NEUROLEPTICS

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Transcript NEUROLEPTICS

Antipsychotic Drugs

William H. Anderson, Ph.D.

Washoe County Sheriff’s Office Reno, NV

Various Names for These Drugs

ANTIPSYCHOTICS

MAJOR TRANQUILIZERS

NEUROLEPTICS

PSYCHOTROPIC AGENTS

Schizophrenia

Disturbance lasting at least 6 months & including at least 1 month of 2 or more of the following positive symptoms:

 Positive symptoms include      Delusions beliefs that are contrary to reality & can involve control, grandeur, or persecution Hallucinations stimuli perceptions that occur in the absence of  often auditory and/or olfactory Disorganized speech Grossly disorganized or catatonic behavior Negative symptoms

DMS-IV

Schizophrenia

Negative symptoms:  Alogia-Poverty of speech and low initiative  Avolition-lack of will  Anhedonia-absence of pleasure  Affective flattening-lack of emotional expression Mood symptoms:  Depression, Anxiety, Hopelessness, etc.

 Social or occupational dysfunction

DMS-IV

Schizophrenia

 Common onset 15-25 years of age  1% general population develops at some point in their lives  Common major mental illness in 65+ years  Smoking: 3 times more likely in schizophrenia than general population  Excessive mortality  20% shorter life expectancy  10% suicide rate

Antipsychotic Medications

 Antipsychotic medications diminish the thought disorder evident in schizophrenia  AP medications have similar efficacy (mostly act on positive symptoms)  AP medications require weeks to take effect

Antipsychotic Medications

    We don’t know how they work but they act upon many receptors  D 1 , D 2 , D 4 , D 5 , 5HT 2 , 5HT 6 , 5HT 7 , alpha 1 adrenergic, H 1 , cholinergic - muscarinic, nicotinic They have many side effects and serious toxicities We are not sure of their therapeutic range There is overlap between therapeutic and toxic blood concentrations for some - many are difficult to analyze - they are ubiquitous

Antipsychotic Medications Receptor Oriented Side Effects

     Sedation – Antihistaminic Weight gain – Antiserotonergic EPS, prolactin release – Antidopaminergic Urinary retention, dry mouth, blurred vision, constipation, sinus tachcardia, cognitionand memory effects – Anticholinergic Orthostatic hypotension, reflex tachycardia – Anti-alpha 1 -adrenergic

Introduction of Antipsychotics in the US

1950 1960 1970 1980 1990 2000 Era of “Typical Antipsychotics”

Terms used to categorize antipsychotics

 Typical  Conventional  Classic  Standard  1 st Generation vs. vs. vs. vs.

vs. Atypical Novel New Modern 2 nd Generation

Classes of Antipsychotic Medications

  Typical   (e.g. CPZ) Block D2 receptors Produce neurological effects ( neuroleptics …) Atypical     Greater separation between AP action and extrapyramidal activity Block D4 receptors: Clozapine acts on D4 receptors in the accumbens (but not in the striatum) Less risk of extrapyramidal (EP) effects Negative symptoms may respond to atypical AP medications (e.g. risperdal)

Typical vs. Atypical

  Typical     High D 2 Low 5-HT 2A D 1 =D 2 Increases NT in caudate and nucleus accumbens Atypical     High 5-HT 2A Lower D 2 Low D 1 Increases NT in nucleus accumbens only

Antipsychotics: ADME

 Large interindividual variation in bioavailability  GI absorption tends to be incomplete  High degree of first pass metabolism  Large to very large V d  Weak bases  Highly protein bound

Antipsychotics: ADME

 Extensive hepatic metabolism  CYP 450  Possible CYP 450 polymorphism  Significant active metabolite profile

Phenothiazine Antipsychotics

Mellaril ® Prolixin ® Serentil ® Stelazine ® Thorazine ® Trilafon ® Vesprin ® (thioridazine) (fluphenazine) (mesoridazine) (trifluoperazine) (chlorpromazine) (perphenazine) (triflupromazine)

Phenothiazines

CH 3 N CH 3 N CH 3 N S

Chlorpromazine

Cl N S

Thioridazine

S CH 3

ADDITIONAL CLASSICAL ANITPSYCHOTICS

Haldol ® Loxitane ® Moban ® Navane ® (haloperidol), Haldol Decanoate (loxapine) (molindone) (thiothixene)

