Marker drugs

A method should be able both to quantify the amount of marker drug residue present in the sample and to identify the compound unambiguously. Historically, this required two distinct procedures a determinative procedure used to quantify the analyte, and a confirmatory procedure used to unequivocally identify the analyte. The need for two procedures was driven by the limitations of available technology. Most determinative methods over the last two decades have been based on liquid chromatography, usually with ultraviolet (UV)/visible or fluorescence defection. Limitations of cost. 

Detection. Identification of the presence or absence of a particular substance, i.e., disease marker, drug of abuse or environmental pollutant. 

Lateral-flqw, fiQy -tirrQUgh, or solid Cardiac markers, drugs, CRP, allergy, and fertility... 

Time-resolved fluorescence Cardiac markers, drugs, CRP... 

The effect of the latent acidic excipient maleic anhydride on the rate of release of a marker drug is shown in Fig. 9 [31]. These data clearly show the effect on polymer erosion rate and the consequent ability to vary erosion rates by relatively minor adjustments in the concentration of the acidic excipient. 

The pharmacokinetics and metabolism of phenazone (largely used as an investigational marker drug of enzyme induction or inhibition) were studied in two groups of patients with prostate cancer before and after they took either bicalutamide 50 mg daily (7 patients) or 150 mg daily (11 patients) for 12 weeks. Small changes in the phenazone pharmacokinetics were found (half-life reduced by 16.3% with the 50 mg bicalutamide dos-... 

The multiple surface plasmon resonance (SPR) sensor was appUed for detection and quantification of dextromethorphan (36) with the use of molecularly imprinted P-CD polymer [81]. The cough suppressant 36 is a marker drug used to identify the activity of the CYP2D6 class of p450 monooxygenases. It was found that the sensor may be used to measure the consumption of 36 by CYP enzymes. 

Headache is a common adverse reaction but should decrease widi continued therapy. If headache persists or becomes severe, notify die primary healdi care provider because a change in dosage may be needed. In patients who get headaches, die headaches may be a marker of the drug s effectiveness. Fhtients should not try to avoid headaches by altering die treatment schedule because loss of headache may be associated with simultaneous loss of drug effectiveness. Aspirin or acetaminophen may be used for headache relief. 

Many authors reported poor elimination of antiepileptic drug carbamazepine [6,13,17,49, 54]. Pharmacokinetic data indicate that only 1-2% of carbamazepine is excreted unmetabolized. However, glucuronide conjugates of carbamazepine can presumably be cleaved in the sewage, and thus increase its environmental concentrations [51]. This is confirmed by its high ubiquity in the enviromnent at concentration levels of several hundred nanograms per liter in different surface waters. Due to its recalcitrant nature, it can be used as anthropogeiuc marker for the contamination of aquatic environment. 

The rate of polymer erosion in the presence of incorporated anhydride and release of an incorporated drug depends on the pK of the diacid formed by hydrolysis of the anhydride and its concentration in the matrix (20). This dependence is shown in Fig. 7 for 2,3-pyridine dicarboxylic anhydride and for phthaUc anhydride. In this study, methylene blue was used as a marker. The methylene blue release rate depends both on the pK and on the concentration of diacid hydrolysis product in the matrix. However, at anhydride concentrations greater than 2 wt%, the erosion rate reaches a limiting value and further increases in anhydride concentration have no effect on the rate of polymer hydrolysis. Presumably at that point Vj, the rate of water intrusion into the matrix, becomes rate limiting. 

Convincing evidence for a surface erosion process is shown in Fig. 8, which shows the concomitant release of the incorporated marker, methylene blue, release of the anhydride excipient hydrolysis product, succinic acid, and total weight loss of the device. According to these data, the release of an incorporated drug from an anhydride-catalyzed erosion of poly (ortho esters) can be unambiguously described by a polymer surface erosion mechanism. 

Beeler A, Zaccaria L, Kawabata T, et al CD69 upregulation on T cells as an in vitro marker for delayed-type drug hypersensitivity. Allergy 2008 63 181-188. 

The first issue lies in the whole realm of the human disease process itself. Many adverse drug events mimic diseases and vice versa. Is an adverse event really an adverse event, or is it merely a natural occurrence of a disease process that is entirely independent of drug exposure The science of drug safety is often complicated by the lack of objective markers of drug toxicity that can systematically separate a disease process from an adverse drug event process [2]. Clinical trials, often viewed as the gold standard to assess efficacy, are simply too limited in scope to answer safety questions in a systematic way. 

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