Palatin Technologies, Inc. (0KF3.L) LSE

Currency In USD

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Palatin Technologies, Inc.

Address

Cedar Brook Corporate Center

Cranbury, NJ 08512

United States of America (the)

Phone

609 495 2200

Sector

Healthcare

Industry

Biotechnology

Employees

30

First IPO Date

January 29, 2018

Key Executives

NameTitlePayYear Born
Carl SpanaCo-Founder, President, Chief Executive Officer & Director738,5001962
Stephen T. WillsChief Financial Officer, Chief Operating Officer, Executive Vice President, Treasurer & Secretary687,9601957
Stephen A. SlusherChief Legal Officer0N/A
John DoddSenior Vice President of Preclinical Development0N/A
Robert JordanSenior Vice President of Program Operations0N/A
James E. HattersleySenior Vice President of Business Development01960
Burns McClellanVice President of Investor Relations0N/A
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Description

Palatin Technologies, Inc., established in Cranbury, New Jersey, in 1986, is a biopharmaceutical company focused on developing specialized, receptor-targeting therapeutics for various medical conditions within the United States. The firm's flagship product, Vyleesi, is an approved melanocortin receptor (MCr) agonist designed to treat hypoactive sexual desire disorder in premenopausal women. Beyond Vyleesi, Palatin's robust pipeline features several investigational compounds: Oral PL8177: A selective MC1r agonist peptide that has successfully completed Phase I clinical trials for the treatment of inflammatory bowel diseases. PL9643: A peptide melanocortin agonist active at multiple melanocortin receptors, including MC1r and MC5r, being developed for anti-inflammatory ocular conditions such as dry eye disease. Additionally, the company is exploring other melanocortin peptides for diabetic retinopathy. PL3994: A synthetic mimetic of the endogenous neuropeptide hormone atrial natriuretic peptide and a natriuretic peptide receptor (NPR)-A agonist, intended for cardiovascular applications. PL5028: An NPR-A and NPR-binder under development to address cardiovascular and fibrotic diseases, including the reduction of cardiac hypertrophy and fibrosis.

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