Extrapyramidal Symptoms

  Clinical Symptoms    Tremor Dystonic reactions Pseudo parkinsonism Akathisia Therapy to Prevent EPS  Treat EPS with benztropine (Cogentin  ), trihexyphenidyl (Artane  ), biperiden (Akineton  ) or diphenhydramine  Tardive dyskinesias  Potentially irreversible

   

Acute Dystonia

(First week to month) Severe spasm of the muscles of the tongue, neck or back • These result in torticallis, facial grimacing Oculogyric Crisis: involuntary upward deviation of the eyes Opisthotonus: tetanic spasm of the back muscles causing the trunk to arch forward while head and lower limbs are thrust backward. • These may result in joint dislocation Laryngeal dystonia: can impair respiration

Pseudo-Parkinsonism

         bradykinesia  slowing of movement pill rolling mask-like faces hyper salivation (drooling) resting tremor rigidity shuffling gait cog wheeling stooped posture

Akathisia

 Inability to sit or remain quiet  characterized by  pacing  squirming  the need to be in motion  profound sense of restlessness

Tardive Dyskinesia

 Involuntary choreoathetiod movements of tongue and face     choreoathetiod: twisting, writhing worm-like movements   lip smacking tongue flicking motions  may also produce movements of limbs, toes, fingers Risk increases with length of time on medication and dosage of medication. These symptoms are non-reversible for most patients.

There is no effective treatment for TD

Sudden Death Syndrome

 Phenothiazines  Large daily doses (>1000 mg)  Mechanism:  Asphyxiation  seizure  ventricular fibrillation   CV collapse during hypotensive crisis Some atypical drugs also cause sudden death

Neuroleptic Malignant Syndrome

 Loss of thermal regulation  Contributing Factors:    ambient heat & dehydration underlying brain damage & dementia high neuroleptic dose (genetic vulnerability?)  Treatment  neuroleptic withdrawal   intensive supportive care (hydration, temp. reg.) medications (dantrolene or pergolide)

Phenothiazine Lethality

 Phenothiazines are generally safe drugs even when taken in overdose.

 Their therapeutic indices ~200.

 Deaths due to overdose have been reported, but these are rare.

Emergency Department Episodes 1994-2001 Estimated From SAMSHA DAWN Data

3500 3000 2500 2000 1500 1000 500 0 19 94 19 96 19 98 20 00 chlorpromazine fluphenazine perphenazine thioridazine trifluoperazine

Thioridazine (Mellaril

)

 1959 Formulations:      Tablets (10-100 mg) Liquid (30-100 mg/mL) Initial dose  25 mg po t.i.d.

Maximum: 800 mg/day Titrate down to maintenance dose

N S N CH 3 S CH 3

Thioridazine: Pharmacology

   V d : 18 L/kg Half-life:  26-36 hr Metabolism  in the gastric mucosa and during first pass

N S

 12 metabolites  Pathways:      Oxidation (e.g. mesoridazine*, sulforidazine*) Ring oxidation (e.g. ring sulfoxide) N-Demethylation Hydroxylation Glucuronidation

N CH 3 S CH 3

Thioridazine: Dosing

 Single Acute Oral  Average serum   4 hr 25 mg: 0.05 mg/L parent 0.17 mg/L mesoridazine 0.05 mg/L sulforidazine  Peak plasma  100 mg: 0.24 mg/L thioridazine (1.7 hr) 0.32 mg/L mesoridazine (4 hr) 0.08 mg/L sulforidazine (6.9 hr)

N S N CH 3 S CH 3

Liver Establishes Overdose

A. Poklis, Chap 31, Casarett & Doull’s Toxicology: the Basic Science of Poisoning. C.D. Klaassen, ed. 2001

Suicide via Chlorpromazine

Subject

62 year old white female

assisted living complex

private apartment

history

schizophrenia

paranoia

reclusive

tobacco use

Suicide via Chlorpromazine

Investigation

found by apartment manager

living room couch

last contact 10 days prior

no evidence of disturbance or struggle

ME case

unknown/ possible natural cause

autopsy ordered

two letters with wording indicating suicidal intent

Suicide via Chlorpromazine

Autopsy

Pulmonary emphysema, moderate diffuse

  

