Travoprost and Timolol eye drops are a combination of a prostanoid receptor agonist and a non-selective beta-blocker. It is used as eye drops in the treatment of patients with raised intraocular pressure or glaucoma who have not responded adequately to monotherapy.
Travoprost and timolol Uses:
Note: Not approved in the US
-
Elevated intraocular pressure:
- Used for reducing intraocular pressure (IOP) in patients with open-angle glaucoma or ocular hypertension who show an inadequate response to topical beta-blockers, prostaglandin analogs, or other IOP-reducing agents and in whom combination therapy is appropriate.
- Limitations of use: Not indicated for use as initial therapy.
Travoprost and Timolol dose in Adults
Travoprost and Timolol dose in the treatment of elevated intraocular pressure:
- Ophthalmic: Instill 1 drop into the affected eye(s) once a day in the morning or evening
Use in Children:
Not indicated.
Pregnancy Risk Category: D
- Combination products are not recommended for women who are pregnant, or trying to get pregnant.
Use during breastfeeding:
- After ophthalmic administration, human breast milk was found to contain timolol. It is unknown if travoprost is secreted in human milk.
- According to the manufacturer discontinuing nursing or discontinuing the drug use should be based on the maternal importance of the drug.
- You can also contact individual agents.
Dose in Kidney Disease:
No dosage adjustments have been provided in the manufacturer's labeling (has not been studied); use cautiously.
Dose in Liver disease:
No dosage adjustments have been provided in the manufacturer's labeling
Also, see individual agents. Based on long-term studies.
Common Side Effects of Travoprost and Timolol:
-
Ophthalmic:
- Ocular hyperemia
- Eye Irritation
- Eye Pruritus
- Xerophthalmia
- Increased Eyelash Length
- Iris Discoloration
- Blurred Vision
- Eye Pain
- Photophobia
- Punctate Keratitis
Contraindications to Travoprost and Timolol:
- Hypersensitivity to travoprost or timolol or any other component in the formulation
- Bronchial asthma history or bronchial asthma
- Severe (COPD).
- Sino-atrial block or sick sinus syndrome
- Sinus bradycardia
- Atrioventricular block, 2nd or 3rd degree
- Cardiac failure with severe consequences
- Cardiogenic shock
- Women who are pregnant or trying to get pregnant.
Warnings and precautions
-
Anaphylactic reactions
- Patients with a history of severe allergic reactions to allergens should be cautious. Beta-blockers users may become more sensitive to repeated challenges.
- Anaphylaxis treatment (eg, epinephrine) in patients taking beta-blockers may be ineffective or may promote undesirable effects.
-
CNS depression:
- CNS depression can lead to mental or physical impairments. Patients should be aware that driving or operating machinery requires mental alertness.
-
Ocular effects
- After filtration, choroidal detachment has been linked to the use of agents that reduce or suppress aqueous humor formation.
- Patients with choroidal detachment should stop using it if they are chronically or recurrently afflicted.
- Prostaglandin analogs like travoprost have been linked to macular edema in patients with a torn posterior capsule.
- Permanently increasing or changing the brown pigmentation of the eyelid skin, iris, and eyelashes can be possible.
- Additionally, eyelash lengths and/or number may vary between eyes. These changes may be gradual and not noticeable for many months or years.
- Also, periorbital and lid modifications, including deepening the eyelids sulcus have been observed.
- The long-term effects and possible eye injury are not known.
-
Angle-closure glaucoma:
- Not to be used alone for acute angle-closure treatment glaucoma.
-
Cardiovascular disease
- Avoid cardiovascular disease (eg coronary heart disease and Prinzmetal angina) and low blood pressure. It is important to properly control heart failure patients before initiating therapy.
- Patients with severe cardiovascular disease should be monitored for signs of heart attack.
- Reports of severe cardiac reactions, including heart failure, have been made.
- Before initiating, it is important to consider any conduction abnormalities.
-
Cerebrovascular disease
- Cerebrovascular Insufficiency should be treated with caution. Patients who have signs/symptoms of reduced cerebral blood flow after treatment initiation should consider alternative therapies.
-
Diabetes:
- Patients with diabetes mellitus should be cautious when using this product. It may mask or worsen hypoglycemia symptoms.
