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Lanoxin (Digoxin)

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Lanoxin is an effective medication which is used in treatment of certain types of fast heartbeats such as atrial fibrillation or fluttering arrhythmia and heart failure. It also treats angina. This drug can also be used after heart attack.

Other names for this medication:
Agoxin, Apo-digoxin, Cardiacin, Cardiogoxin, Digacin, Digazolan, Digibind, Digitek, Digobal, Digocard-g, Digohan, Digoregen, Digosin, Digossina, Digoxanova, Digoxen, Digoxine, Digoxinum, Eudigox, Fargoxin, Halfdigoxin, Lanadicor, Lanibos, Lanicor, Lenoxin, Pms-digoxin, Purgoxin, Sigmaxin, Vidaxil

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Also known as:  Digoxin.


Lanoxin target is struggle against certain types of fast heartbeats such as atrial fibrillation or fluttering arrhythmia and heart failure. It is also treats angina. This drug can also be used after heart attack. The effectiveness of Lanoxin is in keeping the heart rhythm under control and to make heart work better (regularly and strongly). It is cardiac (or digitalis) glycosides.

Generic name of Lanoxin is Digoxin.

Lanoxin is also known as Digoxin, Digitalis, Digitek, Lanoxicaps.

Brand names of Lanoxin are Lanoxicaps, Lanoxin, Cardoxin, Digitek, Lanoxin Elixir Pediatric.


Take Lanoxin tablets (0.25 mg), capsules and pediatric elixir (liquid) orally.

Elderly people (> 65 years) should take the lowest dose.

Take Lanoxin at the same time once a day with water.

Do not crush or chew it.

If you want to achieve most effective results do not stop taking Lanoxin suddenly.


If you overdose Lanoxin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Lanoxin overdosage: confusion, irregular heartbeats, nausea, seizures, vomiting, extremely fast or slow heartbeats, hallucinations, tiredness, problems with vision, diarrhea, lack of appetite.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Lanoxin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Lanoxin if you are allergic to Lanoxin components.

Do not take Lanoxin if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Lanoxin if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Lanoxin in case of taking medicines as a steroid medicine (prednisone (such as Deltasone), methylprednisolone (such as Medrol), prednisolone (such as Prelone, Pediapred), dexamethasone (such as Decadron)); a cancer chemotherapy drug; amphotericin B (such as Fungizone); indomethacin (such as Indocin); rifampin (such as Rifadin, Rimactane); cholestyramine (such as Questran, Prevalite) or colestipol (such as Colestid); a thyroid medication; a beta-blocker (atenolol (such as Tenormin), propranolol (such as Inderal), acebutolol (such as Sectral), metoprolol (such as Lopressor), carteolol (such as Cartrol), labetalol (such as Normodyne, Trandate) or nadolol (such as Corgard)); a diuretic (hydrochlorothiazide (such as HCTZ, HydroDiuril, others), chlorothiazide (such as Diuril), chlorthalidone (such as Hygroton, Thalitone), furosemide (such as Lasix), torsemide (such as Demadex), bumetanide (such as Bumex), ethacrynic acid (such as Edecrin), triamterene (such as Dyrenium, Maxzide, Dyazide), amiloride (such as Midamor), spironolactone (such as Aldactone), eplerenone (such as Inspra)); metoclopramide (such as Reglan); tetracycline (such as Broadspec, Emtet, Panmycin, Sumycin, Tetracap); erythromycin (such as E.E.S., E-Mycin, Eryc, Ery-Tab, PCE) or clarithromycin (such as Biaxin); sulfasalazine (such as Azulfidine); sulfasalazine (such as Azulfidine); another medicines for irregular heartbeats (quinidine (such as Quinidex, Quinora, Cardioquin), amiodarone (such as Cordarone) or propafenone (such as Rythmol)); itraconazole (such as Sporanox); a calcium channel blocker (diltiazem (such as Cardizem, Dilacor XR, Tiazac), amlodipine (such as Norvasc), felodipine (such as Plendil), nifedipine (such as Procardia, Adalat), verapamil (such as Verelan, Calan, Isoptin, Covera-HS)), an antacid or laxative that contains aluminum, magnesium or kaolin-pectin (such as Maalox, Rolaids, Mylanta, Milk of Magnesia).

