GDP

GDP-α-D-mannose disodium gives a competitive inhibition with respect to GTP (Ki 14.7 μM) and an uncompetitive inhibition with respect to mannose-1-P (Ki 115 μM).GDP-α-D-mannose disodium is the donor substrate for mannosyltransferases and the precursor of

GDP-D-mannose disodium is a natural product for research related to life sciences and the catalog number is T65209.

Guanosine 5'-diphosphate (GDP) as Potential Iron Mobilizer, Preventing the Hepcidin-Ferroportin Interaction and Modulating the Interleukin-6 Stat-3 Pathway.

GDP-L-fucose is a nucleotide sugar widely found in fungi and plants, playing a role in both the slave and secondary remedial metabolic pathways.

GDP-L-fucose disodium, a nucleotide sugar, serves as a crucial substrate for fucose oligosaccharides biosynthesis by providing the fucose moiety. Its formation follows two metabolic pathways: the primary de novo pathway and the secondary remedial pathway [1].

6-T-GDP (6-Thioguanosine 5'-diphosphate) is a metabolite of thiopurine. It inhibits the activity of Rac1, thereby reducing the transcription of inflammatory factors and the expression of cell adhesion molecules, which ultimately suppresses leukocyte migration and the occurrence of tissue inflammation.

GDP-D-Rha6F2 is an inhibitor of GMDS (GDP-mannose-4,6-dehydratase), binding to the active site of GMDS. It effectively inhibits the conversion of GDP-mannose.

GDP366, a dual inhibitor of survivin and Op18, induces cell growth inhibition, cellular senescence, and mitotic catastrophe in human cancer cells.

Sp-GDPαS acts as a regulator for GDP-binding proteins and exhibits greater metabolic stability than GTP.

Gdpflrfamide is a neuropeptide that existed in the snail Lymnaea stagnalis.

Adagrasib (MRTX849) is an orally active and selective covalent inhibitor of KRAS G12C. Adagrasib binds to the GDP state of the inactive conformation of KRAS G12C and inhibits KRAS and its downstream signaling. Adagrasib exhibits inhibitory activity against KRAS G12C mutant tumors.

Sotorasib (AMG-510) is an orally active and selective covalent inhibitor of KRAS G12C. Sotorasib binds to the GDP state of the inactive conformation of KRAS G12C and inhibits KRAS and its downstream signaling. Sotorasib exhibits inhibitory activity against KRAS G12C mutant tumors.

0990CL is an effective heterotrimer Gαi subunit specific inhibitor, which can interact with purified Go± in GDP-bound state, and can block α2AR mediated cAMP regulation. In the cell model, low concentration of 0990CL could partially restore cAMP level, and high concentration of 0990CL (10μM) began to have negative effects on cell viability.

Guanosine 5'-diphosphate disodium salt (5'-GDP-Na2) is a nucleoside diphosphate, is a potential iron mobilizer, which prevents the hepcidin-ferroportin interaction and modulating the interleukin-6 (IL-6) stat-3 pathway.

AMG410 is a non-covalent, bimodal GDP (OFF) and GTP (ON)-binding pan-KRAS inhibitor with Kd (GDP) = 1 nM and Kd (GTP) = 22 nM, which enables circulation-independent blockade of KRAS. AMG410 is more than 100-fold selective for KRAS than HRAS and NRAS2, binds on the same variegated pocket as KRAS G12C inhibitors, and has high potency in KRAS G12D, G12V, G12C, G13D and other mutants, IC 50 = 1-4 nM. AMG140 regresses tumors and reduces phosphorylated ERK levels in colorectal, pancreatic and lung models of KRAS mutations.

HJC0197 selectively blocks cAMP-induced Epac activation. HJC0197 is an effective exchange protein. Which straightly activated by cAMP (Epac) antagonist (IC50=5.9 μM for Epac2).

KRASG12C IN-15 (Compound 21) is an orally active KRASG12C inhibitor that effectively blocks SOS1-mediated GDP GTP exchange with an IC50 of 19 nM. It inhibits ERK phosphorylation with an IC50 of 0.051 μM and reduces the viability of KRASG12C mutant MIA PaCa-2 cells with an IC50 of 0.023 μM. Additionally, KRASG12C IN-15 demonstrates antitumor activity in a MIA PaCa-2 xenograft mouse model.

UCM 608 (2-Phenylmelatonin) is an antagonist of melatonin-induced contractile responses at low concentrations and induces an increase in GDP-GTP exchange.

6-Alkynyl-fucose, a widely used fucosylation probe, acts by strongly inhibiting fucosylation and GDP-fucose synthetase FX and halting hepatoma invasion.

Guanosine 5'-diphosphate (GDP) is a purine nucleotide and biosynthetic precursor of guanosine 5'-triphosphate .1It has been used to study the conformations of GTPases.2GDP (100 μM) activates sulfonylurea receptor 2B (SUR2B) linked to the inward-rectifier potassium channel 6.1 (Kir6.1) in HEK293T cells in a patch-clamp assay.3 1.Berg, J.M., Tymoczko, J.L., and Stryer, L.Biochemistry(2002) 2.Vetter, I.R., and Wittinghofer, A.The guanine nucleotide-binding switch in three dimensionsScience294(5545)1299-1304(2001) 3.Yamada, M., Isomoto, S., Matsumoto, S., et al.Sulphonylurea receptor 2B and Kir6.1 form a sulphonylurea-sensitive but ATP-insensitive K+ channelJ. Physiol.499(Pt 3)715-720(1997)

7-Methylguanosine 5'-diphosphate (7-Methyl-GDP) sodium, a cap analog, is utilized in the synthesis of mRNA cap analogues[1].

Son of sevenless homolog 1 (Sos1) is a guanine nucleotide exchange factor (GEF) that directs the exchange of Ras-GDP to Ras-GTP by binding to SH3 domains of the growth factor receptor-bound protein 2 (Grb2), leading to the activation of ERK. Ras inhibitory peptide is a synthetic peptide that contains the sequence PVPPR, which corresponds to a region within human Sos1 that interacts with an SH3 domain of Grb2. It specifically blocks the interaction of the GEF with Grb2, preventing an interaction that is essential for Ras activation by receptor tyrosine kinases, including epidermal growth factor receptor.

RMC-0331 (RM-023) is an orally available and potent SOS1 inhibitor with potential anticancer activity, blocking RAS activation by disrupting RAS-SOS1 interactions.

KRA-533, a potent KRAS agonist, directly targets the GTP/GDP binding pocket within the KRAS protein, inhibiting GTP cleavage. This inhibition leads to the buildup of constitutively active GTP-bound KRAS, which subsequently activates both apoptotic and autophagic cell death pathways specifically in cancer cells.