Table 5.
Pentasaccharides.
Study | Compound | Assays* | Activity | Lit. no.‡ | Ref. |
---|---|---|---|---|---|
Martin-Lomas (2000) |
IG-41 | Lipogenesis PDH phosphatase cAMP-dependent protein kinase |
Inactive | 1a | [36] |
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Misek (1992) | IG-42 | Lipolysis | 70% inhibition at 132 μM, IC50= 60 μM |
VSG-IPG | [4] |
Glucose-6-phosphatase activity | 90% inhibitionat 160 μM, IC50 = 109 μM |
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Fructose-1,6-bisphosphatase activity | 100% inhibition at 226 μM, IC50= 136 μM. |
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Gluconeogenesis | 67% inhibitionat 102 μM, IC50= 84 μM |
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Misek (1992) | Protein phosphorylation/ dephosphorylation |
Blocked IPT-dependent phosphorylation at 200 μM ~ 90% dephosphorylation at 150 μM, IC50 = 75 μM |
VSG-IPG | [4] | |
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Frick (1998) | IG-43 | Lipogenesis | Activity‘A’§ | 20 | [45] |
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Frick (1998) | IG-44 | Lipogenesis | Activity‘C’§ | 29 | [45] |
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Frick (1998) | IG-45 | Lipogenesis | Activity‘B’§ | 23 | [45] |
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Frick (1998) | IG-46 | Lipogenesis | Activity‘C’§ | 13 | [45] |
Frick (1999) | 44% MIR, EC50 = 40 μM | Q | [101] | ||
Glucose transport | 18% MIR, EC50 = 30 μM |
Details of assays (in alphabetical order) are given in the text.
The number assigned to this compound in the cited publication.
Note: for Muller’s SAR study [45] aggregate activities were reported as follows: “A”, MIR < 20%; “B”, MIR 20–49%, EC20 25–200 μM; “C”, MIR 50–80%, EC50 10–100 μM; “D”, MIR > 80%, EC50 3–30 μM.
IPG: Inositol phosphate-glycan; Lit. no.: Literacy number; MIR: Maximal insulin response.