1. 1H NMR (700 MHz, CD3OD) δ: 1.33/1.49 [each 3H, s, (CH3)2C]), 2.46 (1H, br d-like, J = ca. 9.5 Hz, H-5), 2.49 (1H, br dd-like, J = ca. 10.9, 10.9 Hz, H-1ax), 2.90 (1H, dd, J = 15.0, 8.0 Hz, H-1’a), 3.18 (1H, dd, J = 9.2, 9.2 Hz, H-3), 3.20 (1H, dd, J = 10.9, 4.9 Hz, H-1eq), 3.38 (1H, br d, J = 15.0 Hz, H-1’b), 3.43 (1H, dd, J = 9.5, 9.2 Hz, H-4), 3.55 (1H, ddd, J = 10.9, 9.2, 4.9 Hz, H-2), 3.85 (1H, dd, J = 11.6, 7.2 Hz, H-4’a), 3.89 (1H, dd, J = 12.0, 2.4 Hz, H-6a), 4.02 (1H, dd, J = 12.0, 3.0 Hz, H-6b), 4.05 (1H, ddd, J = 8.8, 7.2, 5.3, H-3’), 4.09 (1H, br dd, J = 8.8, 8.0 Hz, H-2’), 4.10 (1H, dd, J = 11.6, 5.3 Hz, H-4’b). 13C NMR (125 MHz, CD3OD) δ: 20.3/28.0 [(CH3)2C], 54.2 (C-1’), 58.06 (C-6), 58.12 (C-1), 63.8 (C-4’), 67.7 (C-5), 69.9 (C-2), 70.5 (C-2’), 71.1 (C-4), 72.2 (C-3’), 80.0 (C-3), 100.5 [(CH3)2C]. FABMS m/z: (pos.) 388 [M+H]+. FAB-HR-MS m/z: 388.1277 (C13H26O10NS requires 388.1278).

1,5-Dideoxy-1,5-{N-[(2S,3S)-2,4-dihydroxy-3-(sulfooxy)butyl]iminoonium}-D-glucitol Inner Salt (10)
A solution of 17 (600 mg, 1.55 mmol) and 0.5% hydrochloric acid (8 mL) was stirred at rt for 2.5 h. After removal of the solvent at reduced pressure, the residue (540 mg) was purified on column chromatography (MeCN–H2O, 3:1) to give the title compound 10 (414 mg, 77%) as a colorless oil, [α]D23 +9.2 (c 1.55, MeOH). IR (neat): 3344, 2511, 1651, 1268, 1219, 1069 cm–1. 1H NMR (700 MHz, CD3OD) δ: 2.44 (1H, br dd-like, J = ca. 9.7, 9.7 Hz, H-1ax), 2.51 (1H, br, H-5), 2.76 (1H, br dd-like, J = ca. 14.0, 9.0 Hz, H-1’a), 3.21 (1H, dd, J = 9.2, 9.2 Hz, H-3), 3.22 (1H, br-d like, J = ca. 9.7 Hz, H-1eq), 3.26 (1H, m, H-1’b), 3.38 (1H, dd, J = 9.2, 9.2 Hz, H-4), 3.58 (1H, ddd, J = 9.7, 9.2, 4.8 Hz, H-2), 3.81 (1H, dd, J = 12.0, 4.4 Hz, H-4’a), 3.86 (1H, dd, J = 12.0, 3.6 Hz, H-6a), 3.92 (1H, dd, J = 12.0, 4.0 Hz, H-4’b), 3.99 (1H, dd, J = 12.0, 2.4 Hz, H-6b), 4.13 (1H, br ddd, J = ca. 9.0 4.0, 4.0 Hz, H-2’), 4.28 (1H, ddd-like, J = 4.4, 4.0, 4.0 Hz, H-3’). 13C NMR (175 MHz, CD3OD) δ: 55.4 (C-1’), 58.1 (C-1), 59.1 (C-6), 62.1 (C-4’), 68.4 (C-5), 69.5 (C-2’), 69.8 (C-2), 71.4 (C-4), 80.0 (C-3), 82.0 (C-3’). FABMS m/z: (pos.) 348 [M+H]+, (neg.) 346 [M–H]–. FAB-HR-MS m/z: 348.0964 (C10H22O10NS requires 348.0965).

