<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>30(4)</volume><submitter>Choi W</submitter><pubmed_abstract>&lt;h4>Purpose&lt;/h4>Dry eye syndrome is commonly thought of as an inflammatory disease, and we have previously presented data showing the effectiveness of topical TNF-α blocker agents for the treatment of this condition. The purpose of this study was to investigate the effectiveness of the TNF-α blocking agent HL036337 compared to cyclosporine A for the treatment of dry eye induced inflammation in order to establish whether HL036337 represents a more effective method for suppressing inflammation. The efficacy of HL036337 and cyclosporine A was determined using an experimental murine dry eye model.&lt;h4>Methods&lt;/h4>The TNF-α blocker HL036337 is a modified form of TNF receptor I. Using dry eye induced C57BL/6 mice (n = 45), corneal erosion was measured at day 4 and 7 after topical treatment with cyclosporine A or HL036337. To determine the effective treatment dose, 0.25, 0.5, 1, 2.5, and 5 mg/mL of HL036337 were topically administered twice per day to dry eye induced murine corneas for 1 week.&lt;h4>Results&lt;/h4>The optimal concentration of the TNF-α blocker HL036337 for treatment of dry eye induced corneal erosion was determined to be 1 mg/mL. Dry eye induced corneal erosion was improved after 1 week with topically applied cyclosporine A and HL036337 at 1 mg/mL.&lt;h4>Conclusions&lt;/h4>HL036337 administered topically at 1 mg/mL effectively improved corneal erosion induced by dry eye. This finding may also suggest that inhibition of TNF-α can improve dry eye syndrome.</pubmed_abstract><journal>Korean journal of ophthalmology : KJO</journal><pagination>302-8</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4965606</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The Effect of TNF-α Blocker HL036337 and Its Best Concentration to Inhibit Dry Eye Inflammation.</pubmed_title><pmcid>PMC4965606</pmcid><pubmed_authors>Noh H</pubmed_authors><pubmed_authors>Song YJ</pubmed_authors><pubmed_authors>Yeo A</pubmed_authors><pubmed_authors>Choi W</pubmed_authors><pubmed_authors>Jang H</pubmed_authors><pubmed_authors>Lee HK</pubmed_authors><pubmed_authors>Ahn HK</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Effect of TNF-α Blocker HL036337 and Its Best Concentration to Inhibit Dry Eye Inflammation.</name><description>&lt;h4>Purpose&lt;/h4>Dry eye syndrome is commonly thought of as an inflammatory disease, and we have previously presented data showing the effectiveness of topical TNF-α blocker agents for the treatment of this condition. The purpose of this study was to investigate the effectiveness of the TNF-α blocking agent HL036337 compared to cyclosporine A for the treatment of dry eye induced inflammation in order to establish whether HL036337 represents a more effective method for suppressing inflammation. The efficacy of HL036337 and cyclosporine A was determined using an experimental murine dry eye model.&lt;h4>Methods&lt;/h4>The TNF-α blocker HL036337 is a modified form of TNF receptor I. Using dry eye induced C57BL/6 mice (n = 45), corneal erosion was measured at day 4 and 7 after topical treatment with cyclosporine A or HL036337. To determine the effective treatment dose, 0.25, 0.5, 1, 2.5, and 5 mg/mL of HL036337 were topically administered twice per day to dry eye induced murine corneas for 1 week.&lt;h4>Results&lt;/h4>The optimal concentration of the TNF-α blocker HL036337 for treatment of dry eye induced corneal erosion was determined to be 1 mg/mL. Dry eye induced corneal erosion was improved after 1 week with topically applied cyclosporine A and HL036337 at 1 mg/mL.&lt;h4>Conclusions&lt;/h4>HL036337 administered topically at 1 mg/mL effectively improved corneal erosion induced by dry eye. This finding may also suggest that inhibition of TNF-α can improve dry eye syndrome.</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Aug</publication><modification>2024-10-18T08:28:43.843Z</modification><creation>2019-06-06T16:08:08Z</creation></dates><accession>S-EPMC4965606</accession><cross_references><pubmed>27478358</pubmed><doi>10.3341/kjo.2016.30.4.302</doi></cross_references></HashMap>