Be careful with Lanoxin if you have allergies to medicines, foods, or other substances.

Be careful with Lanoxin if you suffer from or have a history of thyroid disease, cancer, kidney disease, heart arrhythmias.

Use Lanoxin with great care in case you want to undergo an operation (dental or any other).

Elderly people (> 65 years) should take the lowest dose.

Avoid alcohol.

Avoid machine driving.

Do not stop taking Lanoxin suddenly.

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This study assesses the role of prednisone and endogenous digoxin-like immunoreactivity (EDLI) in the increased Na+ pump activity in renal allograft patients. Red blood cell (RBC) Na+ transport activities and plasma concentrations of EDLI were measured in ten controls and ten renal allograft recipients (5 hypertensive) while undergoing treatment with cyclosporin, prednisone, and azathioprine, and also after prednisone withdrawal. As compared to controls, prednisone-treated patients showed an increased Na+ pump activity (0.323/h vs 0.571, P less than 0.05) and decreased RBC Na+ concentration (6.69 mM vs 4.99, P less than 0.05). They also showed a decrease in the activity of cotransport, countertransport, and passive Na+ efflux (0.02/h vs 0.005, P less than 0.05; 207 mumol/l vs 35, P less than 0.05; 0.02/h vs 0.005 respectively, P less than 0.05). After prednisone withdrawal, normotensive and hypertensive patients showed RBC Na+ transport system activities and RBC Na+ concentration similar to those of controls. EDLI was not detected in controls or in patients. We conclude that prednisone treatment increased the Na+ pump activity, and decreased the RBC Na+ concentration. Moreover, it induced a decrease in the activity of secondary RBC Na+ transport systems. This study provides no evidence for a modulatory role of EDLI in the RBC Na+ pump activity. Neither parameters can be presumed to be a marker of hypertension in these patients.

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Using Non-small cell lung cancer (NSCLC) as subject, to explore the characteristics of immune response in immunological microenvironment at the tumor site and its effect on anti-tumor immunity.

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A prospective analysis of the samples from 100 requests to monitor patients being treated with digoxin. The samples were processed in AxSYM® and Architect®. The techniques were assessed using the linear regression coefficient, determination coefficient, mean absolute error, mean squared prediction error and the Bland-Altman method.

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The epidemiology and etiology, pathophysiology, diagnosis, and treatment of congestive heart failure (CHF) are reviewed. CHF affects as many as 4 million Americans and is one of the most prevalent causes of death in hospitalized patients. Major risk factors for developing CHF include advanced age, male sex, hypertension, coronary artery disease, smoking, hypercholesterolemia, diabetes mellitus, and rheumatic heart disease. Heart failure results from decreased intrinsic myocardial contractility caused by one or more of three changes: (1) altered adrenergic nervous system function, (2) impaired delivery of calcium to contractile elements in the heart, and (3) reduced myosin-ATPase activity in the myocardium. The disease is progressive, and no intervention has yet been found to stop it effectively. CHF is diagnosed based on subjective signs and symptoms and objective assessment using auscultation, ECG, chest roentgenogram, laboratory tests, and noninvasive and invasive tests. Treatment of CHF begins with restriction of physical activity and sodium intake. Pharmacologic interventions start with either digitalis glycosides or thiazide diuretics; both may be used concomitantly as the disease progresses. Current studies are focusing on the use of angiotensin-converting enzyme inhibitors as first-line agents for CHF. When CHF worsens, loop diuretics are substituted for or added to the thiazide diuretics, and vasodilators are added to reduce the workload on the heart. Other inotropic agents, including the new bipyridine derivatives, may also be used. In patients not responding to these and other aggressive therapeutic interventions, cardiac transplantation is the only option. Despite advances in management of CHF, little improvement in overall survival has been demonstrated, and no intervention has stopped or reversed the progression of CHF.

