while the making and using of various embodiments of the present invention are discussed in detail below , it should be appreciated that the present invention provides many applicable inventive concepts that can be embodied in a wide variety of specific contexts . the specific embodiments discussed herein are merely illustrative of specific ways to make and use the invention and do not delimit the scope of the invention . to facilitate the understanding of this invention , a number of terms are defined below . terms defined herein have meanings as commonly understood by a person of ordinary skill in the areas relevant to the present invention . terms such as “ a ”, “ an ” and “ the ” are not intended to refer to only a singular entity , but include the general class of which a specific example may be used for illustration . the terminology herein is used to describe specific embodiments of the invention , but their usage does not delimit the invention , except as outlined in the claims . non - limiting exemplary lysophosphatidylglycerols for use with the present invention include lysophosphatidylcholines , lauroyl - lysophosphatidylcholine , myristoyl - lysophosphatidylcholine , palmitoyl - lysophosphatidylcholine , stearoyl - lysophosphatidylcholine , arachidoyl - lysophosphatidylcholine , oleoyl - lysophosphatidylcholine , linoleoyl - lysophosphatidylcholine , linolenoyl - lysophosphatidylcholine or erucoyl - lysophosphatidylcholine . asymmetric phosphatidylcholines are referred to as 1 - acyl , 2 - acyl - sn - glycero - 3 - phosphocholines , wherein the acyl groups are different from each other . symmetric phosphatidylcholines are referred to as 1 , 2 - diacyl - sn - glycero - 3 - phosphocholines . as used herein , the abbreviation “ pc ” refers to phosphatidylcholine . the phosphatidylcholine 1 , 2 - dimyristoyl - sn - glycero - 3 - phosphocholine is abbreviated herein as “ dmpc .” the phosphatidylcholine 1 , 2 - dioleoyl - sn - glycero - 3 - phosphocholine is abbreviated herein as “ dopc .” the phosphatidylcholine 1 , 2 - dipalmitoyl - sn - glycero - 3 - phosphocholine is abbreviated herein as “ dppc .” the single fatty acid chain version of these short or long chain fatty acids are referred to as the “ lyso ” forms when only a single fatty acid chain is attached to the glyceryl backbone . wherein r 1 or r 2 can be any even or odd - chain fatty acid , and r 3 can be h , acyl , alkyl , aryl , amino acid , alkenes , alkynes , and wherein a short chain fatty acid is up to 5 carbons , a medium chain is 6 to 12 carbons , a long chain is 13 - 21 carbons and a very long chain fatty acid is greater than 22 carbons , including both even and odd chain fatty acids . in one example , the fatty acids have 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 35 , 40 , 45 , 50 , 55 or long fatty acids , which can be saturated or unsaturated . the present invention can be used with any qt prolonging drug , including but not limited to those listed at : www . crediblemeds . org , albuterol ( salbutamol ), alfuzosin , amantadine , amiodarone , amisulpride , amitriptyline , amoxapine , amphetamine , anagrelide , apomorphine , arformoterol , aripiprazole , arsenic trioxide , astemizole , atazanavir , atomoxetine , azithromycin , bedaquiline , bepridil , bortezomib , bosutinib , chloral hydrate , chloroquine , chlorpromazine , ciprofloxacin , cisapride , citalopram , clarithromycin , clomipramine , clozapine , cocaine , crizotinib , dabrafenib , dasatinib , desipramine , dexmedetomidine , dexmethylphenidate , dextroamphetamine ( d - amphetamine ), dihydroartemisinin + piperaquine , diphenhydramine , disopyramide , dobutamine , dofetilide , dolasetron , domperidone , dopamine , doxepin , dronedarone , droperidol , ephedrine , epinephrine ( adrenaline ), eribulin , erythromycin , escitalopram , famotidine , felbamate , fenfluramine , fingolimod , flecainide , fluconazole , fluoxetine , formoterol , foscarnet , fosphenytoin , furosemide ( frusemide ), galantamine , gatifloxacin , gemifloxacin , granisetron , halofantrine , haloperidol , hydrochlorothiazide , ibutilide , iloperidone , imipramine ( melipramine ), indapamide , isoproterenol , isradipine , itraconazole , ivabradine , ketoconazole , lapatinib , levalbuterol ( levsalbutamol ), levofloxacin , levomethadyl , lisdexamfetamine , lithium , mesoridazine , metaproterenol , methadone , methamphetamine ( methamfetamine ), methylphenidate , midodrine , mifepristone , mirabegron , mirtazapine , moexipril / hctz , moxifloxacin , nelfinavir , nicardipine , nilotinib , norepinephrine ( noradrenaline ), norfloxacin , nortriptyline , ofloxacin , olanzapine , ondansetron , oxytocin , paliperidone , paroxetine , pasireotide , pazopanib , pentamidine , perflutren lipid microspheres , phentermine , phenylephrine , phenylpropanolamine , pimozide , posaconazole , probucol , procainamide , promethazine , protriptyline , pseudoephedrine , quetiapine , quinidine , quinine sulfate , ranolazine , rilpivirine , risperidone , ritodrine , ritonavir , roxithromycin , salmeterol , saquinavir , sertindole , sertraline , sevoflurane , sibutramine , solifenacin , sorafenib , sotalol , sparfloxacin , sulpiride , sunitinib , tacrolimus , tamoxifen , telaprevir , telavancin , telithromycin , terbutaline , terfenadine , tetrabenazine , thioridazine , tizanidine , tolterodine , toremifene , trazodone , trimethoprim - sulfa , trimipramine , vandetanib , vardenafil , vemurafenib , venlafaxine , voriconazole , vorinostat , or ziprasidone . human ether - a - go - go - related gene ( herg ) potassium channel anti - blockade by liposome and fragments . potassium channels conduct the rapid component of the delayed rectifier potassium current , kir , which is crucial for repolarization of cardiac action potentials . a reduction in herg currents due to either genetic defects or adverse drug effects can lead to hereditary or acquired long qt syndromes characterized by action potential prolongation , lengthening of the qt interval on the surface ecg , and an increased risk for “ torsade de pointes ” arrhythmias and sudden death . this undesirable side effect of non - antiarrhythmic compounds has prompted the withdrawal of drugs from the market . studies on mechanisms of herg channel inhibition provide significant insights into the molecular factors that determine state -, voltage -, and use - dependency of herg current block . mutations altering properties of the high - affinity drug binding site in herg and its interaction with drug molecules cause current increase and hereditary short qt syndrome with a high risk for life - threatening arrhythmias . ( thomas d1 , 2006 ). the types and distributions of inwardly rectifying potassium ( kir ) channels are one of the major determinants of the electrophysiological properties of cardiac myocytes . inward rectifier potassium ( kir ) channels regulate cell excitability and transport of k + ions across cell membranes . the potassium channel from streptomyces lividans is an integral membrane protein with sequence similarity to all known k + channels , particularly in the pore region . x - ray analysis with data to 3 . 2 angstroms reveals that four identical subunits create an inverted teepee , or cone , cradling the selectivity filter of the pore in its outer end . the narrow selectivity filter is only 12 angstroms long , whereas the remainder of the pore is wider and lined with hydrophobic amino acids . a large water - filled cavity and helix dipoles are positioned so as to overcome electrostatic destabilization of an ion in the pore at the center of the bilayer . main chain carbonyl oxygen atoms from the k + channel signature sequence line the selectivity filter , which is held open by structural constraints to coordinate k + ions but not smaller na + ions . the selectivity filter contains two k + ions about 7 . 5 angstroms apart . ion channels exhibit ion selectivity through pore architecture that conducts specific ions . this configuration promotes ion conduction by exploiting electrostatic repulsive forces to overcome attractive forces between k + ions and the selectivity filter . the architecture of the pore establishes the physical principles underlying selective k + conduction . ( doyle d a , 1998 ). another member of the inward - rectifier family of potassium channels is the prokaryotic kirbac1 . 1 channel . the structure of the kir channel assembly in the closed state , when refined to a resolution of 3 . 65 angstroms contains a main activation gate and structural elements involved in gating . on the basis of structural evidence , gating involves coupling between the intracellular and membrane domains suggesting that initiation of gating by membrane or intracellular signals represents different entry points to a common mechanistic pathway . ( kuo , a 2003 ). kir channels in the cardiac myocytes may be actively regulated by means of the change in pip ( 2 ) level rather than by downstream signal transduction pathways . the classical inward rectifier k (+) channel ), kir2 . 1 , kir6 . 2 / sur2a ( atp - sensitive k (+) channel ) and kir3 . 1 / 3 . 4 ( muscarinic k (+) channels ) in cardiac myocytes are commonly upregulated by a membrane lipid , phosphatidylinositol 4 , 5 - bisphosphates ( pip ( 2 )). pip ( 2 ) interaction sites appear to be conserved by positively charged amino acid residues and the putative alpha - helix in the c - terminals of kir channels . pip ( 2 ) level in the plasma membrane is regulated by tagonist stimulation ( takano m i 2003 ). inward rectifier potassium channels are characterized by two transmembrane helices per subunit , plus an intracellular c - terminal domain that controls channel gating in response to changes in concentration of various ligands . based on the crystal structure of the tetrameric c - terminal domain of kir3 . 