VYZULTA: Available in Pharmacies Nationwide.

Why the VYZULTA dual mechanism of action
may be an option for your glaucoma patients

› VYZULTA targets 2 outflow pathways to reduce elevated IOP1

Two pathways help regulate IOP1

Aqueous humor outflow happens through 2 pathways:

  • Trabecular meshwork
  • Uveoscleral pathway

The trabecular meshwork

  • The eye's primary outflow pathway
  • Made up of the trabecular meshwork and Schlemm’s canal2-4

The uveoscleral pathway

  • The remaining aqueous humor exits the eye through this secondary pathway, called the uveoscleral pathway2,4

Both outflow pathways are important in the regulation of IOP, and slowing the progression of glaucoma and delaying the onset of ocular hypertension5

VYZULTA is metabolized and targets each outflow pathway1,6,7

VYZULTA targets 2 pathways to increase aqueous humor outflow

VYZULTA is metabolized into 2 moieties1,6,7

  • Latanoprost acid, a prostaglandin analog, works primarily within the uveoscleral pathway2,8
  • Butanediol mononitrate releases nitric oxide, which is thought to relax the trabecular meshwork9-12

Nitric oxide plays a role in controlling IOP9-12

  • Evidence of reduced levels of nitric oxide have been found in glaucoma patients' eyes13-15
  • A key role of endogenous nitric oxide is vascular smooth muscle relaxation to regulate blood flow

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INDICATION

VYZULTA (latanoprostene bunod ophthalmic solution), 0.024% is indicated for the reduction of intraocular pressure (IOP) in patients with open-angle glaucoma or ocular hypertension.

IMPORTANT SAFETY INFORMATION 
  • Increased pigmentation of the iris and periorbital tissue (eyelid) can occur. Iris pigmentation is likely to be permanent
  • Gradual changes to eyelashes, including increased length, increased thickness, and number of eyelashes, may occur. These changes are usually reversible upon treatment discontinuation
  • Use with caution in patients with a history of intraocular inflammation (iritis/uveitis). VYZULTA should generally not be used in patients with active intraocular inflammation
  • Macular edema, including cystoid macular edema, has been reported during treatment with prostaglandin analogs. Use with caution in aphakic patients, in pseudophakic patients with a torn posterior lens capsule, or in patients with known risk factors for macular edema
  • There have been reports of bacterial keratitis associated with the use of multiple-dose containers of topical ophthalmic products that were inadvertently contaminated by patients
  • Contact lenses should be removed prior to the administration of VYZULTA and may be reinserted 15 minutes after administration
  • Most common ocular adverse reactions with incidence ≥2% are conjunctival hyperemia (6%), eye irritation (4%), eye pain (3%), and instillation site pain (2%)
1. VYZULTA Prescribing Information. Bausch & Lomb Incorporated. 2017.
2. Braunger BM, Fuchshofer R, Tamm ER. The aqueous humor outflow pathways in glaucoma: a unifying concept of disease mechanisms and causative treatment. Eur J Pharm Biopharm. 2015;95(Pt B):173-181.
3. Tamm ER, Braunger BM, Fuchshofer R. Intraocular pressure and the mechanisms involved in resistance of the aqueous humor flow in the trabecular meshwork outflow pathways. Prog Mol Biol Transl Sci. 2015;134:301-314.
4. Winkler NS, Fautsch MP. Effects of prostaglandin analogues on aqueous humor outflow pathways. J Ocul Pharmacol Ther. 2014;30(2-3):102-109.
5. Cavet ME, DeCory HH. The role of nitric oxide in the intraocular pressure lowering efficacy of latanoprostene bunod: review of nonclinical studies. J Ocul Pharmacol Ther. 2017 Aug 7. doi: 10.1089/jop.2016.0188. [Epub ahead of print]
6. Krauss AH, Impagnatiello F, Toris CB, et al. Ocular hypotensive activity of BOL-303259-X, a nitric oxide donating prostaglandin F2alpha agonist, in preclinical models. Exp Eye Res. 2011;93:250-255.
7. Cavet ME, Vollmer TR, Harrington KL, VanDerMeid K, Richardson ME. Regulation of endothelin-1–induced trabecular meshwork cell contractility by latanoprostene bunod. Invest Ophthalmol Vis Sci. 2015;56(6):4108-4116.
8. Weinreb RN, Khaw PT. Primary open-angle glaucoma. Lancet. 2004;363:1711-1720.
9. Cavet ME, Vittitow JL, Impagnatiello F, et al. Nitric oxide (NO): an emerging target for the treatment of glaucoma. Invest Ophthalmol Vis Sci. 2014;55:5005-5015.
10. Buys ES, Potter LR, Pasquale LR, Ksander BR. Regulation of intraocular pressure by soluble and membrane guanylate cyclases and their role in glaucoma. Front Mol Neurosci. 2014 May 19;7;38. doi: 10.3389/fnmol.2014.00038. eCollection 2014.
11. Schneemann A, Dijkstra BG, van den Berg TJ, et al. Nitric oxide/guanylate cyclase pathways and flow in anterior segment perfusion. Graefes Arch Clin Exp Ophthalmol. 2002;240:936-941.
12. Wiederholt M, Sturm A, Lepple-Wienhues A. Relaxation of trabecular meshwork and ciliary muscle by release of nitric oxide. Invest Ophthalmol Vis Sci. 1994;35:2515-2520.
13. Doganay S, Evereklioglu C, Turkoz Y, et al. Decreased nitric oxide production in primary open-angle glaucoma. Eur J Ophthalmol. 2002;12:44-48.
14. Galassi F, Renieri G, Sodi A, et al. Nitric oxide proxies and ocular perfusion pressure in primary open angle glaucoma. Br J Ophthalmol. 2004;88:757-760.
15. Nathanson JA, McKee M. Alterations of ocular nitric oxide synthase in human glaucoma. Invest Ophthalmol Vis Sci. 1995;36:1774-1784.

