General Instruction for Writing Report for Continuous

Guru Nanak Institute of Pharmaceutical Science and

Technology
157/ F, Nilgunj Road, Panihati, Kolkata 700114

Title of Work: Beta Blockers for Glaucoma

Paper Code: R21_PT513A

Paper Name: Medicinal Chemistry I

Report Submitted for the Evaluation of Continuous Assessment II

Submitted by

Name: Sovan Sarkar

Roll No: 186012111012

Program: B.Pharm

Semester: 5

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Sl.
Title Pg. No.
No.

1. Abstract 3

2. Introduction 4

3. Discussion 4-8

4. Conclusion 9

5. References 10

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 Abstract

glaucoma is an autoimmune disorders affecting neuromuscular connection is characterised by

having degree of weakness and voluntary muscles caused by antibodies produced against ne
uromuscular junction resulting in a decrease number of receptor
the main cause of glaucoma is production of antibodies causes the condition antibody attack a
acetylcholine that results in muscle weakness and that characterises the contrary condition de
velopment of antibody started to neuromuscular junction number one third
of neuromuscular receptor are reduced
structural damage to neuromuscular junction this will result in a weakness and easy fatigabily
of I eyelid facial muscle and then name and respiratory muscle.

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 Introduction

Glaucoma is a group of diseases characterized by a progressive form of optic nerve damage.

This is generally but not necessarily associated with raised (> 21 mmHg) intraocular tension
(i.o.t) but the causative agent is unknown and there are many risk factors. The chief therapeutic
measure is to lower i.o.t., either by reducing secretion of aqueous\of i.o.t. retards progression
of optic nerve damage even in normal/low i.o.t. glaucoma.

the main cause of glaucoma is production of antibodies causes the condition antibody attack a
acetylcholine that results in muscle weakness and that characterises the contrary condition de
velopment of antibody started to neuromuscular junction number one third
of neuromuscular receptor are reduced
structural damage to neuromuscular junction this will result in a weakness and easy fatigabilit
y of I lead facial muscle and then name and respiratory muscle

The site of formation and pathway of drainage of aqueous humour as well as sites of action of
antiglaucoma drugs is illustrated.

1. Major amount of aqueous (~90%) drains through the trabecular route, while ~10% fluid
passes into the connective tissue spaces within the ciliary muscle—then via
vessels. Glaucoma is seen in two principal clinical forms:

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A. Open angle (wide angle, chronic simple) glaucoma

It is probably a genetically predisposed degenerative disease affecting patency of the

trabecular meshwork which is gradually lost past middle age. The i.o.t. rises insidiously
and progressively. Ocular hypotensive drugs are used on a long-term basis and constitute
the definitive treatment in majority of cases

Alpha Adrenergic Dipivefrine

Blocker
Aparlonidine

Carbonic Anhydrase Acetazolamide

Inhibitor
Dorzolamide

Beta Blocker Timolol Betaxolol

Miotics Pilocarpine

Prostaglandins Lantoprost

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 B. Angle closure (narrow angle, acute congestive) glaucoma

It occurs in individuals with a narrow iridocorneal

shallow anterior chamber and an angle. The i.o.t. remains normal until an attack is precipitated,
usually by mydriasis. The i.o.t rises rapidly to very high values (40–60 mmHg).
It is an emergent condition with marked congestion of eyes and severe headache. Failure to
lower i.o.t. quickly may result in loss of sight.

Osmotic Agent Mannitol Glycerol

Carbonic Anhydrase Acetazolamide

Inhibitor

Beta Blocker Timolol

Miotics Pilocarpine

Prostaglandins Lantoprost

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β Adrenergic blockers

Topical β blockers have been the first line drug till recently, but PG F2α analogues are the
preferred drugs now. In contrast to miotics, the β blockers do not affect pupil size, tone of
ciliary muscle or outflow facility, but lower i.o.t. by reducing aqueous formation. This probably
results from down regulation of adenylyl cyclase due to β2 receptor blockade in the ciliary
epithelium and a secondary effect due to reduction in ocular blood flow. They are as effective
as miotics and produce less ocular side effects. Ocular β blockers are lipophilic with high ocular
capture (to reduce systemic effects) and have no weak local anaesthetic activity (to avoid
corneal hypoesthesia and damage).

Ocular side effects of β blockers These are generally mild and infrequent—stinging, redness
and dryness of eye, corneal hypoesthesia, allergic conjunctivitis and blurred vision.