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I compared the feeding responses of five species ofPeromyscus mice (aztecus, polionotus, melanotis, leucopus, andmaniculatus) to three bitter-tasting cardenolides (ouabain, digoxin, and digitoxin) that differ greatly in lipophilic character.Peromyscus, like other muroid rodents, are unusual in that they can ingest relatively large amounts of cardenolides without adverse physiologic effects. In experiment 1, I determined avoidance thresholds for the three cardenolides with 48 hr, two-choice tests. Mice exhibited large interspecific differences in avoidance threshold, and the interspecific ranking of the thresholds (maniculatus=leucopus >melanotis >polionotus >aztecus) was the same for each of the cardenolides. In experiment 2, I reevaluated the avoidance thresholds, but this time monitored the pattern of intake (i.e., bout lengths) during initial feeding encounters with cardenolidelaced diets. For each cardenolide, mice were subjected to three tests. In test 1, they received a control diet; in test 2, a diet containing the cardenolide at a concentration 1 log, unit below the avoidance threshold (as determined in experiment 1); and in test 3, a diet containing the cardenolide at the avoidance threshold concentration. Results were similar across all species and cardenolide types: Bout lengths in tests 1 and 2 were statistically equal, whereas those in test 3 were significantly shorter than those in test 1. The rapid rejection of cardenolide-laced diets in test 3 is consistent with a preingestive (i.e., gustatory) mechanism underlying the avoidance thresholds. I conclude (1) thatPeromyscus species differ substantially in taste sensitivity to cardenolides and that these differences may influence each species' respective ability to eat cardenolide-laced insects; and (2) that a species' relative taste sensitivity to one cardenolide predicts its sensitivity to other cardenolides.

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The organization of eukaryotic chromosomes into euchromatin and heterochromatin represents an enigmatic aspect of genome evolution. Constitutive heterochromatin is a basic, yet still poorly understood component of eukaryotic genomes and its molecular characterization by means of standard genomic approaches is intrinsically difficult. Drosophila melanogaster polytene chromosomes do not seem to be particularly useful to map heterochromatin sequences because the typical features of heterochromatin, organized as it is into a chromocenter, limit cytogenetic analysis. In contrast, constitutive heterochromatin has been well-defined at the cytological level in mitotic chromosomes of neuroblasts and has been subdivided into several bands with differential staining properties. Fluorescence in situ hybridization (FISH) using Bacterial Artificial Chromosomes (BAC) probes that carry large genomic portions defined by sequence annotation has yielded a "revolution" in the field of cytogenetics because it has allowed the mapping of multiple genes at once, thus rendering constitutive heterochromatin amenable to easy and fast cytogenetics analyses. Indeed, BAC-based FISH approaches on Drosophila mitotic chromosomes have made it possible to correlate genomic sequences to their cytogenetic location, aiming to build an integrated map of the pericentric heterochromatin. This chapter presents our standard protocols for BAC-based FISH, aimed at mapping large chromosomal regions of mitotic heterochromatin in Drosophila melanogaster.

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Survival following out-of-hospital cardiac arrest (OHCA) from ventricular fibrillation (VF) is poor and dependent on a rapid emergency response system. Improvements in emergent early response have resulted in a higher percentage of patients surviving to admission. However, the admission variables that predict both short- and long-term survival in a region with high discharge survival following OHCA require further study in order to identify survivors at subsequent highest risk.

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The disposition of flecainide appeared to be influenced by the CYP3A5*3 and possibly the CYP1A2*1F polymorphisms, particularly in subjects with CYP2D6 variant alleles.

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Hospitalized elderly patients taking digitoxin had a lower rate of toxicity than those taking digoxin.