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INDICATION

VYZULTA (latanoprostene bunod ophthalmic solution), 0.024% is indicated for the reduction of intraocular pressure (IOP) in patients with open-angle glaucoma or ocular hypertension.

IMPORTANT SAFETY INFORMATION 
  • Increased pigmentation of the iris and periorbital tissue (eyelid) can occur. Iris pigmentation is likely to be permanent
  • Gradual changes to eyelashes, including increased length, increased thickness, and number of eyelashes, may occur. These changes are usually reversible upon treatment discontinuation
  • Use with caution in patients with a history of intraocular inflammation (iritis/uveitis). VYZULTA should generally not be used in patients with active intraocular inflammation
  • Macular edema, including cystoid macular edema, has been reported during treatment with prostaglandin analogs. Use with caution in aphakic patients, in pseudophakic patients with a torn posterior lens capsule, or in patients with known risk factors for macular edema
  • There have been reports of bacterial keratitis associated with the use of multiple-dose containers of topical ophthalmic products that were inadvertently contaminated by patients
  • Contact lenses should be removed prior to the administration of VYZULTA and may be reinserted 15 minutes after administration
  • Most common ocular adverse reactions with incidence ≥2% are conjunctival hyperemia (6%), eye irritation (4%), eye pain (3%), and instillation site pain (2%)
1. VYZULTA Prescribing Information. Bausch & Lomb Incorporated. 2017.
2. Braunger BM, Fuchshofer R, Tamm ER. The aqueous humor outflow pathways in glaucoma: a unifying concept of disease mechanisms and causative treatment. Eur J Pharm Biopharm. 2015;95(Pt B):173-181.
3. Tamm ER, Braunger BM, Fuchshofer R. Intraocular pressure and the mechanisms involved in resistance of the aqueous humor flow in the trabecular meshwork outflow pathways. Prog Mol Biol Transl Sci. 2015;134:301-314.
4. Winkler NS, Fautsch MP. Effects of prostaglandin analogues on aqueous humor outflow pathways. J Ocul Pharmacol Ther. 2014;30(2-3):102-109.
5. Cavet ME, DeCory HH. The role of nitric oxide in the intraocular pressure lowering efficacy of latanoprostene bunod: review of nonclinical studies. J Ocul Pharmacol Ther. 2017 Aug 7. doi: 10.1089/jop.2016.0188. [Epub ahead of print].
6. Krauss AH, Impagnatiello F, Toris CB, et al. Ocular hypotensive activity of BOL-303259-X, a nitric oxide donating prostaglandin F2alpha agonist, in preclinical models. Exp Eye Res. 2011;93:250-255.
7. Cavet ME, Vollmer TR, Harrington KL, VanDerMeid K, Richardson ME. Regulation of endothelin-1–induced trabecular meshwork cell contractility by latanoprostene bunod. Invest Ophthalmol Vis Sci. 2015;56(6):4108-4116.
8. Weinreb RN, Khaw PT. Primary open-angle glaucoma. Lancet. 2004;363:1711-1720.
9. Cavet ME, Vittitow JL, Impagnatiello F, et al. Nitric oxide (NO): an emerging target for the treatment of glaucoma. Invest Ophthalmol Vis Sci. 2014;55:5005-5015.
10. Buys ES, Potter LR, Pasquale LR, Ksander BR. Regulation of intraocular pressure by soluble and membrane guanylate cyclases and their role in glaucoma. Front Mol Neurosci. 2014 May 19;7;38. doi: 10.3389/fnmol.2014.00038. eCollection 2014.
11. Schneemann A, Dijkstra BG, van den Berg TJ, et al. Nitric oxide/guanylate cyclase pathways and flow in anterior segment perfusion. Graefes Arch Clin Exp Ophthalmol. 2002;240:936-941.
12. Wiederholt M, Sturm A, Lepple-Wienhues A. Relaxation of trabecular meshwork and ciliary muscle by release of nitric oxide. Invest Ophthalmol Vis Sci. 1994;35:2515-2520.
13. Doganay S, Evereklioglu C, Turkoz Y, et al. Decreased nitric oxide production in primary open-angle glaucoma. Eur J Ophthalmol. 2002;12:44-48.
14. Galassi F, Renieri G, Sodi A, et al. Nitric oxide proxies and ocular perfusion pressure in primary open angle glaucoma. Br J Ophthalmol. 2004;88:757-760.
15. Nathanson JA, McKee M. Alterations of ocular nitric oxide synthase in human glaucoma. Invest Ophthalmol Vis Sci. 1995;36:1774-1784.