Probable colloid goiter, thyroid gland Postmortem decomposition, severe Toxicology

Central “blood”

 

chlorpromazine: positive (qns for quantification) alprazolam: 0.17 mg/L

ethanol: 40 mg/dL

Liver

chlorpromazine: 550 mg/kg

Suicide via Chlorpromazine

Disposition

further investigation revealed:

a recent chlorpromazine prescription

 

40-50 tablets (100 mg) missing the decedent’s estranged husband had committed suicide four weeks prior

cause of death

chlorpromazine toxicity

manner of death

suicide

RE Winecker Amer Acad Forensic Sci, 2003

Haloperidol: Dosing

 Single Acute  0.5 to 5 mg  > 100 mg daily  up 1000 mg daily  Peak Plasma  Oral   ≤ 5 hr 10 mg: 3 μ g/L  Intramuscular   20 min 2 mg: 5 μ g/L

F F O CCH 2 CH 2 CH 2 N OH N OH OH Cl Cl

Phenothiazines:

BioAnalytical Considerations

Absorption to glassware Interference (artifacts and mtb’S) Loss of drug in plasma: PROTEIN BINDING Liver important for PM interpretation (10 mg/kg) Postmortem re-distribution (8x) Drug/metabolite stability

Phenothiazines: BioAnalytical Considerations

 Spot tests  Detection in Routine Screens  Liquid/Liquid or Solid Phase Extraction of bases  TLC  GC-NPD, GC-ECD  HPLC  Quantitative Analysis  GC/MS  LOD- 1 to 5 ng/mL

Atypical Antipsychotics

    Serotonin & Dopamine Antagonists Treats both positive & negative symptoms with fewer side effects.

Much Less Extrapyramidal Symptoms Controls  Mood & Behavior -Physical Coordination   Appetite Sleep -Body Temperature

6000 Emergency Department Episodes 1994-2001 Estimated From SAMSHA DAWN Data

olanzapine

5000

quetiapine

4000

risperidone

3000 2000 1000 0 1994 1995 1996 1997 1998 1999 2000 2001

Olanzapine

Chemistry (Zyprexa

®

)

     Structure C 17 H 20 N 4 S MW = 312.44

pKa = 5.0, 7.4

Thienobenzodiazepine Derivative  Organic base

Olanzapine General Information

   FDA Approval in late 1996 Tablets as free base  2.5, 5, 7.5, and 10-mg doses Daily doses range from 10-20 mg a day

Olanzapine

Adverse Effects

       Drowsiness Dry mouth Hypotension Parasthesias CNS Depression Tachycardia Increased mortality in elderly with dementia related psychosis      Life-threatening hyperglycemia Alteration of blood lipids Elongated Q-T intervals Possible weight problems  Gain and loss Constipation

Olanzapine Pharmacokinetics

 

Absorption

  Well absorbed Extensive 1 st pass metabolism - 40 %

Distribution

   Vd T 1/2 Protein Binding 10 -20 L/kg 21 - 54 hours 93 %

Olanzapine Pharmacokinetics

 

Metabolism

   P450 CYP 1A2 & 2D6 N-desmethyl & 2 Hydroxymethylolanzapine Glucuronidation

Elimination

  57 % dose recovered in urine 7 % as unchanged drug

Olanzapine Analytical Considerations

  Thio group very unstable In-vitro   16 % in extraction 40 % during 1 week at 4 O C  Possibly stabilize with 0.25 % ascorbic acid

Olanzapine Analytical Methods

     TLC HPLC GLC GC/MS Internal standards: promazine, ethylmorphine ethyl-olanzapine (Lilly Co)

Olanzapine Therapeutic Steady State Trough Concentrations

Daily Dose

5 10 15 20

Olanzapine, ng/mL

7 9-14 19-21 ~26

Aravagiri et al. Therap Drug Monitor, 1997

Olanzapine Blood Concentrations

     1653 Clinical Specimens Olanzapine (ng/mL) Range 3 - 390 Mean 36 +/- 40 Median 26 86 % of the cases Range: 5-75       58 Postmortem Specimens Olanzapine (ng/mL) Range 10 – 5,000 Mean 358 +/- 758 Median 130 75 % less than 30O 86 % less than 500 Robertson et al. J Forensic Sci, 1999