Systemic adverse effects These are the major limitations in the use of ocular β blockers, and
occur due to absorption through nasolacrimal duct. Life-threatening bronchospasm has been
reported in asthmatic and COPD patients. Bradycardia, CHF and heart block accentuation are
likely, especially in elderly people. In fact, all adverse effects and contraindications of systemic
β blocker therapy apply to ocular β blockers as well. Systemic adverse effects can be minimised
by applying mild pressure on the inner canthus of the eye for about 5 min. after instilling the
eyedrop to prevent entry of the drug into nasolacrimal duct from where it is mainly absorbed

Timolol

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It is the prototype of ocular β blockers is nonselective (β1 + β2) and has no local anaesthetic or
intrinsic sympathomimetic activity. The ocular hypotensive action (20–35% fall in i.o.t.)
becomes evident within 1 hour and lasts for ~12 hours. After chronic dosing, the action is
smooth and well sustained. Some effect on i.o.t. persists for 1–2 weeks following
discontinuation. This feature, in contrast to pilocarpine drops, gives a high level of clinical
safety, i.e. 1 or 2 missed doses will not affect i.o.t. control. However, ~30% cases of open angle
glaucoma fail to achieve the desired level of i.o.t. with timolol alone, and may need additional
medication.

GLUCOMOL, OCUPRES, IOTIM, LOPRES 0.25% and 0.5% eye drops; start with 0.25%
drops BD, change to 0.5% drops\sin case of inadequate response. 0.5% TIMOLAST as eyedrop
for OD use.

Betaxolol
It is β1 selective blocker offering the advantage of less bronchopulmonary and probably less
cardiac, central and metabolic side effects. In addition, it appears to exert a protective effect on
retinal neurones independent of i.o.t. lowering, by blocking some Ca2+ channels an reducing
Na+/Ca2+ influx. This action is more prominent in betaxolol than in timolol. However,
betaxolol is less efficacious in lowering i.o.t. than

Timolol because ocular β receptors are predominantly\sof the β2 subtype. Transient stinging
and burning in the eye is more common with it. Most ophthalmologists prefer to start with
betaxolol and change over to timolol \sonly if i.o.t. control is insufficient or there is local
intolerance to betaxolol.
OPTIPRESS, IOBET, OCUBETA 0.5% eye drops; 1 drop in each eye BD.

Levobunolol
It has been introduced as a once daily alternative to timolol. The ocular and systemic effects
are very similar to timolol except for longer duration of action.
BETAGAN 0.5% ophthalmic soln., 1 drop OD.

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 Conclusion

Glaucoma is a group of diseases characterized by a progressive form of optic nerve damage.

This is generally but not necessarily associated with raised (> 21 mmHg) intraocular tension
(i.o.t) but the causative agent is unknown and there are many risk factors. The chief therapeutic
measure is to lower i.o.t., either by reducing secretion of aqueous\of i.o.t. retards progression
of optic nerve damage even in normal/low i.o.t. glaucoma.
Aside from other drug various beta blockers like timolol has been used to treat Glaucoma.

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 Reference

 Sugrue, Michael F. "New approaches to antiglaucoma therapy." Journal of medicinal

chemistry 40.18 (1997): 2793-2809.
 Wood, J. P. M., et al. "The β-adrenoceptor antagonists metipranolol and timolol are retinal
neuroprotectants: comparison with betaxolol." Experimental eye research 76.4 (2003):
505-516.
 Fini, M. Elizabeth, et al. "Steroid-induced ocular hypertension/glaucoma: Focus on
pharmacogenomics and implications for precision medicine." Progress in retinal and eye
research 56 (2017): 58-83.
 Harris, Alon, Vic Malinovsky, and Bruce Martin. "Correlates of acute exercise-induced
ocular hypotension." Investigative ophthalmology & visual science 35.11 (1994): 3852-
3857.
 Frishman, William H., Moshe S. Fuksbrumer, and Mark Tannenbaum. "Topical
Ophthalmic β‐Adrenergic Blockade for the Treatment of Glaucoma and Ocular
Hypertension." The Journal of Clinical Pharmacology 34.8 (1994): 795-803.
 Frishman, William H., Moshe S. Fuksbrumer, and Mark Tannenbaum. "Topical
Ophthalmic β‐Adrenergic Blockade for the Treatment of Glaucoma and Ocular
Hypertension." The Journal of Clinical Pharmacology 34.8 (1994): 795-803.
 Yu, Dao-Yi, et al. "Effect of betaxolol, timolol and nimodipine on human and pig retinal
arterioles." Experimental eye research 67.1 (1998): 73-81.

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Plagiarirm Check

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