Disease relevance of AD6

• When examined for reactivity with heterologous strains, MAb AD6 recognized high-molecular-weight proteins in 75% of 125 unrelated nontypeable Haemophilus strains and, in addition, reacted with three of three such strains when examined by IEM [1].
• Conversely, HuMAb 19b fails to bind to a peptide from the V3 loop of HIV-1 AD-6 in solid-phase assays, but binds to the same peptide in solution and also to AD-6 gp120 [2].

High impact information on AD6

• Similarly, a mutant cell line (AD6) with normal growth, but a rounded shape due to defective adhesiveness to substratum, showed no bundle formation [3].
• This defect is responsible for all the surface alterations because feeding of GlcNAc to AD6 cells corrects the defects in the synthesis of complex carbohydrates and the exposure of glycoproteins at the outer surface of the plasma membrane [4].
• In AD6, the biosynthesis of complex carbohydrates and glycoproteins is impaired because of a block in the acetylation of GlcN-6-P [4].
• AD6, a mutant derived from 3T3 Balb/c cells, is characterized by low adhesion to substratum, round shape, increase in surface microvilli, increase in agglutinability by concanavalin A, and loss of directional motility [4].
• BTG and PF4 release from blood anticoagulated with sodium citrate was inhibited by AD6 during a 3 h incubation [5].

Biological context of AD6

• We conclude that AD6 is an inhibitor of platelet activation in vitro [5].
• The results indicate that AD6 is an inhibitor of platelet aggregation in vitro with a mode of action different from cyclo-oxygenase blockade [6].
• However, at a pH value of 11 a more rapid hydrolysis of AD6 occurred [7].
• The pharmacokinetics of a lipophilic alkylamino acid (LAA) prodrug of cloricromene (AD6), name CLOR-C4, was studied in rat plasma and brain [8].
• AD6 (20-50 mumols/l), but not acetylsalicylic acid (ASA), incubated with whole blood or PRP, prevented the fall in platelet count and the release of BTG for at least 150 min [9].

Anatomical context of AD6

• The coumarin derivative AD6 is known to inhibit platelet aggregation and release and it possesses vasodilatory properties on coronary arteries of laboratory animals [10].

Associations of AD6 with chemical compounds

• Action of AD6 (8-monochloro-3-beta-diethylaminoethyl-4-methyl-7-ethoxycarbonylmet hox y coumarin) on human platelets in vitro [5].
• Cyclic AMP accumulation induced in WP by prostacyclin was not modified by AD6 (100 microM), while theophylline greatly potentiated prostacyclin action [5].
• The effect of AD6 (8-monochloro-3-beta-diethylamino-ethyl-4-methyl-7-ethoxy- carbonylmethoxycoumarin) on washed human platelet aggregation induced by platelet activating factor (PAF) and epinephrine [6].
• The present report demonstrates that AD6 inhibits the production of labeled arachidonic acid and diglycerides from phospholipids of platelets stimulated with thrombin [10].
• Molecular aspects of cloricromene (AD6) distribution in human platelets and its pharmacological effects [9].

Other interactions of AD6

• Under these circumstances we could observe a reversible aggregation and a partial release of BTG and PF4, AD6 was able to further reduce aggregation and release [5].

Analytical, diagnostic and therapeutic context of AD6

• The formulations were stored at 4 degrees C, and the rate of degradation of AD6 was followed by high performance liquid chromatography (HPLC) [11].
• AD6 inhibited selectively human platelet cyclic GMP phosphodiesterase, which was separated from cyclic AMP phosphodiesterase by DEAE-cellulose chromatography [12].

References