Olanzapine Blood Concentrations

 Suggested that toxicity should be considered at conc above 100 ng/mL  One death due primarily to olanzapine at 160 ng/mL Robertson et al. J Forensic Sci, 1999  Other studies showed postmortem toxicity often above 1000 ng/mL  Literature reports of death at 237, 675, 400 heart (270 carotid) ng/mL

Olanzapine

Postmortem Femoral Blood Concentrations Mode of Death Olanzapine, ng/mL mean range Suicides (5) Accident (11) Natural (5) Homicide (1) Undetermined (2) 400 25 – 1,600 90 25 – 190 50 25 50 180 10; 1,200

D. Anderson, AAFS 2003

Olanzapine Postmortem Redistribution  16 deaths –  Heart/femoral ratio averaged 4.9 (0.7-23) D. Anderson, SOFT 1998

Dual Column NPD

Olanzapine Promazine (IS)

A. RTx-200: trifluoropropyl methyl polysiloxane (Restek) B. RTx-50: 50% phenyl, 50% methyl polysiloxane (Restek)

Jenkins et al. J Anal Toxicol 1998

Quetiapine

G

eneral Information

     Developed in 1993 FDA approval in Sept. 1997 Manufactured by Zeneca Pharmaceuticals Tablets as a fumarate salt (Seroquel ® )  25, 100 & 200 mg dose Daily doses range from 150-750 mg

Quetiapine Chemistry

      Structure C 21 H 25 N 3 O 2 S MW =383.6

pKa=3.3, 6.8

Dibenzothiazepine, organic base Structurally related to Clozapine

Quetiapine

Adverse Effects

       Dizziness Somnolence, sedation Constipation Dry mouth Dyspepsia Tachycardia Hypotension    Hyperglycemia Diabetes Headache

Quetiapine

Pharmacokinetics

 

Absorption

 Rapidly and completely absorbed after oral administration.

Distribution

   Vd T 1/2 Protein Binding 10 L/kg 2.7-9.3 hours 83 %

Quetiapine Pharmacokinetics

 

Metabolism

  CYP3A4  Sulfoxidation - Inactive  Oxidation - Inactive Active Metabolite : 7-Hydroxyquetiapine

Elimination

  73 % dose recovered in urine Less 1% as unchanged drug

Quetiapine

Dosage Regimen

   Peak Plasma conc within 1.5 hours Steady state within 2 days of dosing Dosing    Day 1: Day 2-3: Target: 25 mg bid 25-50 mg bid or tid 300-400 mg a day

Quetiapine Therapeutic Concentrations

  75 mg oral dose mean, 279 ng/mL range, 140 – 365 ng/mL 450 mg daily dose mean, 402 ng/mL range, 195 – 632 ng/mL

Quetiapine

Mode Suicide (22 cases) Accident (24) Natural (33) Total 79 cases* Average Quetiapine (ug/ml or ug/g) Heart Blood 6.6 (14 ) 2.3 (12) 0.65 (7) Femoral Blood 5.3 (12) 2.3 (7) 0.62 (4) Liver 76 (7) 37 (4) 5.4 (3) *Not all cases contained parent drug - metabolites only in some

D. Anderson, AAFS 2003

Toxic Quetiapine Concentrations

    Parker and McIntyre, JAT, 2005 (21 cases)   > than 1 mg/L in peripheral and central blood > than 0.5 mg/L in vitreous > than 5 mg/kg in liver – especially helpful  Wise and Jenkins, JFS, 2005 (3 cases)  Heart blood 0.72-18.37 mg/L Langman, Kaliciak, Carlyle, JAT, 2004 (3 cases)   Blood: 7.2, 16, 5.9 mg/L Liver: 120 mg/kg (only data reported) Similar reports in literature

Quetiapine Analytical Considerations

  Basic Drug      L/L extractions-Various TLC GC/NPD HPLC GC/MS Metabolite Pattern

Quetiapine

Cross-reacts with TCA Immunoassays

    Emit & CEDIA, not Triage  cross-reacts at 100 ug/mL parent drug in urine Normal therapeutic urine <1.0 ug/mL parent drug Patient urine following therapy & overdose, positive yield TCA results Cross-reactivity related to metabolites

Hendrickson & Morocco, J Clin Toxicol 2003

Capillary HP-5 NPD

A

.