1 , it is possible to build a homology model of the atp - binding c - terminal domain of kir6 . 2 . molecular dynamics simulations are used to probe the dynamics of kir c - terminal domains and to explore the relationship between their dynamics and possible mechanisms of channel gating . multiple simulations , each of 10 ns duration , were performed for kir3 . 1 ( crystal structure ) and kir6 . 2 ( homology model ), in both their monomeric and tetrameric forms . the kir6 . 2 simulations were performed with and without bound atp . the results of the simulations reveal comparable conformational stability for the crystal structure and the homology model . there is decrease in conformational flexibility when comparing the monomers with the tetramers , corresponding mainly to the subunit interfaces in the tetramer . the beta - phosphate of atp interacts with the side chain of k185 in the kir6 . 2 model and simulations . the flexibility of the kir6 . 2 tetramer is not changed greatly by the presence of bound atp , other than in two loop regions . principal components analysis of the simulated dynamics suggests loss of symmetry in both the kir3 . 1 and kir6 . 2 tetramers , consistent with “ dimer - of - dimers ” motion of subunits in c - terminal domains of the corresponding kir channels . this is suggestive of a gating model in which a transition between exact tetrameric symmetry and dimer - of - dimers symmetry is associated with a change in transmembrane helix packing coupled to gating of the channel . dimer - of - dimers motion of the c - terminal domain tetramer is also supported by coarse - grained ( anisotropic network model ) calculations . loss of exact rotational symmetry is suggested to play a role in gating in the bacterial kir homolog , kirbac1 . 1 , and in the nicotinic acetylcholine receptor channel . ( haider s i , 2005 ). homotetrameric models of three mammalian kir channels ( kir1 . 1 , kir3 . 1 , and kir6 . 2 ) have been generated , using the kirbac3 . 1 transmembrane and rat kir3 . 1 intracellular domain structures as templates . all three models were explored by 10 ns molecular dynamics simulations in phospholipid bilayers . analysis of the initial structures revealed conservation of potential lipid interaction residues ( trp / tyr and arg / lys side chains near the lipid headgroup - water interfaces ). examination of the intracellular domains revealed key structural differences between kir1 . 1 and kir6 . 2 which may explain the difference in channel inhibition by atp . the behavior of all three models in the md simulations revealed that they have conformational stability similar to that seen for comparable simulations of , for example , structures derived from cryoelectron microscopy data . local distortions of the selectivity filter were seen during the simulations , as observed in previous simulations of kirbac and in simulations and structures of kcsa . these may be related to filter gating of the channel . the intracellular hydrophobic gate does not undergo any substantial changes during the simulations and thus remains functionally closed . analysis of lipid - protein interactions of the kir models emphasizes the key role of the m0 ( or “ slide ”) helix which lies approximately parallel to the bilayer - water interface and forms a link between the transmembrane and intracellular domains of the channel ( haider s i , 2007 ). the potassium - selective transmembrane pore in voltage - activated k + channels is gated by changes in the membrane potential . activation gating ( opening ) occurs in milliseconds and involves a gate at the cytoplasmic side of the pore . substituting cysteine at a particular position in the last transmembrane region ( s6 ) of the homotetrameric shaker k + channel creates metal binding sites at which cd2 + ions can bind with high affinity . the bound cd2 + ions form a bridge between the introduced cysteine in one channel subunit and a native histidine in another subunit , and the bridge traps the gate in the open state . these results suggest that gating involves a rearrangement of the intersubunit contacts at the intracellular end of s6 . the structure of a bacterial k + channel shows that the s6 homologs cross in a bundle , leaving an aperture at the bundle crossing . in the context of this structure , the metal ions form a bridge between a cysteine above the bundle crossing and a histidine below the bundle crossing in a neighboring subunit . results suggest that gating occurs at the bundle crossing , possibly through