Adult: For the treatment of predominantly classic or occult cases due to age-related macular degeneration, pathologic myopia, or presumed ocular histoplasmosis: 6 mg/m2 via infusion over 10 minutes, followed by light activation using a nonthermal diode laser (refer to specific product guidelines on treatment procedure). Re-evaluate patient every 3 months and repeat treatment if choroidal neovascular leakage occurs. Treatment may be given up to 4 times per year.
Reconstitute with 7 mL sterile water for inj to a total volume of 7.5 mL (2 mg/mL). Withdraw the desired dose from the vial and further dilute in 5% dextrose solution for infusion to a total volume of 30 mL.
May cause precipitation with saline solutions.
Porphyria. Severe hepatic impairment.
Mild to moderate hepatic impairment. Pregnancy and lactation.
Significant: Extravasation (if exposed to light, may cause severe pain, swelling, inflammation, blistering, discolouration; localised necrosis), visual disturbances (e.g. abnormal vision, decreased vision, or visual field defects), photosensitivity, hypersensitivity reactions (e.g. anaphylaxis), vasovagal reactions, chest pain, dyspnoea, flushing, syncope. Rarely, convulsions. Eye disorders: Reduced visual acuity, blurred vision, fuzzy vision, photopsia, scotoma, grey or dark haloes, and black spots. Gastrointestinal disorders: Nausea, vomiting. General disorders and administration site conditions: Inj site pain, oedema, inflammation; asthenia. Metabolism and nutrition disorders: Hypercholestrolaemia. Musculoskeletal and connective tissue disorders: Back pain. Nervous system disorders: Headache, dizziness.
This drug may cause abnormal vision, decreased vision, or visual field defects; if affected, do not drive or operate machinery. Avoid exposure to direct sunlight for 2-5 days after treatment. If exposure cannot be avoided, use protective clothing and dark sunglasses. Ambient light exposure is encouraged.
Monitor inj site (to avoid extravasation). Perform fluorescein angiography every 3 months to monitor neovascular leakage.
Symptoms: Non-selective non-perfusion of normal retinal vessels, including the possibility of severe vision decrease; prolonged period of photosensitivity. Management: Prolonged or continued skin or eye protection from direct sunlight or bright indoor light.
Increased risk of photosensitivity reactions with other photosensitising drugs (e.g. tetracyclines, sulfonamides, phenothiazines, sulfonylurea, thiazide diuretics, griseofulvin). May enhance verteporfin tissue-uptake with Ca channel blockers, polymyxin B, and radiation therapy. Decreased efficacy with antioxidants (e.g. β-carotene), free radical scavenging agents (e.g. dimethylsulfoxide, formate, mannitol), drugs that decrease clotting, vasoconstriction, or platelet aggregation (e.g. thromboxane A2 inhibitors).
Alcohol may decrease the therapeutic efficacy of verteporfin.
Description: Verteporfin, a synthetic benzoporphyrin derivative, is a cytotoxic photosensitizing agent. It produces cytotoxic agents upon light activation in the presence of oxygen. When energy absorbed by the porphyrin is transferred to oxygen, highly reactive short-lived singlet oxygen is produced causing damage to biological structures within the diffusion range, thereby resulting in vascular occlusion, cell damage, and in certain conditions, cell death. Pharmacokinetics: Distribution: Enters breast milk (small amounts). Plasma protein binding: approx 90%. Metabolism: Metabolised via hydrolysis by plasma and hepatic esterases to benzoporphyrin derivative diacid (BPD-DA). Excretion: Mainly via the bile (as unchanged drug); urine (<1%). Terminal elimination half-life: 5-6 hours.
Store intact vials between 20-25°C. Protect from light. Reconstituted and diluted solutions are stable for 4 hours at 25°C. Protect from light.
S01LA01 - verteporfin ; Belongs to the class antineovasculatisation agents. Used in the management of neovascular macular degeneration.
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