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Overall, 212 patients (27.28%) received digoxin as the only heart control strategy, 184 received beta-blockers (23.68%), 58 (7.46%) were administered both, and 323 (41.57%) received none of these drugs. Digoxin was not associated with all-cause mortality (estimated hazard ratio=1.42; 95% confidence interval, 0.77-2.60; P=.2), admission due to any cause (estimated hazard ratio=1.03; 95% confidence interval, 0.710-1.498; P=.8), or admission due to cardiovascular causes (estimated hazard ratio=1.193; 95% confidence interval, 0.725-1.965; P=.4). No association was found between digoxin use and all-cause mortality, admission due to any cause, or admission due to cardiovascular causes in patients without heart failure. There was no interaction between digoxin use and sex in all-cause mortality or in survival free of admission due to any cause. However, an association was found between sex and admission due to cardiovascular causes.

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Prompted by animal studies reporting the accumulation of digitalis-glycosides in ocular tissues, we investigated whether measurement of digoxin levels in human ocular tissues can improve the postmortem diagnosis of lethal digoxin intoxication. Digoxin was measured in the vitreous humor and choroid-retina of patients who had received in-patient treatment with digoxin prior to death (therapeutic group) and in a single case of suicidal intoxication. The results were compared with the digoxin levels in the femoral vein blood, myocardium, kidney and liver, and evaluated in light of the medical history of each patient. In the therapeutic group the mean digoxin level was higher in the choroid-retina than in other tissues and body fluids. The range of variation in levels in the choroid-retina following therapeutic doses was comparable to that in the other tissues. An extremely high level of digoxin was present in the choroid-retina in the case of suicidal intoxication. In all cases, levels in the vitreous humor were very low compared to those in the choroid-retina. Hence, it is unlikely that significant distortion of choroid-retinal levels occurs due to postmortem diffusion of digoxin into the vitreous body. Our results indicate that measurement of digoxin levels in the choroid-retina can aid the postmortem diagnosis of lethal digoxin intoxication.

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lanoxin generic substitution 2015-10-15

The calcium antagonists are a heterogeneous class of Viagra 150 Mg drugs which block the inward movement of calcium into cells through 'slow channels' from extracellular sites. By inhibiting phase 0 depolarisation in cardiac pacemaker cells and phase 2 plateau in myocardium, and by depressing calcium ion flux in smooth muscle cells of blood vessels, these agents may exert profound effects on the cardiovascular system, particularly in susceptible individuals or in overdose. Sinus node depression, impaired atrioventricular (AV) conduction, depressed myocardial contractility, and peripheral vasodilatation may result. Pharmacokinetic features of calcium antagonists include rapid and complete absorption from the gastrointestinal tract, with extensive first-pass hepatic metabolism yielding generally low bioavailability. The volume of distribution is generally large and protein binding is high. Elimination is almost entirely by the liver. Impaired renal function does not affect pharmacokinetics. Verapamil is the most potent inhibitor of cardiac conduction and contractility, with diltiazem also showing such effects. Nifedipine is the most potent vasodilator, but only occasionally impairs the sinus node or AV conduction. Significant pharmacodynamic effects are common during combination therapy with calcium antagonists, especially verapamil and beta-blockers. Verapamil may significantly elevate serum digoxin concentrations and may exert additive negative effects on chronotropism and dromotropism when this combination is used. Overdoses of calcium entry blockers are becoming more frequent and reflect an extension of the known pharmacodynamic profile of these agents. Typical features include confusion or lethargy, hypotension, sinus node depression and cardiac conduction defects. Onset of symptoms may be delayed if a sustained release preparation is ingested. Management of calcium antagonist overdose includes gut decontamination with lavage and activated charcoal. All symptomatic patients and patients with a history of ingesting a sustained release preparation should be admitted for ECG monitoring. If bradycardia and/or conduction defects contribute to hypotension, atropine or isoprenaline (isoproterenol) may accelerate the ventricular rate. Transvenous pacing may be required. Depressed myocardial contractility usually responds well to calcium chloride or calcium gluconate administration, but further inotropic support may be required. Peripheral vasodilation should be managed with intravenous fluids and a pressor agent such as dopamine or norepinephrine (noradrenaline).