7-Hydroxyquetiapine B. quetiapine metabolite C. quetiapine metabolite D. quetiapine

Anderson & Fritz J Anal Toxicol 2000

Quetiapine GC/MS

   Quetiapine: Major Metabolite: Minor Metabolites: 210, 239, 144, 253, 321 227, 210, 209, & 251 210, 239, 209, 251 210, 209, 239, 251, 322

Suicide via Quetiapine

 Subject   44 year old white female - homemaker History - depression  medications  bupropion    fluoxetine dextroamphetamine quetiapine

Suicide via Quetiapine

 Investigation     found by neighbors 3 p.m.

last seen alive 9:30 a.m. no evidence of disturbance or struggle  body in bedroom an autopsy ordered   a letter addressed to “my dear husband” - wording indicating suicide a bottle of quetiapine - 70 pills missing

Suicide via Quetiapine

 Autopsy     Mild pulmonary congestion and edema Healing contusions of abdomen and thigh Granular material in stomach Toxicology  Central blood   Trace: bupropion, detromethorphan, doxylamine Fluoxetine: 0.7 mg/L     Norfluoxetine: 1.1 mg/L

Quetiapine: 230 mg/L

Peripheral blood 

Quetiapine: 43 mg/L

Liver 

Quetiapine: 200 mg/kg

Suicide via Quetiapine

 Disposition of death   cause - quetiapine toxicity manner - suicide

RE Winecker Amer Acad Forensic Sci, 2003

Risperidone General Information

   Available since 1993 Tablets 0.25, 0.5, 1, 2, 3, 4-mg Solution 1 mg/ml

Risperidone Chemistry

    C 23 H 27 FN 4 O 2 MW = 410.49

pKa = ??

Benzisoxazole Derivative

Risperidone Pharmacokinetics

  

Dosing

  Initial Dose  1 mg bid Increase 1 mg bid on 2nd and 3rd day  Maximum 3 mg bid Dosage adjustments at 1-week intervals

Bioavailability

68-82 % Distribution

 Vd 0.7-2.1 L/kg

Risperidone

Pharmacokinetics

Metabolism

  Hydroxylation  9-Hydroxyrisperidone

(9-OH-R)

 Active

-

equivalent to risperidone  CYP2D6 polymorphism  ~ 6-10% caucasians  ~ 1% Asian Oxidative N-dealkylation  inactive

Risperidone Pharmacokinetics

 

Plasma half-life

  risperidone ~ 3 hr (fast) risperidone ~ 20 hr (slow)  9-OH-risperidone ~ 21 hr (fast)  9-OH-risperidone

Elimination

  ~ 30 hr (slow) 70% dose recovered in urine 15% dose recovered in feces

Risperidone Pharmacokinetics

  Blood/plasma ratio 0.67

Time to peak plasma concentration   risperidone 9-OH-risperidone ~ 1 hr ~ 3 hr (fast) ~ 17 hr (slow)  Time to steady state  risperidone  9-OH-risperidone ~ 1 day (fast -EM) ~ 5 day (slow-PM) ~ 5 days (fast)

Risperidone Therapeutic Steady State Plasma Concentrations, ng/mL

Dose, mg Risperidone 9-hydroxyrisperidone 2 6 10 16 3.2

9.2

13 15 Recent Case WCSO – None Detected 11 34 60 98 Long Term Care Facility – Dose to patient 0.5 mg/day Were they providing adequate care and giving prescribed dose?