-
Uveitis/Iritis:
- Patients with active intraocular inflammation (iritis/uveitis), and patients at high risk for developing uveitis should be treated with caution.
-
Myasthenia gravis:
- Patients with myasthenia Gravis should be cautious; it may worsen the condition or cause other myasthenic symptoms (diplopia and ptosis).
-
Orthostatic hypotension
- Patients with orthostatic hypotension should be cautious; it may worsen their symptoms.
-
Raynaud's Disease and Peripheral Vascular Disease (PVD).
- Patients with Raynaud disease and PVD can experience symptoms of arterial insufficiency that are either exacerbated or precipitated.
- Be cautious.
- For the detection of arterial obstruction, it is important to monitor its progression.
-
Renal impairment
- Patients with impaired renal function should be cautious.
-
Respiratory disease
- Patients with COPD (eg chronic bronchitis or emphysema), of mild or moderate severity, bronchospastic diseases or history of, should not take beta-blockers.
- There have been severe respiratory reactions, including fatalities, with ophthalmic usage. This was due to bronchospasm among patients with asthma.
- Use of this product is not recommended for patients with severe COPD or bronchial symptoms.
-
Thyroid disease:
- Hyperthyroidism signs (eg, Tachycardia) can be disguised.
- If there are suspicions of thyrotoxicosis, it is important to monitor and treat the patient. Sudden withdrawal symptoms of hyperthyroidism can be dangerous.
Travoprost and timolol (United States: Not available): Drug Interaction
|
Acetylcholinesterase Inhibitors |
May enhance the bradycardic effect of Beta-Blockers. |
|
Ajmaline |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Alpha1-Blockers |
Beta-Blockers may enhance the orthostatic hypotensive effect of Alpha1Blockers. The risk associated with ophthalmic products is probably less than systemic products. |
|
Aminoquinolines (Antimalarial) |
May decrease the metabolism of Beta-Blockers. |
|
Amiodarone |
May enhance the bradycardic effect of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase the serum concentration of Beta-Blockers. |
|
Antipsychotic Agents (Phenothiazines) |
May enhance the hypotensive effect of Beta-Blockers. Beta-Blockers may decrease the metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease the metabolism of Beta-Blockers. |
|
Barbiturates |
May decrease the serum concentration of Beta-Blockers. |
|
Bradycardia-Causing Agents |
May enhance the bradycardic effect of other Bradycardia-Causing Agents. |
|
Bretylium |
May enhance the bradycardic effect of Bradycardia-Causing Agents. Bretylium may also enhance atrioventricular (AV) blockade in patients receiving AV blocking agents. |
|
Bupivacaine |
Beta-Blockers may increase the serum concentration of Bupivacaine. |
|
Calcium Channel Blockers (Nondihydropyridine) |
May enhance the hypotensive effect of BetaBlockers. Bradycardia and signs of heart failure have also been reported. Calcium Channel Blockers (Nondihydropyridine) may increase the serum concentration of Beta-Blockers. Exceptions: Bepridil. |
|
Cardiac Glycosides |
Beta-Blockers may enhance the bradycardic effect of Cardiac Glycosides. |
|
Cholinergic Agonists |
Beta-Blockers may enhance the adverse/toxic effect of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Management: Administer these agents in combination with caution, and monitor for conduction disturbances. Avoid methacholine with any beta blocker due to the potential for additive bronchoconstriction. |
|
CloBAZam |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Cobicistat |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
CYP2D6 Inhibitors (Moderate) |
May decrease the metabolism of CYP2D6 Substrates (High risk with Inhibitors). |
|
CYP2D6 Inhibitors (Strong) |
May increase the serum concentration of Timolol (Ophthalmic). |
|
Darunavir |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Dipyridamole |
May enhance the bradycardic effect of Beta-Blockers. |
|
Disopyramide |
May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. |
|
EPINEPHrine (Nasal) |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Nasal). |
|
EPINEPHrine (Oral Inhalation) |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Oral Inhalation). |
|
