carvedilol and its optically pure isomers were tested in various cell lines for their cytotoxic activity and it was found that these compounds can effectively be used for inhibition of tumors and cancer and for treatment of cancer or tumor . such indications exhibited by these compounds are surprising as carvedilol is generally known to act as an anti - hypertensive drug and cytotoxic activity is not expected . the modulation of growth factor dependent proliferation as well as protein kinase c , a key signaling intermediate involved in cross talk of g protein coupled signaling and receptor tyrosine kinases explained the observed anticancer effects of the molecule . pharmaceutical compositions containing an effective amount of the compounds of the invention as described herein above may be prepared according to methods known in the art . by “ effective amount ”, the applicants intend an amount that will produce tumor or cancer inhibiting effects or anti - cancer or anti - tumor effects without causing undue harmful side effects . the pharmaceutical compositions may provide from about 10 mg to 1000 mg of carvedilol or its isomers , per unit dose . the actual dosage for humans and animals will vary depending upon the body weight of the subject , stage of affliction etc . the composition may be administered either alone or as a mixture with other therapeutic agents . the compositions may be formulated in various physical forms suitable for administration such as tablets , capsules , solutions , injectables , lozenges , powders , aqueous or oily suspensions , syrups , elixirs , implants or aqueous solutions etc . the compositions containing carvedilol or an optically pure isomer thereof as active ingredients , may be formulated as tablets , if intended for oral use , or lyophilized powders for parenteral administration . the powders may be reconstituted by adding suitable diluents or pharmaceutically acceptable carriers prior to use . tablets containing carvedilol or an optically pure isomer thereof as active ingredient may include , along with non - toxic pharmaceutically acceptable excipients . such excepients may be for example , inert diluents , such as calcium carbonate , sodium carbonate , lactose , calcium phosphate or sodium phosphate ; granulating and disintegrating agents , for example , corn starch , or alginic acid ; binding agents , for example starch , gelatin or acacia , and lubricating agents , for example magnesium stearate , stearic acid or talc . the tablets may be uncoated or they may be coated by known techniques . compositions for oral use may also be presented as hard gelatin capsules wherein the active ingredient comprises carvedilol or an isomer thereof mixed with an inert solid diluent , for example , calcium carbonate , calcium phosphate or kaolin , or as soft gelatin capsules wherein the active ingredient is mixed with water or an oil medium , for example peanut oil , liquid paraffin or olive oil . the pharmaceutical compositions may also be formulated as solutions , when intended for systemic or parenteral administration . systemic administration refers to oral , rectal , nasal , transdermal and parentral ( i . e ., intramuscular , intraperitoneal , subcutaneous or intravenous ). the liquid formulation is generally buffered , isotonic or aqueous solution . examples of suitable diluents are normal isotonic saline solution , standard 5 % dextrose in water or buffered sodium or ammonium acetate solution . formulations suitable for parenteral administration , may also be used for oral administration or contained in a metered dose inhaler or nebulizer . it may be desirable to add excipients such as ethanol , polyvinylpyrrolidone , gelatin , hydroxy cellulose , acacia , polyethylene glycol , mannitol , sodium chloride or sodium citrate . alternatively , the compounds of the invention may be prepared in a emulsion or syrup for oral administration . pharmaceutically acceptable solid or liquid carriers may be added to enhance or stabilize the composition , or to facilitate preparation of the composition . liquid carriers include syrup , peanut oil , olive oil , glycerin , saline , ethanol , and water . solid carriers include starch , lactose , calcium sulfate dihydrate , terra alba , magnesium stearate or stearic acid , talc , pectin , acacia , agar or gelatin . the carrier may also include a sustained release material such as glyceryl monostearate or glyceryl distearate , alone or with a wax . the amount of solid carrier varies but , preferably , will be between about 20 mg to about 1 g per dosage unit . the pharmaceutical preparations are made following the conventional techniques of pharmacy involving milling , mixing , granulating , and compressing , when necessary , for tablet forms ; or milling , mixing and filling for hard gelatin capsule forms . when a liquid carrier is used , the preparation will be in the form of a syrup , elixir , emulsion or an aqueous or non - aqueous suspension . such a liquid formulation may be administered directly or filled into a soft gelatin capsule . the compositions may contain additives selected from the group consisting of sweetening agents , flavoring agents , coloring agents and preserving agents . the nature of pharmaceutical composition employed will , of course , depend on the desired route of administration . the present invention provides for method ( s ) for the treatment of cancer or tumors , said method comprising the steps of administering to the subject an effective amount of carvedilol or an isomer thereof to a patient in need thereof . the present invention provides for method ( s ) for the inhibition of cancer or tumors , said method comprising the steps of administering to the subject an effective amount of carvedilol or an isomer thereof to a patient in need thereof . an effective amount of carvedilol or an isomer thereof is an amount sufficient to treat the cancer or tumor or inhibit the growth and / or replication of the cancer or tumor . the patient can be human , mammal or other animal . the dosage in human beings for treatment of cancer or a tumor or inhibition of tumor or cancer includes the active ingredient ( carvedilol or an isomer thereof ) in combination with conventional pharmaceutical agents . the usual dosage is about 3 to 30 g of active ingredient as a single dose or divided doses . the preferred and actual dosage will be determined according to the specific compositions formulated , mode of administration , the site of administration and the patient being treated . no unexpected or toxic effects were observed when the compounds of the invention were tested for treatment of cancer or tumors or inhibition of tumors or cancer . the invention is further described in detail by the following examples which are given for illustration of the invention and not intended to limit the scope thereof in any manner . in vitro cytotoxic activity of carvedilol and its isomers was determined by performing the mtt cytotoxicity assay ( mosmann t ., j immunological methods , 65 : 55 ; 1983 ). briefly , the cultured tumor cells were separately seeded in a 96 - well culture plate and co - incubated with carvedilol or its isomers dissolved in methanol , dimethyl formamide , dimethyl sulfoxide or isopropyl alcohol with relevant controls at 37 ° c . in a co 2 incubator . after 72 hours , the assay was terminated and percent cyotoxicities calculated . as shown in table 1 , carvedilol shows good in vitro cytotoxicity in human colon , ovary , melanoma , leukemia , glioblastoma , prostate , oral and lung tumor cell lines with ed 50 values less than 20 μg / ml . these results demonstrate that carvedilol is a potential anti - cancer agent with broad - spectrum anticancer activity . further , fig1 shows the high cytotoxicity effect of carvedilol on all of the above - mentioned tumor cell lines , except oral , at a fixed concentration of 20 μg / ml . the anti - tumor activity of the optically pure isomers of carvedilol s (−) and r (+) were evaluated in a 72 - hour mtt cytotoxicity assay ( mosmann t ., j immunological methods , 65 : 55 ; 1983 ) as explained above . carvedilol and its isomers were evaluated in human tumor cell lines molt - 4 ( leukemia ), ptc ( colon ), kb ( oral ), l132 ( lung ) u87mg ( glioblastoma ), hbl100 ( breast ), b16f10 ( melanoma ), miapaca . 