National Medical Services, Toxi-News,2001

      Dizziness Somnolence Nausea Hypotension Anxiety Headache

Risperidone Adverse Effects

      Tachycardia EKG changes Confusion Lethargy Drooling Sudden death in elderly with dementia

Risperidone

Overdose Cases

 8 cases: 20 - 300 mg ingested     No fatalities Drowsiness & sedation Tachycardia & hypotension Extrapyramidal symptoms

MM McMullin, AAFS 1995

Risperidone Analytical Considerations

       Large MW & Polar molecule Low Therapeutic Concentrations RIA (Janssen) ToxiLab R f 0.25 Ris/9-OH, brown stage IV Liquid-liquid extraction GC: Thermal degradation HPLC: diode-array or MS

Risperidone Toxic & Lethal Concentrations

  100 mg ingestion  1,070/100 ng/ml (Ris/9-OH-R)-Admission Blood  74/50 ng/ml - 48 hours post ingestion Suicidal Ingestion  1,800 ng/ml Blood  14,400 ng/ml Urine Lee et al., J. Clin., Psychopharm., 1997 Springfield & Bodiford, J Anal Toxicol, 1996

Clozapine General Information  Available since 1989  Tablets 25, 100 mg   C 18 H 19 ClN 4 MW = 326.83

  pKa = 3.7, 7.6

Tricyclic dibenzodiazepine derivative

Clozapine Pharmacokinetics      Dosing   Initial 12.5 mg once or twice per day Increase to 300-450 mg/day after two weeks Bioavailability Vd 50-60% 2-7 L/kg Half-Life Metabolism    6-17 hrs.

N-demethylation, N-oxidation, oxidation of chlorine-containing ring, and thiomethyl conjugation.

N-desmethylclozapine has very little activity; others inactive Metabolized by P450 CYP1A2

Clozapine Pharmacokinetics    Elimination    50% dose excreted in urine 30% dose excreted in feces Trace amounts of unchanged drug excreted in urine in therapeutic dosing Blood/plasma ratio 0.80

Time to peak plasma concentration  3 hrs Range: 1-6.3 hrs

Clozapine T herapeutic Steady State Plasma Concentrations    500 mg daily for 12 weeks    Clozapine 0.472 mg/L Norclozapine 0.201 mg/L in those who responded to treatment Clozapine 0.328 mg/L Norclozapine 0.156 mg/L in those unresponsive to treatment Threshold for response 0.350–0.400 mg/L but adverse effects over twice as high at 0.350 or greater as compared to below 0.350

200-700 mg/day  0.03-1.016 mg/L All studies show wide variations in concentrations as a function of dose

Clozapine Adverse Affects   Agranulocytosis   Risk so high that drug should be reserved for use in   Severely ill patients who show inadequate response to conventional antipsychotics Reducing the risk of recurrent suicidal behavior Patients must have a baseline WBC and ANC before initiation of therapy as well as regular WBC and ANC during treatment and for a least 4 weeks after discontinuation of treatment.

Seizures  Greater chance at higher dose

Clozapine Adverse Affects       Myocarditis –  Potentially fatal especially in first month of therapy Orthostatic hypotension Increased mortality in elerdly patients with dementia-related physhosis Hyperglycemia NMS – Neuroleptic Malignant Syndrone Anticholinergic toxicity

Clozapine Analytical Considerations    Not a difficult drug to assay Gas Chromatography  FID, NPD, MS  Concern over N-oxide reduction to clozapine HPLC  UV, electrochemical detection, MS

Clozapine Concentrations in Non-Lethal Overdose Cases    Pediatric patients  Confusion, ataxia, hyper-hypo tonic disorders  0.51; 0.54 mg/L Adults (accidental overdose)  Seizures  1.3; 2.2 ; 3.8 mg/L Adults (intentional overdose – 7 cases)  2.9 – 9.5 mg/L

Clozapine Concentrations in Fatal Overdose Cases Average Blood (mg/L) 5.2

Liver (mg/kg) 46 Range 1.2 - 13 19 - 85  Baselt, Disposition of Toxic Drugs and Chemical in Man, Seventh Ed., 2004

Ziprasidone

(Geodon ® )      Available since 1992 Capsules 20,40,60,80 mg Solution for injection  20 mg/mL C 21 H 21 ClN 4 OS MW = 412  If you are a mass spectrometer

Ziprasidone Pharmacology

      High affinity for:  D 2 , D 3 , 5HT 2A , 5HT 2C ,5HT 1A , 5HT 1D ,  1 Moderate affinity for H 1 Antagonist for:  D 2 , 5HT 2A , 5HT 1D Agonist for 5HT 1A High 5HT/D Inhibits serotonin and norepinephrine reuptake No affinity for muscarinic receptor

