Deoxygalactonojirimycin derivatives

Organic compounds -- part of the class 532-570 series – Organic compounds – Carbohydrates or derivatives

Reexamination Certificate

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C536S004100

Reexamination Certificate

active

06291657

ABSTRACT:

BACKGROUND OF THE INVENTION
This invention relates to novel N-alkyl derivatives of deoxygalactonojirimycin (DGJ) in which said alkyl groups contain from 3-6 carbon atoms. These novel compounds are useful for selectively inhibiting glycolipid synthesis.
In applicants' copending application Ser. No. 08/061,645, filed May 13, 1993, now U.S. Pat. No. 5,399,567 certain N-alkyl derivatives of deoxynojirimycin (DNJ) are disclosed as effective inhibitors of glycolipid biosynthesis. N-alkylated derivatives of DNJ were also previously known to be inhibitors of the N-linked oligosaccharide processing enzymes, &agr;-glucosidase I and II. Saunier et al.,
J. Biol. Chem
. 257, 14155-14166 (1982); Elbein,
Ann. Rev. Biochem
. 56, 497-534 (1987). As glucose analogues, they also have potential to inhibit glucosyltransferases. Newbrun et al.,
Arch. Oral Biol
. 28, 516-536 (1983); Wang et al.,
Tetrahedron Lett
. 34, 403-406 (1993). Their inhibitory activity against the glucosidases has led to the development of these compounds as antihyperglycemic agents and antiviral agents. See, e.g., PCT Int'l. Appln. WO 87/03903 and U.S. Pat. Nos.: 4,065,562; 4,182,767; 4,533,668; 4,639,436; 4,849,430; 5,011,829; and 5,030,638.
BRIEF DESCRIPTION OF THE INVENTION
In accordance with the present invention, novel N-alkyl derivatives of deoxygalactonojirimycin (DGJ) are provided in which said alkyl contains from 3-6 carbon atoms and preferably from 4-6 carbon atoms. These novel compounds are useful for selectively inhibiting glycolipid synthesis. The length of the N-alkyl chain has been found to be important to said inhibitory activity since the non-alkylated DGJ and the N-methyl and N-ethyl derivatives of DGJ were each found to be inactive for such inhibition. The N-propyl derivative of DGJ was partially active. Thus, a minimum alkyl chain length of 3 carbon atoms has been found to be essential for efficacy.
The biosynthesis of glycolipids in cells capable of producing glycolipids can be selectively inhibited by treating said cells with a glycolipid inhibitory effective amount of an N-alkyl derivative of DGJ of the present invention. These inhibitory compounds can be used at concentrations of about 10-fold less than the effective antiviral concentrations of the corresponding N-alkyl derivatives of DNJ. Illustratively, the N-butyl DGJ is inhibitory of glycolipid biosynthesis at relatively low concentration of about 50 &mgr;M compared to the 0.5 mM level of concentration of N-butyl DNJ in cell culture systems for &agr;-glucosidase I inhibition (Karlsson et al.,
J. Biol. Chem
. 268, 570-576 (1993).
The active N-alkyl derivatives of DGJ have a significant advantage since, unlike the previously described N-alkyl derivatives of DNJ, they selectively inhibit biosynthesis of glycolipids without effect either on the maturation of N-linked oligosaccharides or lysosomal glucocerebrosidase. For example, in contrast to N-butyl DNJ, the N-butyl DGJ of the present invention surprisingly does not inhibit the processing &agr;-glucosidases I and II or lysosomal &bgr;-glucocerobrosidase. Likewise, the only prior reported experimental evidence using deoxygalactonojirimycin indicates that N-alkylation (N-heptyldeoxygalactonojirimycin) provides a modest increase in the affinity towards certain &bgr;-glucosidases [Legler & Pohl, Carb. Res. 155, 119 (1986)]. The inhibitory results described herein for the novel N-alkylated deoxygalactonojirimycin analogues in which the alkyl contains from 3 to 6 carbon atoms were unexpected in view of the corresponding activity of related iminosugar compounds.
Further uniqueness of the present invention is seen by the finding that the exemplary N-butyl and N-hexyl derivatives of DGJ completely prevented glycolipid biosynthesis, whereas the N-butyl derivatives of mannose, fucose and N-acetylglucosamine were without effect on glycolipid biosynthesis.