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Mean score of erectile dysfunction was 14.02 ± 6.26 and 80% of heart failure patient had erectile dysfunction. Erectile dysfunction was Geodon Maximum Dose significantly associated with age (P < 0.001), education (P = 0.019), occupation (P = 0.002), hemoglobin level (P = 0.003), left ventricular ejection fraction (P = 0.030), cholesterol level (P = 0.001), renal dysfunction (P = 0.009), use of digoxin (P = 0.014), angiotensin converting enzyme inhibitors (P < 0.001), beta blocker (P = 0.001), diuretics (P = 0.035), depression (P < 0.001) and quality of life (P < 0.001).

lanoxin drug classification 2015-03-06

Clarithromycin is a macrolide antibacterial that differs in chemical structure from erythromycin by the methylation of the hydroxyl group at position 6 on the lactone ring. The pharmacokinetic advantages that clarithromycin has over erythromycin include increased oral bioavailability (52 to 55%), increased plasma concentrations (mean maximum concentrations ranged from 1.01 to 1.52 mg/L and 2.41 to 2.85 mg/L after multiple 250 and 500 mg doses, respectively), and a longer elimination half-life (3.3 to 4.9 hours) to allow twice daily administration. In addition, clarithromycin has extensive diffusion into saliva, sputum, lung tissue, epithelial lining fluid, alveolar macrophages, neutrophils, tonsils, nasal mucosa and middle ear fluid. Clarithromycin is primarily metabolised by cytochrome P450 (CYP) 3A isozymes and has an active metabolite, 14-hydroxyclarithromycin. The reported mean values of total body clearance and renal clearance in adults have ranged from 29.2 to 58.1 L/h and 6.7 to 12.8 L/h, respectively. In patients with severe renal impairment, increased plasma concentrations and a prolonged elimination half-life for clarithromycin and its metabolite have been reported. A dosage adjustment for clarithromycin should be considered in patients with a creatinine clearance < 1.8 L/h. The recommended goal for dosage regimens of clarithromycin is to ensure that the time that unbound drug concentrations in the blood remains above the minimum inhibitory concentration is at least 40 to 60% of the dosage interval. However, the concentrations and in vitro activity of 14-hydroxyclarithromycin must be considered for pathogens such as Haemophilus influenzae. In addition, clarithromycin achieves significantly higher drug concentrations in the epithelial lining fluid and alveolar macrophages, the potential sites of extracellular and intracellular respiratory tract pathogens, respectively. Further studies are needed to determine the importance of these concentrations of clarithromycin at the site of infection. Clarithromycin can increase the steady-state concentrations of drugs that are primarily depend upon CYP3A metabolism (e.g., astemidole, cisapride, pimozide, midazolam and triazolam). This can be clinically important for drugs that Albenza Syrup have a narrow therapeutic index, such as carbamazepine, cyclosporin, digoxin, theophylline and warfarin. Potent inhibitors of CYP3A (e.g., omeprazole and ritonavir) may also alter the metabolism of clarithromycin and its metabolites. Rifampicin (rifampin) and rifabutin are potent enzyme inducers and several small studies have suggested that these agents may significantly decrease serum clarithromycin concentrations. Overall, the pharmacokinetic and pharmacodynamic studies suggest that fewer serious drug interactions occur with clarithromycin compared with older macrolides such as erythromycin and troleandomycin.

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As of August 13, 2002, 334 patients have been enrolled from 68 participating centers. Enrollment is expected to be concluded in May 2003 with a minimum follow-up of 2 Paxil Dosage Reduction years.

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PAR calculated between the end and the beginning of the VM using the last two beats and the first three beats of the straining phase Trileptal User Reviews and simultaneous measurement of PCWP.