Ziprasidone Pharmacokinetics

    Dosing   Schizophrenia  Initial 20 mg BID with food  If necessary, may increase slowly to 80 mg BID Bipolar mania    40 mg BID with food Increase to 60 or 80 mg BID on second day Adjust dose efficacy and tolerance to 40-80 mg BID Bioavailability 60% Vd 1.5 L/kg Half-Life 4 – 8 hrs

Ziprasidone Pharmacokinetics

 Metabolism   12 known metabolites  Therapeutic affect primarily due to parent drug Major circulating metabolites are:     Benzisothiazole (BITP) sulphoxide BITP-sulphone Ziprasidone sulphoxide S-methyl-dihydroziprasidone  Metabolism mediated by P450 CYP3A4  CYP1A2 to a much lesser extent

Ziprasidone Pharmacokinetics

  Elimination   20% in urine  Only trace amounts of unchanged drug 66% in feces Time to peak plasma concentration  2 – 6 hrs

Ziprasidone Adverse Affects

 During Therapy    Sedation Headache Postural hypotension      NMS Tardive dyskensia Prolongation of QT interval Less weight gain than other atypicals Dizziness   Overdose    Several cases all non-fatal QT changes (minimal) Delerium     Hemodynamic instability Diarrhea Urinary retention No EPS If you have a fatal case, let me know!

Ziprasidone Blood Concentrations   4 healthy males administered 20 mg Ziprasidone for 11 days  Mean plasma concentration 45.4 ng/mL with a range of 28.8-62 ng/mL 39 males administered fixed doses of 10, 40, and 40 escalated to 80, and 40 escalated to 120 mg  On day 18, peak plasma concentrations were  14.8, 44.6, 118.6, 139.4 ng/mL

Ziprasidone Analytical Consideratioins   Extraction   Liquid-liquid C 18 cartridges Detection/Quantification   HPLC – UV detection LC/MS/MS

Aripiprazole (Abilify

®

)

     Available since 2002 Tablets  10, 15, 20, 30 mg Oral Solution  1 mg/mL C 23 H 27 Cl 2 N 3 O 2 MW = 448.38

Aripiprazole Pharmacology

     High Affinity for:  D 2 , D3, 5HT1A, 5HT2A Moderate affinity for:  D4, 5HT 2C , 5H T7 ,  1 , H 1 , serotonin reuptake site No affinity for muscarinic receptors * Partial agonist D 2 Antagonist at 5HT 2A and 5HT 1A *

Aripiprazole Pharmacokinetics

    Dosing  10 or 15 mg qd Bioavailability  Tablets 87% Solution near 100% Vd = 4.9 L/kg Half-Life   Aripiprazole 75 hrs EM 146 hrs PM Dehydroariprazole 94 hrs

Aripiprazole Pharmacokinetics

 Metabolism    Dehydrogenation and hydroxylation  CYP3A4 and CYP2D6 N-dealkylation  CYP3A4 Active metabolite  Dehydroaripiprazole    Approximately = parent About 40% of parent in EM Measure total active moiety

Aripiprazole Pharmacokinetics

   Elimination   25% of dose excreted in urine  Less than 1% excreted unchanged 55% excreted in feces Time to peak plasma concentration  3-5 hrs Steady state attained within 14 days for both active moieties

Aripiprazole Adverse Affects

 Schizophrenia and Bipolar Disorder  Headache, Nausea       Vomiting, Constipation Anxiety, agitation Insomnia, sleepiness Dizziness Akathisia, EPS Drug Interactions  Overdose  Nausea, vomiting, asthenia, diarrhea, somnolence   Tachycardia, EPS CNS depression  Somnolence, transient loss of consciousness, CNS effects for 2 weeks

Aripiprazole Concentration in Blood

    27-year-old female Ingested 330 mg of aripiprazole Total active moiety of 716 ng/mL    According to manufacture = ~ 6X upper limit of therapeutic dosing One clinical study suggest range for aripiprazole of 146-254 ng/mL (metabolite not measured) Not aware of a death case – doesn’t mean there isn’t one Analysis  Clean up by direct injection of diluted sample and column switching  LC/MS/MS or with UV detection

Acknowledgement

 The presenter would like to thank Dr. Alphonse Poklis for the organizational concept for this presentation.