Disease relevance of Pgt-1A

• Prophylaxis with the novel immunomodulator pidotimod reduces the frequency and severity of upper respiratory tract infections in children with Down's syndrome [1].
• The beneficial effects of pidotimod were also confirmed by a series of recordings made over the 90-day treatment period which showed a significant reduction in the number of days of fever, severity of the signs and symptoms of the acute episodes and use of antibiotics and antipyretic drugs [1].
• Pidotimod activity against chronic bronchitis exacerbations [2].
• Immunoactivity of pidotimod against episodes of recurrent tonsillitis in childhood [3].
• Protective effects of pidotimod against experimental bacterial infections in mice [4].

High impact information on Pgt-1A

• Immune modulator pidotimod decreases the in vitro expression of CD30 in peripheral blood mononuclear cells of atopic asthmatic and normal children [5].
• In this study we investigated the ability of the synthetic immunomodulator pidotimod to affect in vitro the phenotype and/or cytokine profile of blood cells in relation to atopic asthma [5].
• The in vitro addition of increasing concentrations of Pidotimod (10, 25 and 50 ug/ml) was able to enhance PBMC proliferation and IL2 production significantly [6].
• Experiments were performed to analyze the possible effect of the immunomodulating agent Pidotimod (3-L-pyroglutamyl-L-thiazolidine-4-carboxylic acid) on mouse Natural Killer (NK) cell activity and glucocorticoid hormone(GCH)-induced thymocyte apoptosis [7].
• Pidotimod stimulates natural killer cell activity and inhibits thymocyte cell death [7].

Chemical compound and disease context of Pgt-1A

• The therapeutic efficacy of the synthetic immunostimulant pidotimod ((R)-3-[(S)-(5-oxo-2-pyrrolidinyl) carbonyl]-thiazolidine-4-carboxylic acid, PGT/1A, CAS 121808-62-6) was evaluated in a double-blind placebo-controlled study in parallel groups in the management of recurrences in 235 children with recurrent tonsillitis [3].
• Finally, pidotimod showed an additive or synergic activity in combination with beta-lactam antibiotics (cefotaxime, ampicillin) against bacterial infections in mice [4].

Biological context of Pgt-1A

• Effect of food on the bioavailability of pidotimod in healthy volunteers [8].
• Pharmacokinetics of pidotimod in rats and dogs [9].
• Macrophage functions, anion superoxide production and the non-stimulated ex vivo chemotaxis reveal that pidotimod significantly reduces the immunodepressant action of prednisolone; particularly in i.p. treated mice the chemotaxis is likely to be restored to the levels of the non-immunodepressed controls [10].
• A significant trend to normalization of the immune response, evidenced by chemotaxis and leukocyte phagocytosis index, was found only in patients treated with pidotimod [11].
• Ex vivo evaluation of pidotimod activity on cell-mediated immunity [12].

Anatomical context of Pgt-1A

• A 12% increase in CD 3 lymphocytes compartment was observed with pidotimod 400 mg/day [12].
• On the basis of the known effects of pidotimod on immune system, this effect is due to an immunostimulating effect of this drug [13].
• Clinical evaluation and changes of the respiratory epithelium function after administration of Pidotimod in Greek children with recurrent respiratory tract infections [14].
• Therapeutic efficacy and safety of pidotimod in the treatment of urinary tract infections in children [15].
• A significant trend to normalization of the immune response, expressed by chemotaxis and index of leukocyte phagocytosis, was found only in patients treated with pidotimod [15].

Associations of Pgt-1A with other chemical compounds

• The pharmacokinetic studies on pidotimod ((R)-3-[(S)-(5-oxo-2-pyrrolidinyl) carbonyl]-thiazolidine-4-carboxylic acid, PGT/1A, CAS 121808-62-6) a new biological response modifier, following intravenous, intramuscular or oral administrations in rats and dogs are reported in this paper [9].
• The action of pidotimod on humoral immunity is showed in two tests where the antibody response is induced by a thymus dependent (sheep erythrocytes) or a thymus independent (lipopolysaccharide) antigen [10].

Gene context of Pgt-1A

• However, MO from mice received mPDN plus pidotimod fully recovered the capacity to produce TNF-alpha and NO in response to the same stimuli [16].
• The results indicate that in vivo treatment with Pidotimod (200 mg/Kg ip for 5 days) causes a significant increase in NK activity and in vitro treatment produces a significant reduction of dexamethasone-induced thymocyte apoptosis [7].
• On the other hand, treatment with pidotimod did not influence the responsiveness of 2 month-old rat lymphocytes to mitogens, nor affected IL-2 production [17].
• This paper reports the toxicological evaluation of pidotimod ((R)-3-[(S)-(5-oxo-2-pyrrolidinyl) carbonyl]-thiazolidine-4-carboxylic acid, PGT/1A, CAS 121808-62-6) [18].
• An evaluation of the expression of CD25 (after in vitro stimulation of circulating mononuclear cells with PHA) before and after treatment with the two products revealed a significant increase in CD25+ cells in the group treated with pidotimod but not in the group treated with placebo [19].

Analytical, diagnostic and therapeutic context of Pgt-1A

• There was a significant reduction in the frequency, severity and duration of infectious episodes in the pidotimod-treated group vs the untreated control group [1].
• In the rat the pharmacokinetic parameters obtained after oral administration demonstrate that pidotimod is a very fast absorbed, distributed and eliminated drug (t1/2el = 1 h) and that it shows high total clearance and distribution volume [9].
• A new HPLC method for pidotimod plasma levels determination [20].
• A significant decrease in the risk of relapses was observed in patients treated with pidotimod (35%), as well as a reduction of hospitalization (86%) and a decreased antibiotic therapy (47%) [11].
• The results indicate that pidotimod has a beneficial effect in children with recurrent respiratory infections: the percentage of patients presenting symptoms affecting the upper and lower airways was significantly lower after treatment with the active drug than after treatment with placebo [19].

References