RHC 3288 [1-methyl-2(1,3,4-oxadiazol-2(3H)-one-5-yl) benzimidazole] and related compounds. Novel inhibitors of histamine release from rat mast cells and human basophils.

  title={RHC 3288 [1-methyl-2(1,3,4-oxadiazol-2(3H)-one-5-yl) benzimidazole] and related compounds. Novel inhibitors of histamine release from rat mast cells and human basophils.},
  author={Atul S. Khandwala and Stephen M. Coutts and Vernetta Dally-Meade and N. Jariwala and John Herr Musser and R Brown and Howard Jones and Bernard Loev and Ira Weinryb},
  journal={Biochemical pharmacology},
  volume={32 22},
5 Citations

Rosmarinic Acid as a Novel Agent in the Treatment of Allergies and Asthma

Rosmarinic acid has shown free radical scavenging ability and suppression of allergic immunoglobulin and inflammatory responses of polymorphonuclear leukocytes, which may underlie its effectiveness in the treatment of allergic disorders, as demonstrated in clinical trials.

Density functional theory study of a silver N-heterocyclic carbene complex

Geometry optimization was carried out by using the density functional theory method with B3LYP applying 6-31G* basis set by plotting the X-ray single crystal structure in the gas phase. Some solven...



Pharmacology of a new orally active antiallergic: pyrido[1,2-a]pyrimidine, ucb L140 (CHINOIN 1045) in rats.

Results suggest that the action of ucb L140 is similar to that of DSCG in inhibiting the release of allergic mediators from mast cells and therefore may present antiallergic activity.

RHC 3024: antiallergic activity in vitro and comparison with disodium cromoglycate and other antiallergic agents.

RHC 3024 is a potent inhibitor of mediator release with a mechanism of action similar to that of DSCG, M&B 22,948, PRD-92-Ea and AH-7725 and the in vitro activity profiles of proxicromil, doxantrazole, ICI 74,917 and WY-16,922 are different from RHC3024.

Antiallergic activity of tiaramide (RHC 2592-A).

Data indicate that tiaramide is a unique inhibitor of histamine release whose mechanism of action differs from that of DSCG, and which in vivo is converted to a more potent metabolite.

A binding site on mast cells and basophils for the anti-allergic drug cromolyn

It is shown here that these drug–bead conjugates (DBC) do prevent the drug penetrating into the cell without reducing its ability to inhibit histamine release, and a specific Ca2+-dependent binding of the DBC to the membranes of rat peritoneal mast cells (RPMC) and basophils.

Inhibitory effect of traxanox sodium on IgE-mediated histamine release from passively-sensitized mast cells of the rat in vitro.

Results suggest that traxanox sodium is a more potent inhibitor than DSCG on the histamine release from the mast cells of the rat, and a part of its antiallergic action is due to a selective inhibition of the immunological release of allergic mediators from themast cell.

Perspectives on the in vitro evaluation of anti‐anaphylactic agents

Use of in vitro models of anaphylaxis in this way allows an early judgment to be made about the extent to which a new compound presents a novel anti‐allergic profile.

The inhibition by disodium cromoglycate in vitro of anaphylactically induced histamine release from rat peritoneal mast cells.

It is suggested that DSCG acts indirectly, inducing the formation of an unstable species in mast cells from a precursor present in a limited amount, using rat peritoneal mast cells as an example.

The site of action of the histamine releaser compound 45/80 in causing mast cell degranulation.

The studies indicate the presence of a receptor for 48/80 on the mast cell membrane which can trigger histamine release.


Histamine release by the combination of dextran, PS, and calcium is inhibited by cromoglycate in the same range (1–30 μm) that inhibits anaphylactic histamine release from rat peritoneal cells.

Prevention of calcium ionophore-induced release of histamine in rat mast cells by disodium cromoglycate.

The results confirm the observations of Foreman et al. (10) that calcium-specific ionophores can initiate histamine release and explain the biphasic nature of the drug9s dose response in most in vitro cells systems.