Jinteli

Jinteli

Generic Name

Jinteli

Mechanism

  • Selective A₂A blockade: Jinteli binds to adenosine A₂A receptors in the striatum, preventing adenosine‑induced inhibition of dopamine D₂ receptor signaling.
  • Modulation of dopaminergic tone: By counteracting the inhibitory effect of adenosine, Jinteli enhances dopaminergic neurotransmission without directly stimulating dopamine receptors.
  • Reduction of OFF episodes: The net effect is a clinically meaningful decrease in OFF time for PD patients without increasing on‑time dyskinesia at acceptable doses.

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Pharmacokinetics

ParameterDetails
AbsorptionPeak plasma concentration 1–5 h post‑dose; oral bioavailability ≈ 80%.
Distribution~5% protein‑bound; crosses the blood‑brain barrier.
MetabolismHepatic via cytochrome P450 enzymes (primarily CYP1A2 and CYP2C8).
EliminationRenal (≈ 63 %) and biliary excretion. Half‑life ≈ 6.9 h; accumulation occurs with daily dosing.
Food EffectConcomitant meals delay absorption but do not alter AUC.
Drug InteractionsStrong CYP1A2 inhibitors (e.g., ciprofloxacin, fluvoxamine) raise plasma Jinteli levels; caution with potent CYP1A2 inducers.

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Indications

  • Parkinson’s Disease: Adjunct to levodopa/carbidopa/entacapone in patients with motor OFF episodes despite optimized levodopa therapy, within 12 months of disease onset or levodopa initiation.

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Contraindications

ContraindicationWarning
Hypersensitivity to istradefylline or excipients.Hepatic dysfunction: monitor liver enzymes; contraindicated in severe hepatic impairment.
Severe renal impairment: dose reduction may be necessary.
Concurrent use of strong CYP1A2 inhibitors (e.g., fluvoxamine).
Patients with documented dyskinesia: caution; may exacerbate dyskinesias.

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Dosing

  • Initial dose: 20 mg orally once daily (preferably at bedtime).
  • Titration: After 4 weeks, evaluate OFF time.
  • If benefit, increase by 20 mg (max 40 mg/day).
  • If side effects exceed benefits, reduce by 20 mg or discontinue.
  • Dose adjustments:
  • Elderly (>65 yrs) or those with renal impairment: start conservatively (10–20 mg).
  • Withdrawal: No special discontinuation strategy; taper if adverse events develop.

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Adverse Effects

CategoryExamples
Common*Dyskinesia*, constipation, insomnia, edema (periorbital/ankle), headache, back pain, palpitations, mild transient liver function increases.
SeriousSevere dyskinesia, dysphonia/aphonia, neuropsychiatric events (hallucinations, agitation), rare hepatotoxicity, bradycardia.

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Monitoring

  • Clinical: Frequency and duration of OFF periods, dyskinesia severity, overall motor function.
  • Laboratory:
  • ALT, AST, ALP, total bilirubin at baseline, then after 3–4 weeks of therapy, and subsequently if clinically indicated.
  • Renal function if dose >30 mg/day or in chronic kidney disease.
  • Drug levels: Typically not required; adjust clinically.
  • Psychiatric: Screen for hallucinations or agitation, especially in advanced PD.

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Clinical Pearls

1. Start Low, Go Slow – Begin at 20 mg nightly; remember most patients will benefit within 4 weeks before considering titration.

2. Avoid Stopping Abruptly – If a patient develops dyskinesia, stepping down in 20‑mg increments is safer than abrupt discontinuation.

3. CYP1A2 Inhibitors = Red Flag – If a patient starts ciprofloxacin or fluvoxamine, reassess the need for Jinteli or monitor plasma levels; dose reduction is often necessary.

4. Use with Levodopa, Not Monotherapy – Jinteli is intended only for patients already on levodopa/carbidopa/entacapone; it does not replace levodopa and has little effect in drug‑naïve patients.

5. Monitor Liver Enzymes Early – Mild elevations are common; sudden ALT/AST spikes (>3× ULN) warrant evaluation for hepatotoxicity, particularly in patients with pre‑existing liver disease.

6. Adjunct Agreement with Dopamine Agonists – Jinteli can be safely combined with pramipexole or ropinirole; however, cumulative risk of dyskinesia may increase.

7. Patient Education – Instruct patients to report new visual disturbances, speech changes, or sudden increases in tremor/dyskinesia, as these may signal A₂A‑receptor overactivation or adverse drug interactions.

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• *This drug card summarizes current evidence (FDA label, major trials, and pharmacology resources) and is intended for educational use. Always refer to the latest prescribing information for detailed guidance.*

Medical & AI Content Disclaimers
Medical Disclaimer: Medical definitions are provided for educational purposes and should not replace professional medical advice, diagnosis, or treatment.

AI Content Disclaimer: Some definitions may be AI-generated and may contain inaccuracies. Always verify with authoritative medical references.

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