The inhibitory effect of these compounds on the biosynthesis of glycolipids is illustrated herein in the myeloid cell line HL-60 and in the lymphoid cell line H9. These are well-known, widely distributed and readily available human cell lines. For example, HL-60 cells are promyelocitic cells described by Collins et al.,
Nature
270, 347-349 (1977). They are also readily available from the American Type Culture Collection, Rockville, Md, U.S.A., under accession number ATCC CCL 240. H9 cells are of lymphoid origin described by Gallo and Popovic,
Science
224, 497-500 (1984). They are also readily available from the same depository under accession number ATCC HTB 176.
The inhibition of glycolipid biosynthesis by these N-alkyl derivatives of DGJ is further demonstrated herein by the reduction of the binding of cholera toxin to the illustrative cell line H9 when cultured in the presence on N-butyl DGJ. These compounds thus are also useful as anti-microbial agents by inhibiting the and bacterial toxins as illustrated hereinafter in Tables 1 and 2, respectively.
The inhibitory effect upon the biosynthesis of glycolipids is further illustrated by the ability of the N-butyl and N-hexyl derivatives of DGJ to offset glucoceramide accumulation in a standard, state-of-the-art in vitro model of Gaucher's disease. In this model, the murine macrophage cell line WEHI-3B was cultured in the presence of an irreversible glucocerebrosidase inhibitor, conduritol &bgr; epoxide (CBE), to mimic the inherited disorder found in Gaucher's disease. WEHI-3B cells are well-known, widely distributed and readily available murine macrophage cells. They are described in
Cancer Res
. 37, 546-550 (1977), and are readily available from the American Type Culture Collection, Rockville, Md, under accession number ATCC TIB 68. The compounds of the invention prevent lysosomal glycolipid storage which is useful for the management of Gaucher's disease and other glycolipid storage disorders as illustrated hereinafter in Table 3. Gaucher's disease is an autosomal recessive disorder characterized by an impaired ability to degrade glucocerebroside (glucosyl ceramide, Glc-Cer) due to mutations in the gene encoding &bgr;-glucocerebrosidase (&bgr;-D-glucosyl-N-acylsphingosine glucohydrolase, EC 3.2.1.45). This defect results in the lysosomal accumulation of Glc-Cer in cells of the macrophage-monocyte system [Barranger and Ginns, in
The Metabolic Basis of Inherited Diseases
, ed. Scriver et al., pp. 1677-1698, McGraw-Hill, New York, (1989); Beutler,
Science
256, 794-799 (1992)]. By slowing the rate of glycolipid synthesis, the impaired catabolism of Glc-Cer can be offset, thereby leading to the maintenance of a balanced level of Glc-Cer.
The clinical management of Gaucher's disease currently relies upon either symptomatic treatment of patients or enzyme replacement therapy [Beutler,
Proc. Natl. Acad. Sci. USA
90, 5384-5390 (1993)]. In view of the prohibitive cost of enzyme replacement therapy and the requirement for intravenous administration of glucocerebrosidase, an orally available alternative therapy based around substrate deprivation constitutes a useful alternative. The N-alkyl derivatives of DGJ are water-soluble sugar analogs and, therefore, orally active. Since the N-alkyl DGJ compounds exhibit fewer complicating enzyme inhibitory characteristics than &agr;-and &bgr;-glucosidase inhibitors, they also constitute a preferable alternative to the N-alkyl DNJ compounds for therapeutic management of Gaucher's disease and other glycolipid storage disorders. The N-alkyl DGJ may also be used in combination with glucocerebrosidase for the treatment of Gaucher's disease.


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patent: 4533668 (1985-08-01), Matsumara et al.
patent: 4639436 (1987-01-01), Junge et al.
patent: 4849430 (1989-07-01), Fleet et al.
patent: 5011829 (1991-04-01), Hirsch
patent: 5030638 (1991-07-01), Partis et al.
patent: 5128347 (1992-07-01), Getman
patent: 536402 (1993-04-01), None
patent: 8703903 (1987-07-01), None
Merck Manual, p 106-108, 978-979 1982.*
Chem

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