a change in the conformation of the bundle itself ( holmgren m l 2002 ). activated gating in voltage - activated k + channels are a potassium - selective transmembrane pore gated by changes in the membrane potential . this activation gating ( opening ) occurs in milliseconds and involves a gate at the cytoplasmic side of the pore . substituting cysteine at a particular position in the last transmembrane region ( s6 ) of the homotetrameric shaker k + channel creates metal binding sites at which cd2 + ions can bind with high affinity . the bound cd2 + ions form a bridge between the introduced cysteine in one channel subunit and a native histidine in another subunit , and the bridge traps the gate in the open state . these results suggest that gating involves a rearrangement of the intersubunit contacts at the intracellular end of s6 . the structure of a bacterial k + channel shows that the s6 homologs cross in a bundle , leaving an aperture at the bundle crossing . in the context of this structure , the metal ions form a bridge between a cysteine above the bundle crossing and a histidine below the bundle crossing in a neighboring subunit . results suggest that gating occurs at the bundle crossing , possibly through a change in the conformation of the bundle itself ( holmgren m l 2002 ). the human ether - à - go - go gene related cardiac tetrameric potassium channel . when mutated can render patients sensitive to over 163 drugs which may inhibit ion conduction and deregulate action potentials . ( credible meds ) prolongation of the action potential follows effects in the potassium channel . ion channel active drugs may directly increase the qtc interval , and increase the risk of torsade de point and sudden cardiac death . ( table 1 ) exacerbation of cardiomyocyte potassium channel sensitivity to drugs may also be associated with metabolic diseased states including diabetes ( veglio m , 2002 ) or may be of idiopathic origin . for these reasons , evaluation of drug effects on cardiomyocyte potassium channel function is a critical step during drug development , and when serious , may be an obstacle to regulatory approval . in whole - cell patch - clamp experiments , curcumin inhibited herg k + currents in hek293 cells stably expressing herg channels in a dose - dependent manner , with ic 50 value of 5 . 55 μm . the deactivation , inactivation and the recovery time from inactivation of herg channels were significantly changed by acute treatment of 10 μm curcumin . incubation of 20 μm curcumin for 24 h reduced the hek293 cell viability . intravenous injection of 20 mg of curcumin in rabbits did not affect the cardiac repolarization manifested by qtc values . ( hu c w 2012 ). however , signpath pharma has discovered specific molecules which antagonize qtc prolonging drugs ( helson l , 2002 ranjan a , 2014 , shopp g , 2014 ). these molecules are specific liposomes , or components of liposomes which were initially bound to lipophilic drugs to permit intravenous solubility at physiological conditions , and reduce adverse events . the loci of action appears to be in intra - channel ion selectivity or gating site ( s ) controlling potassium ion movement : a key functional component of regulation of action potentials which lead downstream to myocyte contraction . the mechanism of human ether - d - go - go related gene channels blocade may be analogous to the effects of externally applied quaternary ammonium derivatives which indirectly may suggest the mechanism of action of the anti - blockading effect of the dmpc / dmpg liposome or its metabolites . the inhibitory constants and the relative binding energies for channel inhibition indicate that more hydrophobic quaternary ammoniums have higher affinity blockade while cation - x interactions or size effects are not a deterministic factor in channel inhibition by quaternary ammoniums . also hydrophobic quaternary ammoniums either with a longer tail group or with a bigger head group than tetraethylammonium permeate the cell membrane to easily access the high - affinity internal binding site in the gene channel and exert a stronger blockade . although these data suggest that the basis for the ameliorating effect liposome , or its components is the higher competitive affinity for binding sites by the , dmpc and dmpg compared to qtc prolonging drugs ( ), its constitutive lack of ion transport modulation , i . e . liposome or its fragments do not impede k + ion transport indicates that by way of explanation , and in no way a limitation of these claims , these data suggest that the basis for the ameliorating effect liposome , or its components , is the higher competitive affinity for binding sites by the dmpc and dmpg compared to qtc prolonging drugs , its constitutive lack of ion transport