Epinephrine (Racemic) |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of Epinephrine (Racemic). |
|
EPINEPHrine (Systemic) |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Systemic). |
|
Imatinib |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Insulins |
Beta-Blockers may enhance the hypoglycemic effect of Insulins. |
|
Ivabradine |
Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. |
|
Lacosamide |
Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. |
|
Lidocaine (Systemic) |
Beta-Blockers may increase the serum concentration of Lidocaine (Systemic). |
|
Lidocaine (Topical) |
Beta-Blockers may increase the serum concentration of Lidocaine (Topical). |
|
Lumefantrine |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Mepivacaine |
Beta-Blockers may increase the serum concentration of Mepivacaine. |
|
Methoxyflurane |
May enhance the hypotensive effect of Beta-Blockers. |
|
Midodrine |
May enhance the bradycardic effect of Bradycardia-Causing Agents. |
|
NIFEdipine |
May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. |
|
Nonsteroidal Anti-Inflammatory Agents |
May diminish the antihypertensive effect of BetaBlockers. |
|
Nonsteroidal Anti-Inflammatory Agents |
May diminish the therapeutic effect of Prostaglandins (Ophthalmic). Nonsteroidal Anti-Inflammatory Agents may also enhance the therapeutic effects of Prostaglandins (Ophthalmic). |
|
Nonsteroidal Anti-Inflammatory Agents (Ophthalmic) |
May diminish the therapeutic effect of Prostaglandins (Ophthalmic). Nonsteroidal Anti-Inflammatory Agents (Ophthalmic) may enhance the therapeutic effect of Prostaglandins (Ophthalmic). |
|
Opioids (Anilidopiperidine) |
May enhance the bradycardic effect of Beta-Blockers. Opioids (Anilidopiperidine) may enhance the hypotensive effect of Beta-Blockers. |
|
Panobinostat |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Peginterferon Alfa-2b |
May decrease the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Peginterferon Alfa-2b may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Perhexiline |
CYP2D6 Substrates (High risk with Inhibitors) may increase the serum concentration of Perhexiline. Perhexiline may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Propafenone |
May increase the serum concentration of Beta-Blockers. Propafenone possesses some independent beta blocking activity. |
|
QuiNINE |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Regorafenib |
May enhance the bradycardic effect of Beta-Blockers. |
|
Reserpine |
May enhance the hypotensive effect of Beta-Blockers. |
|
Rifamycin Derivatives |
May decrease the serum concentration of Beta-Blockers. Exceptions: Rifabutin. |
|
Ruxolitinib |
May enhance the bradycardic effect of Bradycardia-Causing Agents. Management: Ruxolitinib Canadian product labeling recommends avoiding use with bradycardia-causing agents to the extent possible. |
|
Selective Serotonin Reuptake Inhibitors |
May increase the serum concentration of Beta-Blockers. Exceptions: Citalopram; Escitalopram; FluvoxaMINE. |
|
Sulfonylureas |
Beta-Blockers may enhance the hypoglycemic effect of Sulfonylureas. Cardioselective beta-blockers (eg, acebutolol, atenolol, metoprolol, and penbutolol) may be safer than nonselective beta-blockers. All beta-blockers appear to mask tachycardia as an initial symptom of hypoglycemia. Ophthalmic beta-blockers are probably associated with lower risk than systemic agents. |
|
Terlipressin |
May enhance the bradycardic effect of Bradycardia-Causing Agents. |
|
Tofacitinib |
May enhance the bradycardic effect of Bradycardia-Causing Agents. |
|
Risk Factor D (Consider therapy modification) |
|
|
Abiraterone Acetate |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Management: Avoid concurrent use of abiraterone with CYP2D6 substrates that have a narrow therapeutic index whenever possible. When concurrent use is not avoidable, monitor patients closely for signs/symptoms of toxicity. |
|
Alpha2-Agonists |
May enhance the AV-blocking effect of Beta-Blockers. Sinus node dysfunction may also be enhanced. Beta-Blockers may enhance the rebound hypertensive effect of Alpha2Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Exceptions: Apraclonidine. |
|
Asunaprevir |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Ceritinib |
|
|