2 ( pancreas ) and pa - 1 ( ovary ) in a range of concentrations . the ed 50 value ( the test concentration which causes 50 % cytotoxicity ) as calculated graphically was used to compare the relative cytotoxic potential of carvedilol and its isomers . as shown in table 2 , the active isomers have retained the cytotoxic potential of the parent compound carvedilol . this shows that the optically pure isomers of carvedilol are potential anti - cancer agents with the advantage of reduced compounded toxicities associated with the parent compound . the effect of carvedilol on epidermal growth factor ( egf ) dependent proliferation was determined by the quantitation of percent viable cells in sera free conditions in vitro . briefly , 10000 human pancreatic cancer cells ( miapaca2 ) were seeded per well in a 96 - well culture plate in dmem containing 5 % fcs . all experiments were carried out in triplicates at 37 ° c . in a co 2 incubator . the cells were incubated for a period of 12 hours , washed once with pbs and the medium was changed to dmem without fetal calf serum ( fcs ). carvedilol was dissolved in 1 % dmso in dmem . the cells were incubated with carvedilol at a concentration of 20 ug / l for a period of 16 hours . the untreated control cells were treated with 1 % dmso in dmem . the cells were washed with pbs and incubated with varying concentrations of egf in dmem without fcs for a period of 48 hours . the percent viable cells in absence and presence of carvedilol was determined in an mtt assay in vitro . as shown in fig2 carvedilol inhibits the egf dependent proliferation in pancreatic cancer cells in a dose dependent manner in vitro . effect of carvedilol on platelet derived growth factor ( pdgf ) dependent proliferation in vitro the effect of carvedilol on platelet derived growth factor ( pdgf ) dependent proliferation was determined by the quantitation of percent viable cells in sera free conditions in vitro . briefly , 10000 human pancreatic cancer cells ( miapaca2 ) were seeded per well in a 96 - well culture plate in dmem containing 5 % fetal calf serum ( fcs ). all experiments were carried out in triplicates at 37 ° c . in a co 2 incubator . the cells were incubated for a period of 12 hours , washed once with pbs and the medium was changed to dmem without fcs . carvedilol was dissolved in 1 % dmso in dmem the cells were incubated with carvedilol at a concentration of 20 ug / ml for a period of 16 hours . the untreated control cells were treated with 1 % dmso in dmem . the cells were washed with pbs , to remove carvedilol and incubated with varying concentrations of pdgf in dmem without fcs for a period of 48 hours . the percent viable cells in absence and presence of carvedilol was determined in an mtt assay in vitro . fig3 shows that carvedilol inhibits the pdgf dependent proliferation in human pancreatic cancer cells in a dose dependent manner in vitro . effect of intracellular blocking of protein kinase c ( pkc ) on the cytotoxicity of carvedilol in vitro the effect of pkc activation , on the cytotoxicity of carvedilol was studied by the intracellular blocking of pkc , in cytotoxicity abrogation assays . briefly , 10000 human pancreatic cancer cells ( miapaca2 ) were seeded per well in a 96 - well culture plate in dmem containing 5 % fcs . all experiments were carried out in triplicate at 37 ° c . in co 2 incubator . the plates were incubated overnight to allow complete reattachment of the cells . subsequently , the medium was replaced with dmem . the cells were incubated with varying concentrations of bisindolylmaleimide , the specific inhibitor of pkc for a period of three hours . bisindolylmaleimide was dissolved in 1 % dmso the control cells were treated with 1 % dmso . the cells were washed with pbs , and the medium was changed to fresh dmem . carvedilol was added to the cells preincubated with or without bisindolylmaleimide for 48 hours . carvedilol was added every 24 hours . the percent cytotoxicity of carvedilol in cells preincubated with or without bisindolylmaleimide at non toxic concentrations was calculated , and the percent abrogation in the cytotoxicity determined . table 3 shows the data on modulation of cytotoxicity of carvedilol in presence or absence of bisindolylmaleimide . as seen in table 3 , blocking of pkc by bisindolylmaleimide , abrogates the cytotoxicity of carvedilol to a significant extent , suggesting a role for it in the observed anticancer action of carvedilol . briefly , 10000 human pancreatic cancer cells ( miapaca2 ) were seeded per well in a 96 - well culture plate in dmem containing 5 % fcs . all experiments were carried out in triplicate at 37 ° c . in co 2 incubator . the plates were incubated overnight to allow complete reattachment of the cells . subsequently , the medium was replaced with dmem . the cells were incubated with varying concentrations of wortmannin , the specific inhibitor of pi3 kinase for a period of three hours . wortmannin was dissolved in 0 . 