modulation , i . e ., liposome , or its fragments , do not impede k + ion transport and indicates that the site of the mechanism of dmpc or dmpg protection may be in the selectivity segment of the channel or in the hydration surrounding the ion . additionally , based upon these herg channel data the structures of these liposome components may be informative for designing or selecting other molecules to prevent drug induced cardiac arrhythmias . this study provides additional information as to the qtc modulating effects by drugs , induced in cardiac myocyte potassium channels , and mitigation by liposomes and liposomal constituents . the latter molecules present an opportunity to probe the k + channels as targets for pharmacological mitigation of drug - induced channelopathies . evaluation of the protective effect of dmpc , dmpg , dmpc / dmpg , lysopg and lysopc against herg inhibition by nilotinib . purpose of the study : the purpose of this study is to evaluate in vitro the protective effect of dmpc , dmpg , dmpc / dmpg , lysopg and lysopc on the rapidly activating delayed - rectifier potassium selective current ( i kr ) generated under normoxic conditions in stably transfected human embryonic kidney cells ( hek 293 cells ). this study was designed as a screen and does not require qa involvement ( non - glp - compliant ). test system : herg - expressing hek 293 transfected cell line . test performed : whole - cell patch - clamp current acquisition and analysis . experimental temperature : 35 ± 2 ° c . 5 minutes of exposure to each concentration in presence of closed circuit perfusion ( 2 ml / min ). 5 minutes for washout periods in presence of a flow - through perfusion ( 2 ml / min ) in addition to a closed circuit perfusion ( 2 ml / min ). the positive control ( nilotinib , 0 . 05 μg / ml ) was added to naive cells obtained from the same cell line and same passage for a period of 5 minutes in presence of a closed circuit perfusion ( 2 ml / min ). cells were under continuous stimulation of the pulses protocol throughout the experiments and cell currents were recorded after 5 minutes of exposure to each condition . 1 recording made in baseline condition 1 recording made in the presence of concentration 1 1 recording made in baseline condition 1 recording made in the presence of the positive control n = number of responsive cells patched on which the whole protocol above could be applied . statistical analysis : statistical comparisons were made using paired student &# 39 ; s t - tests . the currents recorded obtained on day 2 , 3 and 4 were statistically compared to the currents recorded on day 1 . the currents recorded after the positive control ( nilotinib alone ) exposure were compared to the currents recorded in baseline conditions . 1 . timeframe of drug exposure not respected 2 . instability of the seal 3 . no tail current generated by the patched cell 4 . no significant effect of the positive control 5 . more than 10 % variability in capacitance transient amplitude over the duration of the study . effect of the test articles on whole - cell i kr herg currents . whole - cell currents elicited during a voltage pulse were recorded in baseline conditions and following the application of the selected concentration of test article . the cells were depolarized for one second from the holding potential (− 80 mv ) to a maximum value of + 40 mv , starting at − 40 mv and progressing in 10 mv increments . the membrane potential was then repolarized to − 55 mv for one second , and finally returned to − 80 mv . whole - cell tail current amplitude was measured at a holding potential of − 55 mv , following activation of the current from − 40 to + 40 mv . current amplitude was measured at the maximum ( peak ) of this tail current . current density was obtained by dividing current amplitude by cell capacitance measured prior to capacitive transient minimization . current run - down and solvent effect correction . all data points presented in this study report have been corrected for solvent effect and time - dependent current run - down . current run - down and solvent effects were measured simultaneously by applying the experimental design in test - article free conditions over the same time frame as was done with the test article . the loss in current amplitude measured during these so - called vehicle experiments ( representing both solvent effects and time - dependent run - down ) was subtracted from the loss of amplitude measured in the presence of the test article to isolate the effect of the test article , apart from the effect of the solvent and the inevitable run - down in current amplitude over time . this study aimed at quantifying the protective effect of dmpc , dmpg , dmpc / dmpg , lysopg and lysopc against the