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The bidirectional pH-dependent transport of weak Feldene 20mg Capsules bases was studied in Caco-2 cell monolayers in the physiologic pH range of the gastrointestinal tract.

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The authors examined endogenous digitalis-like factor (DLF) concentrations in the serum and urine in 65 patients with acute myocardial infarction. Radioimmunoassay was used for the examination and patients' data were analyzed in detail in relation to sex, risk factors and acute myocardial infarction complications. The concentrations of digitalis-like factor found in the serum of men (0.317 +/- 0.026 micrograms/l) and women (0.256 +/- 0.057 micrograms/l) with acute myocardial infarction were much higher compared with values of healthy men (0.009 +/- 0.004 micrograms/l) and women (0.015 +/- 0.012 micrograms/ Indocin Brand Name l). This finding is in agreement with data published by others and suggests a role of DLF in the pathogenesis of myocardial infarction.

lanoxin drug dose 2017-05-31

In a total study population of 10,932 persons, 419 SCDs occurred during a median follow-up of 9.8 years. In non-users of digoxin, the risk of SCD was not different across genotypes. In digoxin users, homozygous T allele carriers of C1236T (HR 1.90; 95% CI 1.09 Suprax Suspension Coupon to 3.30; allele frequency 0.43), G2677T (HR 1.89; 95% CI 1.10 to 3.24; allele frequency 0.44) and C3435T (HR 1.72; 95% CI 1.03 to 2.87; allele frequency 0.53) had a significantly increased risk of SCD in a recessive model. Interaction between the ABCB1 polymorphisms and digoxin use was significant for C1236T and G2677T in the age-adjusted and sex-adjusted model.

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The hypothalamus secretes an endogenous membrane Na+-K+ ATPase inhibitor, digoxin. A digoxin-mediated model of quantal perception is proposed. In the quantal state, self replication of self-organized macromolecules is possible. This leads to the origin of molecular organisms like prions. Macromolecules group together to form organelle, which in evolutionary terms are independent bacteria. The organelle/bacteria symbiotically cluster together to form the cell. The human organism, including the brain, can be visualized as an organized cluster or colony of unicellular, symbiotically grouped flagellated bacteria. Synaptic connections form in the bacterial cluster leading to the evolution of the primitive neuronal networks, and later the human brain. The role of quantal perception and the observer function of consciousness in the origin of matter is important. Symbiotically clustered intergalactic magnetotactic bacterial networks are important in the evolution of the universe.

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A sensitive and rapid method based on formate-adduct ion detection was developed and fully validated for digoxin determination in rat plasma. For LC/MS/MS detection with formate-adducts as precursor ions, transitions of m/z 825.5→779.9 for digoxin and m/z 809.5→763.4 for the internal standard (digitoxin) were monitored in negative mode. To investigate the impact of formic acid on the mass response and method sensitivity, a formic acid concentration range of 0-0.1% (0, 0.0005%, 0.002%, 0.01%, 0.1%, v/v) was evaluated. A concentration of 0.002% gave the highest sensitivity, which was 16- to 18-fold higher than deprotonated ions, and was designated as the contribution giving the strongest ionization enhancement and adduction. A number of parameters were then varied in order to optimize the method, and a limit of quantitation (LOQ) at 0.2 ng/mL was reached with an injection volume of 5 μL, a total run time of 3 min, and 0.1 mL of rat plasma. A calibration curve was plotted over the range 0.2-50 ng/mL (R(2)=0.9998), and the method was successfully applied to study pharmacokinetics in rat following a single oral administration of digoxin (0.05 mg/kg). Four additional steroid saponins (digitoxin, deslanoside, ginsenoside Rg1 and Rb1) were investigated to assess the impact of formic acid on the mass response of steroid saponins. Compounds with a conjugated lactonic ring in their structures such as digoxin, digitoxin and deslanoside tended to form stable formate-adduct ions more easily. The LC/MS/MS method developed here is therefore well suited for the quantification of steroid saponins that are difficult to deprotonate using other MS approaches.