Abstract: The present invention describes a novel bivalent helically constrained peptide targeted against S100B that is an effective anti-cancer drug against cancers that over-express S100B. This helix mimetic targeted against S100B induces rapid apoptosis in cancer cells that over-express a calcium binding protein S100B through simultaneous inhibition of key growth pathways including activation of p53.

Abstract: The present invention relates to compounds of general formula 1 for the treatment of bronchial asthma by inhibition of IL-4 or IL-5 pathway inhibition. The present invention also relates to the use of compound of general formula 1 for the treatment of bronchial by inhibition of IL-4 or IL-5 pathway. The present invention also relates to the method of treating asthma by inhibition of IL-4 or IL-5 pathway by administration of compound or said composition through oral, intranasal, route or by inhalation to a mammal in need thereof. Compound of general formula 1 may be used for reducing perivascular and peribronchial inflammation.

Abstract: The present invention relates to compounds of general formula 1 for the treatment of malignancy by inhibition of PI3-Akt pathway and or induction of NO. The present invention also relates to the use of compound of general formula 1 for the treatment of malignancy by inhibition of PI3-Akt pathway and or induction of NO. The present invention further relates to a method of treating malignancy by inhibition of PI3-Akt pathway and or induction of NO by administration of compound or said composition to a mammal in need thereof.

Abstract: A novel heterocyclic compound belonging to ‘triazine-aryl-bis-indoles’, useful for the treatment of asthma. The pathway by which this compound inhibits asthma is also demonstrated. The present invention also provides a process for the preparation of above compounds and their derivatives are presented.

Abstract: The present invention describes a novel bivalent helically constrained peptide targeted against S100B that is an effective anti-cancer drug against cancers that over-express S100B. This helix mimetic targeted against S100B induces rapid apoptosis in cancer cells that over-express a calcium binding protein S100B through simultaneous inhibition of key growth pathways including activation of p53.

Abstract: The present invention relates to compounds of general formula 1 for the treatment of bronchial asthma by inhibition of IL-4 or IL-5 pathway inhibition. The present invention also relates to the use of compound of general formula 1 for the treatment of bronchial by inhibition of IL-4 or IL-5 pathway. The present invention also relates to the method of treating asthma by inhibition of IL-4 or IL-5 pathway by administration of compound or said composition through oral, intranasal, route or by inhalation to a mammal in need thereof. Compound of general formula 1 may be used for reducing perivascular and peribronchial inflammation.

Abstract: The present invention relates to a method for the treatment of bronchial asthma and chronic obstructive pulmonary disease (COPD) comprising administering to the patient suffering from asthma and COPD an effective dose of carbazole derivatives or salt thereof, optionally along with pharmaceutically acceptable excipients. Structural formula of the compounds of general formula 1 useful as phosphodiesterase-4 (PDE-4) enzyme inhibitors, inhibitor for signalling molecule for the treatment of asthma and asthma related diseases is given below: wherein R1=H or OCH3; R2?CH3 or CHO; R3?H or OCH3; R4?H or OCH3 Herbal route for the isolation of compound of general formula 1 from the bark of plant Murraya Koenigii and chemical route for the preparation of such compounds from basic compounds such as vanillin is also reported.

Abstract: A novel heterocyclic compound belonging to ‘triazine-aryl-bis-indoles’, useful for the treatment of asthma. The pathway by which this compound inhibits asthma is also demonstrated. The present invention also provides a process for the preparation of above compounds and their derivatives are presented.

Abstract: The present invention relates to a method for the treatment of bronchial asthma and chronic obstructive pulmonary disease (COPD) comprising administering to the patient suffering from asthama and COPD an effective dose of carbazole derivatives or salt thereof, optionally along with pharmaceutically acceptable excipients. Structural formula of the compounds of general formula 1 useful as phosphodiesterase-4 (PDE-4) enzyme inhibitors, inhibitor for signalling molecule for the treatment of asthma and asthma related diseases is given below: wherein R1=H or OCH3; R2?CH3 or CHO; R3?H or OCH3; R4?H or OCH3 Herbal route for the isolation of compound of general formula 1 from the bark of plant Murraya Koenigii and chemical route for the preparation of such compounds from basic compounds such as vanillin is also reported.