Dacomitinib |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Management: Avoid concurrent use of dacomitinib with CYP2D6 subtrates that have a narrow therapeutic index. |
|
Dronedarone |
May enhance the bradycardic effect of Beta-Blockers. Dronedarone may increase the serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in betablocker dose. |
|
Ergot Derivatives |
Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives. Exceptions: Nicergoline. |
|
Fingolimod |
Beta-Blockers may enhance the bradycardic effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and beta-blockers if possible. If coadministration is necessary, patients should have overnight continuous ECG monitoring conducted after the first dose of fingolimod. Monitor patients for bradycardia. |
|
Grass Pollen Allergen Extract (5 Grass Extract) |
Beta-Blockers may enhance the adverse/toxic effect of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. |
|
Siponimod |
Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. |
|
Theophylline Derivatives |
Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Theophylline Derivatives. |
|
Risk Factor X (Avoid combination) |
|
|
Beta2-Agonists |
Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Beta2Agonists. |
|
Floctafenine |
May enhance the adverse/toxic effect of Beta-Blockers. |
|
Methacholine |
Beta-Blockers may enhance the adverse/toxic effect of Methacholine. |
|
Rivastigmine |
May enhance the bradycardic effect of Beta-Blockers. |
Travoprost and timolol (United States: Not available): Drug Interaction
|
Acetylcholinesterase Inhibitors |
May enhance the bradycardic effect of Beta-Blockers. |
|
Ajmaline |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Alpha1-Blockers |
Beta-Blockers may enhance the orthostatic hypotensive effect of Alpha1Blockers. The risk associated with ophthalmic products is probably less than systemic products. |
|
Aminoquinolines (Antimalarial) |
May decrease the metabolism of Beta-Blockers. |
|
Amiodarone |
May enhance the bradycardic effect of Beta-Blockers. Possibly to the point of cardiac arrest. Amiodarone may increase the serum concentration of Beta-Blockers. |
|
Antipsychotic Agents (Phenothiazines) |
May enhance the hypotensive effect of Beta-Blockers. Beta-Blockers may decrease the metabolism of Antipsychotic Agents (Phenothiazines). Antipsychotic Agents (Phenothiazines) may decrease the metabolism of Beta-Blockers. |
|
Barbiturates |
May decrease the serum concentration of Beta-Blockers. |
|
Bradycardia-Causing Agents |
May enhance the bradycardic effect of other Bradycardia-Causing Agents. |
|
Bretylium |
May enhance the bradycardic effect of Bradycardia-Causing Agents. Bretylium may also enhance atrioventricular (AV) blockade in patients receiving AV blocking agents. |
|
Bupivacaine |
Beta-Blockers may increase the serum concentration of Bupivacaine. |
|
Calcium Channel Blockers (Nondihydropyridine) |
May enhance the hypotensive effect of BetaBlockers. Bradycardia and signs of heart failure have also been reported. Calcium Channel Blockers (Nondihydropyridine) may increase the serum concentration of Beta-Blockers. Exceptions: Bepridil. |
|
Cardiac Glycosides |
Beta-Blockers may enhance the bradycardic effect of Cardiac Glycosides. |
|
Cholinergic Agonists |
Beta-Blockers may enhance the adverse/toxic effect of Cholinergic Agonists. Of particular concern are the potential for cardiac conduction abnormalities and bronchoconstriction. Management: Administer these agents in combination with caution, and monitor for conduction disturbances. Avoid methacholine with any beta blocker due to the potential for additive bronchoconstriction. |
|
CloBAZam |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Cobicistat |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
CYP2D6 Inhibitors (Moderate) |
May decrease the metabolism of CYP2D6 Substrates (High risk with Inhibitors). |
|
CYP2D6 Inhibitors (Strong) |
May increase the serum concentration of Timolol (Ophthalmic). |
|
Darunavir |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Dipyridamole |
May enhance the bradycardic effect of Beta-Blockers. |
|
Disopyramide |
May enhance the bradycardic effect of Beta-Blockers. Beta-Blockers may enhance the negative inotropic effect of Disopyramide. |
|