inhibition of the rapidly activating delayed - rectifier potassium selective current ( i kr ) generated under normoxic conditions in stably transfected human embryonic kidney ( hek ) 293 cells caused by the nilotinib . all data points presented in this study have been corrected for solvent effects and time - dependent current run - down . these two parameters were evaluated by applying exactly the same experimental design to the vehicle as that done with the test articles . the currents were measured over the same time course as was done in the presence of the test article . the values obtained , representing both solvent effects and time - dependent run - down , were used to correct the effect of the test articles , if any . this ensures that changes attributable to time or the solvent are not mistakenly attributed to the test articles . dmpc , dmpg , dmpc / dmpg and lysopg alone did not cause any inhibition of the herg tail current density ( n = 3 ). lysopc alone caused 16 % of inhibition of the herg tail current density ( n = 4 ). nilotinib alone , formulated in dmso at 0 . 1 μm , caused 54 . 1 % of inhibition of the herg tail current ( n = 3 ). the inhibition observed is in line with previous data generated in identical conditions , and agrees with reported inhibition values for this compound . nilotinib when formulated in an aqueous solution containing dmpc , dmpg , dmpc / dmpc , lysopg or lysopc ( ratio 1 : 9 ) did not cause any inhibition of the herg tail current . these data suggest that co - formulating nilotinib with dmpc , dmpg , dmpc / dmpc , lysopg and lysopc protects against herg inhibition caused by nilotinib . in this study , the dmpc + nilotinib , dmpg + nilotinib , dmpc / dmpc + nilotinib , lysopg + nilotinib or lysopc + nilotinib were all formulated using the same method . the appropriate amount of nilotinib powder was dissolved in an aqueous solution containing either dmpc , dmpg , dmpc / dmpc , lysopg or lysopc ( ratio 9 : 1 ). the solution was vortexed for 10 minutes before being used in the patch - clamp assay . in contrast , the nilotinib used for the cells exposed to nilotinib alone was dissolved in dmso . additional studies were conducted to determine whether the difference in herg inhibition between dmso - formulated nilotinib and lipid - co - formulated nilotinib resulted from the different formulations ( aqueous or dmso - based ). amongst the mechanisms considered to explain the protection of herg currents were the possibility that dmpc / dmpg or the lyso - variants quenched the nilotinib at the moment of formulation , essentially preventing it from getting into the channel at its receptor site . another possibility was that nilotinib was less soluble in an aqueous solution , and therefore was incompletely solubilized at 0 . 1 μm . to test both hypotheses , nilotinib was formulated in dmso and added into the experimental chamber following the addition of the dmpc or dmpg . this was based on the principle that 1 — adding dmpc / dmpg alone , followed by dmso - formulated nilotinib , would eliminate the possibility of early quenching of nilotinib by the lysosome ; and 2 — that dmso would maintain the solubility of nilotinib ( the “ nilotinib - only ” inhibition of herg was observed when dmso - formulated nilotinib was added to the cells ). it is contemplated that any embodiment discussed in this specification can be implemented with respect to any method , kit , reagent , or composition of the invention , and vice versa . furthermore , compositions of the invention can be used to achieve methods of the invention . it will be understood that particular embodiments described herein are shown by way of illustration and not as limitations of the invention . the principal features of this invention can be employed in various embodiments without departing from the scope of the invention . those skilled in the art will recognize , or be able to ascertain using no more than routine experimentation , numerous equivalents to the specific procedures described herein . such equivalents are considered to be within the scope of this invention and are covered by the claims . all publications and patent applications mentioned in the specification are indicative of the level of skill of those skilled in the art to which this invention pertains . all publications and patent applications are herein incorporated by reference to the same extent as if each individual publication or patent application was specifically and individually indicated to be incorporated by reference . the use of the word “ a ” or “ an ” when used in conjunction with the term “ comprising ” in the claims and / or the specification may mean “ one ,” but it is also consistent with the meaning of “ one or more ,” “ at least one ,” and “ one or more