5 % dmso . the control cells were treated with 0 . 5 % dmso . the cells were washed with pbs , and the medium was changed to fresh dmem . carvedilol was added to the cells preincubated with or without wortamannin for 48 hours . carvedilol was added every 24 hours . the percent cytotoxicity of carvedilol in cells preincubated with or without wortmannin at non toxic concentrations was calculated , and the percent abrogation in the cytotoxicity determined . table 4 shows the data on modulation of cytotoxicity of carvedilol in presence or absence of wortamannin . as seen in table 4 , the blocking of the activity of pi3 kinase by wortamannin abrogates the cytotoxicity of carvedilol , suggesting the role of the kinase in its observed action . the effect of carvedilol on the activity of protein kinase c ( pkc ) was quantitated by an enyme linked immunosorbent assay ( elisa ). briefly 0 . 5 × 10 6 cells of human pancreatic cancer cells ( miapaca2 ) were plated per well in 6 well tissue culture plates in 2 ml of dmem containing 10 % fetal calf serum . the cells were incubated overnight at 37 ° c . and 5 % co 2 . the medium was changed to dmem without serum . carvedilol was dissolved in 1 % dmso in dmem . the cells were incubated with carvedilol at concentrations of 5 - 100 ug / ml for a period of 15 minutes at 37 ° c . in 5 % co 2 . the control cells were treated with 1 % dmso in dmem . the medium containing the carvedilol was aspirated , and the cells were washed with phosphate buffered saline ( pbs ) ( 50 mm , ph 7 . 2 ) twice . the cells were scraped with sterile cell scrapers , and spun at 1500 rpm for 5 minutes . the cell pellet was dissolved in 1 ml of ice cold sample preparation buffer ( 50 mm tris - hcl , 50 mm 2 - mercaptoethanol , 10 mm egta , 5 mm edta , 1 mm pmsf , 10 mm benzamidine , ph 7 . 5 ). the cell pellets were sonicated four to five times each with time intervals of 5 - 10 seconds . the cells were centrifuged at 100 , 000 × g for a period of 60 minutes at 4 ° c . the supernatant was aspirated from each set of experiments . the reaction mixture for quantitation of the pkc activity contained 25 mm tris - hcl ( ph7 . 0 ), 3 mm mgc12 , 0 . 1 mm atp , 2 mm cacl2 , 50 ug / ml phosphatidylserine , 0 . 5 mm edta , 1 mm egta , and 5 mm 2 mercaptoethanol . the lysates from the cells not treated with carvedilol were the control experiments . the reaction mixture was preincubated for 5 minutes at 25 ° c . 50 ug of the cell lysate from different experiments was added to the individual reaction mix and added to microtitre plates coated with substrate for pkc . the plates were incubated for 15 minutes at 25 ° c . in a water bath . the pkc mediated reaction was stopped by the addition of 100 ul of stop solution . the plates were washed 5 times with the wash solution , and 100 ul of the biotinylated antibody to the phosphorylated substrate was added per well . the plates were incubated at 25 ° c . for 60 minutes . the plates were washed 5 times and 100 ul of peroxidase conjugated streptavidin was added to each well . the plates were incubated at 25 ° c . for 60 minutes . the plates were washed five times and 100 ul of substrate was added to each well . the plates were incubated at 25 ° c . for 3 - 4 minutes , and the reaction was stopped by the addition of stop solution . the optical density was read at 492 nm , and the pkc activity expressed as percent of that in control cells . fig4 shows the data on modulation of pkc activity by carvedilol in pancreatic cancer cells as seen below , carvedilol inhibits the pkc activity in a dose dependent manner in human pancreatic cancer cells in vitro . 