EPINEPHrine (Nasal) |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Nasal). |
|
EPINEPHrine (Oral Inhalation) |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Oral Inhalation). |
|
Epinephrine (Racemic) |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of Epinephrine (Racemic). |
|
EPINEPHrine (Systemic) |
Beta-Blockers (Nonselective) may enhance the hypertensive effect of EPINEPHrine (Systemic). |
|
Imatinib |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Insulins |
Beta-Blockers may enhance the hypoglycemic effect of Insulins. |
|
Ivabradine |
Bradycardia-Causing Agents may enhance the bradycardic effect of Ivabradine. |
|
Lacosamide |
Bradycardia-Causing Agents may enhance the AV-blocking effect of Lacosamide. |
|
Lidocaine (Systemic) |
Beta-Blockers may increase the serum concentration of Lidocaine (Systemic). |
|
Lidocaine (Topical) |
Beta-Blockers may increase the serum concentration of Lidocaine (Topical). |
|
Lumefantrine |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Mepivacaine |
Beta-Blockers may increase the serum concentration of Mepivacaine. |
|
Methoxyflurane |
May enhance the hypotensive effect of Beta-Blockers. |
|
Midodrine |
May enhance the bradycardic effect of Bradycardia-Causing Agents. |
|
NIFEdipine |
May enhance the hypotensive effect of Beta-Blockers. NIFEdipine may enhance the negative inotropic effect of Beta-Blockers. |
|
Nonsteroidal Anti-Inflammatory Agents |
May diminish the antihypertensive effect of BetaBlockers. |
|
Nonsteroidal Anti-Inflammatory Agents |
May diminish the therapeutic effect of Prostaglandins (Ophthalmic). Nonsteroidal Anti-Inflammatory Agents may also enhance the therapeutic effects of Prostaglandins (Ophthalmic). |
|
Nonsteroidal Anti-Inflammatory Agents (Ophthalmic) |
May diminish the therapeutic effect of Prostaglandins (Ophthalmic). Nonsteroidal Anti-Inflammatory Agents (Ophthalmic) may enhance the therapeutic effect of Prostaglandins (Ophthalmic). |
|
Opioids (Anilidopiperidine) |
May enhance the bradycardic effect of Beta-Blockers. Opioids (Anilidopiperidine) may enhance the hypotensive effect of Beta-Blockers. |
|
Panobinostat |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Peginterferon Alfa-2b |
May decrease the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Peginterferon Alfa-2b may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Perhexiline |
CYP2D6 Substrates (High risk with Inhibitors) may increase the serum concentration of Perhexiline. Perhexiline may increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Propafenone |
May increase the serum concentration of Beta-Blockers. Propafenone possesses some independent beta blocking activity. |
|
QuiNINE |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Regorafenib |
May enhance the bradycardic effect of Beta-Blockers. |
|
Reserpine |
May enhance the hypotensive effect of Beta-Blockers. |
|
Rifamycin Derivatives |
May decrease the serum concentration of Beta-Blockers. Exceptions: Rifabutin. |
|
Ruxolitinib |
May enhance the bradycardic effect of Bradycardia-Causing Agents. Management: Ruxolitinib Canadian product labeling recommends avoiding use with bradycardia-causing agents to the extent possible. |
|
Selective Serotonin Reuptake Inhibitors |
May increase the serum concentration of Beta-Blockers. Exceptions: Citalopram; Escitalopram; FluvoxaMINE. |
|
Sulfonylureas |
Beta-Blockers may enhance the hypoglycemic effect of Sulfonylureas. Cardioselective beta-blockers (eg, acebutolol, atenolol, metoprolol, and penbutolol) may be safer than nonselective beta-blockers. All beta-blockers appear to mask tachycardia as an initial symptom of hypoglycemia. Ophthalmic beta-blockers are probably associated with lower risk than systemic agents. |
|
Terlipressin |
May enhance the bradycardic effect of Bradycardia-Causing Agents. |
|
Tofacitinib |
May enhance the bradycardic effect of Bradycardia-Causing Agents. |
|
Risk Factor D (Consider therapy modification) |
|
|
Abiraterone Acetate |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Management: Avoid concurrent use of abiraterone with CYP2D6 substrates that have a narrow therapeutic index whenever possible. When concurrent use is not avoidable, monitor patients closely for signs/symptoms of toxicity. |
|
Alpha2-Agonists |