than one .” the use of the term “ or ” in the claims is used to mean “ and / or ” unless explicitly indicated to refer to alternatives only or the alternatives are mutually exclusive , although the disclosure supports a definition that refers to only alternatives and “ and / or .” throughout this application , the term “ about ” is used to indicate that a value includes the inherent variation of error for the device , the method being employed to determine the value , or the variation that exists among the study subjects . as used in this specification and claim ( s ), the words “ comprising ” ( and any form of comprising , such as “ comprise ” and “ comprises ”), “ having ” ( and any form of having , such as “ have ” and “ has ”), “ including ” ( and any form of including , such as “ includes ” and “ include ”) or “ containing ” ( and any form of containing , such as “ contains ” and “ contain ”) are inclusive or open - ended and do not exclude additional , unrecited elements or method steps . in embodiments of any of the compositions and methods provided herein , “ comprising ” may be replaced with “ consisting essentially of ” or “ consisting of ”. as used herein , the phrase “ consisting essentially of ” requires the specified integer ( s ) or steps as well as those that do not materially affect the character or function of the claimed invention . as used herein , the term “ consisting ” is used to indicate the presence of the recited integer ( e . g ., a feature , an element , a characteristic , a property , a method / process step or a limitation ) or group of integers ( e . g ., feature ( s ), element ( s ), characteristic ( s ), propertie ( s ), method / process steps or limitation ( s )) only . the term “ or combinations thereof ” as used herein refers to all permutations and combinations of the listed items preceding the term . for example , “ a , b , c , or combinations thereof ” is intended to include at least one of : a , b , c , ab , ac , bc , or abc , and if order is important in a particular context , also ba , ca , cb , cba , bca , acb , bac , or cab . continuing with this example , expressly included are combinations that contain repeats of one or more item or term , such as bb , aaa , ab , bbc , aaabcccc , cbbaaa , cababb , and so forth . the skilled artisan will understand that typically there is no limit on the number of items or terms in any combination , unless otherwise apparent from the context . as used herein , words of approximation such as , without limitation , “ about ”, “ substantial ” or “ substantially ” refers to a condition that when so modified is understood to not necessarily be absolute or perfect but would be considered close enough to those of ordinary skill in the art to warrant designating the condition as being present . the extent to which the description may vary will depend on how great a change can be instituted and still have one of ordinary skilled in the art recognize the modified feature as still having the required characteristics and capabilities of the unmodified feature . in general , but subject to the preceding discussion , a numerical value herein that is modified by a word of approximation such as “ about ” may vary from the stated value by at least ± 1 , 2 , 3 , 4 , 5 , 6 , 7 , 10 , 12 or 15 %. all of the compositions and / or methods disclosed and claimed herein can be made and executed without undue experimentation in light of the present disclosure . while the compositions and methods of this invention have been described in terms of preferred embodiments , it will be apparent to those of skill in the art that variations may be applied to the compositions and / or methods and in the steps or in the sequence of steps of the method described herein without departing from the concept , spirit and scope of the invention . all such similar substitutes and modifications apparent to those skilled in the art are deemed to be within the spirit , scope and concept of the invention as defined by the appended claims . u . s . patent publication no . 2010 / 0004549 : system and method of serial comparison for detection of long qt syndrome ( lqts ). u . s . patent publication no . 2008 / 0255464 : system and method for diagnosing and treating long qt syndrome .
the present invention includes compositions and methods for preventing one or more cardiac channelopathies or conditions resulting from irregularities or alterations in cardiac patterns caused by an active agent or a drug in a human or animal subject comprising : an amount of a lysophosphatidylglycerol adapted for oral administration effective to reduce or prevent one or more cardiac channelopathies or conditions resulting from irregularities or alterations in cardiac patterns caused by the active agent or drug .