Dry eyedisease compounds…
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pretreatment is the reduction of Cyclosporine stinging in chronic dry eye disease
(62).
Lotemax
ophthalmic suspension, 0.5% completed Phase II studies
(ClinicalTrials.gov Identifier: NCT00560638) in July 2011. From the results it was
confirmed its ability to reduce the eye inflammation rapidly, causing limited side
effects. Additionally in2012Wanandcolleaguesperformeda studyon34patients,
confirming the efficacy of topical 0.5% loteprednoletabonate ophthalmic
suspension for the treatment ofmoderatedryeye (63).
ECABET-‐SODIUM
Bausch&Lomb Inc. is developing aprescriptioneyedrop for the treatment
of dry eye syndrome called
Ecabet
(Accession Number: DB05265).
Sulfodehydroabietic acid monosodium salt pentahydrate or ecabet sodium,
represents a new class of small diffusible molecules capable of increasing the
quantity and quality of mucin produced by conjunctival goblet cells and corneal
epithelia (Figure 8) (64). This ability makes the compound quite interesting as a
treatment for muco-‐deficient dry eye.
Ecabet
possible mechanism of action is
through the targeting of the prostaglandin E2 pathway, inhibiting the pepsin
formation, increasing blood flowand downregulating the reactive oxygen species
on the ocular surface. (65). It ismarketed in Japan by Senju Pharmaceutical as an
oral agent forgastriculcersandgastritis treatment (66). Bausch&Lomborganized
from April 2008 to January 2013 Phase II efficacy and safety studies for
Ecabet
ophthalmic solution with the purpose of treating the dry eye syndrome
(ClinicalTrials.gov Identifier: NCT00667004) in 183 patients. Bausch & Lomb Inc.
didnot yetdistributeresults information.
BOL-‐303242-‐X
Pharmaceutical R&D, Bausch&Lomb Inc., presented thedrugBOL-‐303242-‐
X (mapracorat) (Figure9) a selective glucocorticoid receptor agonist, as apossible
treatment for inflammatory skin and eye diseases. This agonist is binding to the
glucocorticoid receptor with an affinity similar to dexamethasone. Zhang and
colleagues demonstrated during
in vitro
and
in vivo
studies that BOL-‐303242-‐X
inhibited interleukin-‐1
β
(IL-‐1
β
) and induced decreases of inflammation in human
corneal epithelial cells. It is possible that BOL-‐303242-‐X is acting as an anti-‐
inflammatory agent in various primary human ocular cellswith similar activity to
classical steroids. Asmechanismof action it is suggested its interference inhuman
ocular cellsMAPK (p38 and JNK) andNF
κ
B signaling pathways (67). Vollmer T.R.