1 × 10 6 human pancreatic cancer cells ( miapaca2 ) were plated in 6 well plates in rpmi containing 10 % fcs . the cells were incubated for a period of 24 hours at 37 ° c . in 5 % co 2 . the medium was changed to dmem without serum . carvedilol was dissolved in 1 % dmso in dmem . the cells were incubated with carvedilol at concentrations of 10 ug / ml and 20 ug / ml for a period of 4 hours . all experiments were carried out in duplicates . the cells not treated with carvedilol were the control experiments . cells were preincubated with bisindolemaleimide ( 1 um ) , a specific inhibitor of pkc for 4 hours . the medium was aspirated to remove bisindolemaleimide , and the cells were washed twice with pbs . these cells were treated with carvedilol at 10 ug / ml and 20 ug / ml . the medium was removed in all wells after carvedilol treatment , and 1 ml of fresh medium containing arachidonic acid ( 20 um ) was added to the wells . the cells were incubated at 37 ° c . for one hour . indomethacin at a concentration of 10 ug / ml was added to the wells to block the cox enzyme . the intracellular and secreted levels of pge2 were quantitated in cells treated with carvedilol . the cells were lysed ( 2 . 5 % dodecyltrimethylammonium ) and incubated for 10 minutes at room temperature . the cell lysates were transferred to microtitre plate coated with goat anti mouse ig coated plate . 50 microliter of pge2 standards ranging from 2 . 5 to 320 pg / ml were added to the microtitre plate in duplicates . 50 microliter of mouse anti pge2 and 50 microliter of pge2 conjugated peroxidase was added to the wells . the plate was covered and incubated at room temperature for one hour on a microtitre plate shaker . the wells were aspirated and washed 4 times with suitable was buffer . 150 microlire of enzyme substrate was added to all the wells . the plate was incubated for a period of 30 minutes and the colour development was stopped by the addition of 1n sulphuric acid . the od was read at 450 nm . the levels of secreted and intracellular pge2 were quantitated in the cells treated with carvedilol and compared with that in untreated cells . the levels of secreted and intracellular pge2 were quantitated in cells treated with or without bisindolemaleimide . as shown in fig5 carvedilol inhibits the cox2 activity in pancreatic cancer cells in vitro . the blocking of pkc by its specific inhibitor bisindolemaleimide , abrogates the effect of carvedilol on cox 2 activity , suggesting that it may be pkc mediated . the antitumor activity of carvedilol on melanoma tumor xenografts grown in nude mice the in vivo antitumor activity of carvedilol has been demonstrated using the b16f10 melanoma xenograft model . melanoma tumor xenografts were initiated in balb / c athymic mice by subcutaneous inoculation of a single cell suspension of b16f10 cells ( 10 × 10 6 cells / 100 μl ). the tumor - bearing mice were divided into three groups of 4 animals each . carvedilol was prepared at a concentration of 1 . 2 mg / ml so as to deliver a dose of 300 μg per 250 μl and 600 μg per 500 μl by oral gavage once a day . the third group served as control . treatment with carvedilol was initiated on day 8 . the anti - tumor activity was monitored by measuring the tumors using a vernier caliper every fourth day and calculating volumes using the formula 0 . 4 × w 2 × l ( w = smaller dia , l = larger dia ,). fig6 shows the pattern of tumor growth in treated and control tumor - bearing animals and shows the delayed tumor growth and tumor regression in both the doses of carvedilol treated mice . on day 19 , treatment with carvedilol ( 300 ug / day ) caused 37 . 3 % tumor inhibition and carvedilol ( 600 ug / day ) caused 59 . 1 % tumor inhibition based on tumor volumes compared with untreated controls . carvedilol is used clinically in doses ranging between 6 . 5 mg / day to 100 mg / day in humans . since most anti - cancer drugs have very narrow therapeutic indices we determined the therapeutic index of carvedilol in mice . acute toxicity studies were performed using two preferred routes of administration : intravenous and oral administration . a range of doses between 0 . 1 to 10 mg was administered in mice using either the intravenous or oral routes and the animals were observed for two weeks . in swiss albino mice , weighing 25 grams , lethal dose ( 6 mg oral , 1 . 25 mg i . v .) and safe dose ( 3 mg oral , 0 . 15 mg i . v .) was observed . we tested the in vivo antitumor activity of carvedilol in mice using oral doses that were { fraction ( 1 / 10 )} th ( 300 ug / day ) and ⅕ th ( 600 ug / day ) of the safe dose and have shown therapeutic efficacy ( see example 2 ) with a wide therapeutic index .