May enhance the AV-blocking effect of Beta-Blockers. Sinus node dysfunction may also be enhanced. Beta-Blockers may enhance the rebound hypertensive effect of Alpha2Agonists. This effect can occur when the Alpha2-Agonist is abruptly withdrawn. Management: Closely monitor heart rate during treatment with a beta blocker and clonidine. Withdraw beta blockers several days before clonidine withdrawal when possible, and monitor blood pressure closely. Recommendations for other alpha2-agonists are unavailable. Exceptions: Apraclonidine. |
|
Asunaprevir |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). |
|
Ceritinib |
|
|
Dacomitinib |
May increase the serum concentration of CYP2D6 Substrates (High risk with Inhibitors). Management: Avoid concurrent use of dacomitinib with CYP2D6 subtrates that have a narrow therapeutic index. |
|
Dronedarone |
May enhance the bradycardic effect of Beta-Blockers. Dronedarone may increase the serum concentration of Beta-Blockers. This likely applies only to those agents that are metabolized by CYP2D6. Management: Use lower initial beta-blocker doses; adequate tolerance of the combination, based on ECG findings, should be confirmed prior to any increase in betablocker dose. |
|
Ergot Derivatives |
Beta-Blockers may enhance the vasoconstricting effect of Ergot Derivatives. Exceptions: Nicergoline. |
|
Fingolimod |
Beta-Blockers may enhance the bradycardic effect of Fingolimod. Management: Avoid the concomitant use of fingolimod and beta-blockers if possible. If coadministration is necessary, patients should have overnight continuous ECG monitoring conducted after the first dose of fingolimod. Monitor patients for bradycardia. |
|
Grass Pollen Allergen Extract (5 Grass Extract) |
Beta-Blockers may enhance the adverse/toxic effect of Grass Pollen Allergen Extract (5 Grass Extract). More specifically, Beta-Blockers may inhibit the ability to effectively treat severe allergic reactions to Grass Pollen Allergen Extract (5 Grass Extract) with epinephrine. Some other effects of epinephrine may be unaffected or even enhanced (e.g., vasoconstriction) during treatment with Beta-Blockers. |
|
Siponimod |
Bradycardia-Causing Agents may enhance the bradycardic effect of Siponimod. Management: Avoid coadministration of siponimod with drugs that may cause bradycardia. |
|
Theophylline Derivatives |
Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Theophylline Derivatives. |
|
Risk Factor X (Avoid combination) |
|
|
Beta2-Agonists |
Beta-Blockers (Nonselective) may diminish the bronchodilatory effect of Beta2Agonists. |
|
Floctafenine |
May enhance the adverse/toxic effect of Beta-Blockers. |
|
Methacholine |
Beta-Blockers may enhance the adverse/toxic effect of Methacholine. |
|
Rivastigmine |
May enhance the bradycardic effect of Beta-Blockers. |
Monitoring parameters:
- IOP, iris color changes, eyelash changes
- Systemic effects of beta-blockade with ophthalmic administration
How to administer Travoprost and Timolol?
Ophthalmic:
- Hands should be washed before and after use.
- Contact lenses should be removed before administration; before reinserting the contact lenses one should wait 15 minutes.
Method administration is as follows:
- Tilt the head back, pull down the lower eyelid and instill drop into the pocket between eyelid and eye; nasolacrimal occlusion or gently close the eyelid for 2 minutes after application.
- Touching bottle tip should be avoided. Administration of other ophthalmic agents should be separated by 5 minutes.
Mechanism of action of Travoprost and Timolol:
Travoprost is a selective prostanoid FP receptor agonist that lowers intraocular pressure through increased trabecular meshwork, outflow and lowering of intraocular tension
Timolol: Blocks both beta1 and Beta2 adrenergic nerve receptors. This reduces intraocular pressure by decreasing the production of aqueoushumor or possibly increasing the outflow of it. You can contact individual agents (Travoprost or Timolol).
International Brand Names of Travoprost and Timolol:
- APO-Travoprost-Timop
- DuoTrav PQ
- Avatan-T
- Avost Plus
- Duo-Travatan
- DuoTrav
- Kivizidiale
- Tapcom-S
Travoprost and Timolol Brand Names in Pakistan:
No Brands Available in Pakistan.
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