Abstract: The present invention relates to compounds of general formula I for the treatment of malignancy by inhibition of PI3-Akt pathway and or induction of NO. The present invention also relates to the use of compound of general formula I for the treatment of malignancy by inhibition of PI3-Akt pathway and or induction of NO. The present invention further relates to a method of treating malignancy by inhibition of PI3-Akt pathway and or induction of NO by administration of compound or said composition to a mammal in need thereof.

Abstract: A method of treating CD33+ acute and chronic myeloid leukemia in animals including humans, using fraction nos. 1 and 9 obtained from water:methanol fraction by column chromatography, with ratio of water and methanol ranging between 1:5 to 5:1, wherein said water:methanol fraction is obtained from the polar extract of Piper betel by HPLC, with retention time of 3.6 and 24.0 minutes respectively, with said fractions used both individually, and in combination.

Abstract: This invention relates to method of treating human malignancies of different origin that are sensitive to oxidative stress by administering effective amount of extract of Piper betel leaves along with a pharmaceutically acceptable additives

Abstract: A method of treating CD33+ acute and chronic myeloid leukemia in animals including humans, using fraction nos. 1 and 9 obtained from water:methanol fraction by column chromatography, with ratio of water and methanol ranging between 1:5 to 5:1, wherein said water:methanol fraction is obtained from the polar extract of Piper betel by HPLC, with retention time of 3.6 and 24.0 minutes respectively, with said fractions used both individually, and in combination.

Abstract: A method of treating CD33+ acute and chronic myeloid leukemia in animals including humans, using fraction nos. 1 and 9 obtained from water:methanol fraction by column chromatography, with ratio of water and methanol ranging between 1:5 to 5:1, wherein said water:methanol fraction is obtained from the polar extract of Piper betel by HPLC, with retention time of 3.6 and 24.0 minutes respectively, with said fractions used both individually, and in combination.

Abstract: Described is an in vitro method for developing dendritic Langerhans type cells, for use in immunotherapy against cancer or infectious diseases and enhancement of graft survival in mammals. The method includes the steps of: culturing cells selected from peripheral blood monocytes and bone marrow cells in a medium containing platelets obtained from the same species or phylogenetically close species; and incubating the culture at 30 to 40° C. for a period sufficient to enable formation of mature dendritic Langerhans type cells.

Abstract: The present invention provides a method of treating acute and chronic myeloid leukemia (AML & CML) and lymphoid leukemia, said method comprising administering a pharmaceutical composition comprising pharmaceutically effective amount of chlorogenic acid (CA) and 3-o-p-Coumaryl quinic acid (PCQ) isolated from any plant parts of Piper betel or any other source, both individually or in a synergistic combination optionally along with pharmaceutically acceptable additives.

Abstract: A method of treating CD33+ acute and chronic myeloid leukemia in animals including humans, using fraction nos. 1 and 9 obtained from water: methanol fraction by column chromatography, with ratio of water and methanol ranging between 1:5 to 5:1, wherein said water:methanol fraction is obtained from the polar extract of Piper betel by HPLC, with retention time of 3.6 and 24.0 minutes respectively, with said fractions used both individually, and in combination, and a composition comprising the said fraction nos. 1 and 9.

Abstract: A method of treating CD33+ acute and chronic myeloid leukemia in animals including humans, using fraction nos. 1 and 9 obtained from water:methanol fraction by column chromatography, with ratio of water and methanol ranging between 1:5 to 5:1, wherein said water:methanol fraction is obtained from the polar extract of Piper betel by HPLC, with retention time of 3.6 and 24.0 minutes respectively, with said fractions used both individually, and in combination.

Abstract: This invention relates to a pharmaceutical composition useful for treating chronic myeloid leukemia where Bcr-Abl kinase is constitutively expressed in animals and humans, and a treatment of chronic myeloid leukemia (CML) by a composition comprising an effective amount of analogs and/or salts of chlorogenic acid. The analogs are preferably sodium chlorogenate (Na-Chl) or potassium or ammonium salts, which were prepared from Chlorogenic acid or its analogs.

Abstract: This invention relates to use of betel leaf extract to induce IFN? from human peripheral blood mononuclear cells and as a Th1 type immuno modulator, wherein the said method comprises the steps of, preparing water extract of betel leaf, preparation of human peripheral blood mononuclear cells, incubation of hPBMC with betel leaf extract for a period of 18–48 hours, extraction of RNA for cytokine specific RT-PCR or for flow cytometry for the detection of intracellular cytokine protein, subjecting RNA for RT-PCR to obtain PCR products using IFN? specific known primers, and enhancement of IFN? as reflected by IFN? specific band.