and was approved for marketing in Europe in 1989.In October 2001 Forest Laboratories acquired the rights to market the drug in the US.It was approved by the FDA in July 2004.The first generic versions of acamprosate were launched in the US in 2013.As of 2015 acamprosate was in development by Confluence Pharmaceuticals as a potential treatment for fragile X syndrome. The drug was granted orphan status for this use by the FDA in 2013 and by the EMA in 2014. Society and culture
"Acamprosate" is the INN and BAN for this substance. "Acamprosate calcium" is the USAN and JAN. It is also technically known as N-acetylhomotaurine or as calcium acetylhomotaurinate. It is sold under the brand name Campral. Research
In addition to its apparent ability to help patients refrain from drinking, some evidence suggests that acamprosate is neuroprotective (that is, it protects neurons from damage and death caused by the effects of alcohol withdrawal, and possibly other causes of neurotoxicity). See also
Homotaurine (tramiprosate)
List of investigational anxiolytics
List of investigational antidepressants


== References ==
a group of genetically identical eosinophils derived from a significantly mutated ancestor cell. The clone may prove to be benign, pre-malignant, or overtly malignant. The fundamental driver of these hypereosinophilic (or uncommonly eosinophilic) disorders is the mutation which increases the proliferation, survival, and further mutation of cells descendant from the originally mutated cell. There are several subtypes of primary hypereosinophilia. Clonal hypereosinophilia
Clonal hypereosinophilia is hypereosinophilia caused by a pre-malignant or malignant clone of eosinophils that bear mutations in genes for PDGFRA, PDGFRB, or FGFR1 or, alternatively, a chromosome translocation that creates the PCM1-JAK2 fusion gene. These genes code for dysfunctional protein products capable of enhancing proliferation and/or survival of their parent cells which, in consequence, become an evolving and constantly growing clone of eosinophils. These mutations are recognized by the World Health Association as causing distinct entities differing from idiopathic hypereosinophilia and the idiopathic hypereosinophilic syndrome. Presence of these clones may be associated with tissue injury but in any case suggests specific therapy be directed at reducing the size and suppressing the growth of the eosinophil clone. More recently, mutations in other genes have been described as causing a similar type of clonal hypereosinophilia but have not yet been recognized as entities distinct from idiopathic hypereosinophilia and the idiopathic hyperesoniphilic syndrome. These include gene mutations in JAK2, ABL1, and FLT2 and chromosomal translocations that create the ETV6-ACSL6 fusion gene. Chronic eosinophilic leukemia (NOS)
Chronic eosinophilic leukemia, not otherwise specified (i.e.