1,5-Dideoxy-1,5-{N-[(2S,3S)-2,3,4-trihydroxybutyl]imino}-D-glucitol Hydrogen Chloride (12)
A mixture of 10 (150 mg, 0.43 mmol) and 5% methanolic hydrogen chloride (7 mL) was stirred at rt for 1.5 h. After removal of the solvent at reduced pressure, the residue (128 mg) was purified on column chromatography (CHCl3–MeOH–H2O, 12:8:1) to give the title compound 12 (110 mg, 84%) as a colorless oil, [α]D24 +2.8 (c 0.75, MeOH). IR (neat): 3283, 2492, 1651, 1080, 1034 cm-1. 1H NMR (500MHz, CD3OD) δ: 2.246 (1H, dd, J = 11.2, 10.4, H-1ax), 2.250 (1H, ddd, J = 9.2, 3.7, 2.6, H-5), 2.54 (1H, dd, J = 13.7, 6.3 Hz, H-1’a), 3.15 (1H, dd, J = 11.2, 4.9 Hz, H-1eq), 3.158 (1H, dd, J = 9.2, 9.2 Hz, H-3), 3.162 (1H, dd, J = 13.7, 6.1 Hz, H-1’b), 3.31 (1H, dd, J = 9.2, 9.2 Hz, H-4), 3.48 (1H, ddd, J = 10.4, 9.2, 4.9 Hz, H-2), 3.57 (1H, ddd, J = 6.0, 5.4, 3.8 Hz, H-3’), 3.62 (1H, dd, J = 11.2, 5.4 Hz, H-4’a), 3.72 (1H, dd, J = 11.2, 3.8 Hz, H-4’b), 3.77 (1H, ddd-like, J = 6.3, 6.1, 6.0, H-2’), 3.84 (1H, dd, J = 12.3, 3.7 Hz, H-6a), 3.98 (1H, dd, J = 12.3, 2.6 Hz, H-6b). 13C NMR (125 MHz, CD3OD) δ: 55.7 (C-1’), 58.9 (C-1), 59.5 (C-6), 64.7 (C-4’), 68.6 (C-5), 70.28/70.33 (C-2, C-2’), 71.8 (C-4), 76.3 (C-3’), 80.5 (C-3). FABMS m/z: (pos.) 268 [M]+. FAB-HR-MS m/z: 268.1381 (C10H22O7N requires 268.1396).

Enzyme inhibition Assays
Rat small intestinal brush border membrane vesicles were prepared and its suspension in 0.1 M maleate buffer (pH 6.0) was used as small intestinal α-glucosidase of maltase and sucrase. Test compound was dissolved in dimethylsulfoxide DMSO, and the resulting solution was diluted with 0.1 M maleate buffer to prepare the test compound solution (concentration of DMSO: 10%). The substrate solution in the maleate buffer (maltose: 74 mM, sucrose: 74 mM, 100 μL), test compound solution (50 μL), and the enzyme solution (50 μL) were mixed and incubated at 37 °C for 30 min. After incubation, the solution was mixed with water (0.8 mL) and was immediately heated by boiling water for 2 min to stop the reaction. Glucose concentration was then determined by the glucose-oxidase method. Final concentration of DMSO in test solution was 2.5% and no influence of DMSO was detected on the inhibitory activity.

ACKNOWLEDGEMENTS
This work was supported by “High-Tech Research Center” Project for Private Universities: matching fund subsidy from MEXT (Ministry of Education, Culture, Sports. Science and Technology), 2007–2011.

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