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Indiplon (INN and USAN) is a nonbenzodiazepine, hypnotic sedative that was developed in two formulations—an immediate-release formulation for sleep onset, and a modified-release (also called controlled-release or extended-release) version for sleep maintenance.

Mode of action[edit]

Indiplon works by enhancing the action of the inhibitory neurotransmitter GABA, like most other nonbenzodiazepine sedatives. It primarily binds to the α1 subunits of the GABAA receptors in the brain.[1]


Indiplon was discovered at Lederle Laboratories (which was later acquired by Wyeth) in the 1980s and was called CL 285,489.[2]:454 In 1998 Lederle licensed it, along with other early stage drug candidates, to DOV Pharmaceutical, a startup formed by former Lederle employees, and Dov exclusively sublicensed its rights in the drug to Neurocrine Biosciences in that same year.[2] In 2002, Neurocrine entered into an agreement with Pfizer to develop the drug.[2]

Indiplon was originally scheduled for release in 2007, when Sanofi-Aventis' popular hypnotic zolpidem lost its patent rights in the United States and thus became available as a much less expensive generic. In 2002, Neurocrine Biosciences had entered into an agreement with Pfizer to co-market indiplon in the US, in a deal worth a potential $400mn.[3] However, following the issuing of a non-approvable letter for the modified-release 15 mg formulation and an approvable letter with stipulations for the 5 mg and 10 mg immediate-release version by the FDA in May 2006,[4] Pfizer ended its relationship with Neurocrine.[5] Neurocrine's stock price dropped 60% on the news.[6]

Following a resubmission, the FDA in December 2007 deemed Neurocrine's new drug application (NDA) 'approvable' in the 5 and 10 mg formulations,[7] but requested new studies as a prerequisite to approval, including a clinical trial in the elderly, a safety study comparing adverse effects to those of similarly marketed drugs, and a preclinical study examining indiplon's safety in the third trimester of pregnancy.[8]

Following the 2007 FDA letter, Neurocrine decided to discontinue all clinical and marketing development of Indiplon in the United States.[7][8]


  1. ^ Petroski RE, Pomeroy JE, Das R, Bowman H, Yang W, Chen AP, Foster AC (April 2006). "Indiplon is a high-affinity positive allosteric modulator with selectivity for alpha1 subunit-containing GABAA receptors" (PDF). The Journal of Pharmacology and Experimental Therapeutics. 317 (1): 369–77. doi:10.1124/jpet.105.096701. PMID 16399882.
  2. ^ a b c Neubauer DN (2010). "Indiplon". In Monti JS, Pandi-Perumal SR, Möhler H (eds.). GABA and Sleep: Molecular, Functional and Clinical Aspects. Springer Science & Business Media. pp. 453–464. ISBN 9783034602266.
  3. ^ "San Diego's Neurocrine Biosciences Scores Second Big Deal in Two Days". The Motley Fool. 18 June 2010.
  4. ^ "Neurocrine's FDA Nightmare". 16 May 2006.
  5. ^ "Pfizer Drops Neurocrine Deal". 22 June 2006.
  6. ^ "Neurocrine stock price plunges 60 percent:FDA's mixed review of sleeping pill Indiplon could threaten Pfizer-Neurocrine partnership". CNN Money. 15 May 2006.
  7. ^ a b "Neurocrine Receives Approvable Letter for Indiplon Capsules with Additional Safety and Efficacy Data Required by FDA" (Press release). Neurocrine Biosciences, Inc. 2007-12-13. Retrieved 2007-12-13.
  8. ^ a b "Additional Pipeline Projects". Neurocrine. 2012-02-16. Archived from the original on 2012-02-17. Retrieved 2014-06-24.

External links[edit]