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AbbVie set to receive $330m after exiting Reata deal

pharmafile | October 11, 2019 | News story | Medical Communications  

AbbVie is to receive $330 million after Reata Pharmaceuticals reacquired development, manufacturing and commercialisation rights to a portfolio of Nrf2 activators, including bardoxolone and omaveloxolone.

More specifically, Reata stated it has regained rights to bardoxolone outside the US in addition to global rights to omaveloxolone and other Nrf2 activators.

Reata also stated that it will make an upfront payment of $75 million this year with the remainder payable in instalments in the second quarter of 2020 and in the fourth quarter of 2021. AbbVie will also be eligible for low single-digit, tiered royalties from worldwide sales of omaveloxolone and certain next-generation Nrf2 activators, excluding bardoxolone.

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Warren Huff, Chief Executive Officer at Reata, said: “AbbVie has been an excellent partner, and our collaboration was instrumental in the clinical development of bardoxolone and omaveloxolone.

 “Regaining these rights will increase Reata’s strategic flexibility and control regarding the development and commercialisation of our lead drug candidates, and our next-generation Nrf2 activators.

“We have been actively preparing for the commercial launch of bardoxolone and omaveloxolone in the United States, and we will now expand our efforts to include these international territories as well.”

AbbVie initially licensed certain rights to bardoxolone for the treatment of chronic kidney disease from Reata in 2010 in a deal worth $450 million. The following year AbbVie acquired right to Reata’s preclinical agents for a one-time payment of $400 million.

Reata also announced that it has amended its loan and security agreement with Oxford Finance and Silicon Valley Bank to make $75 million available to the drug maker upon positive, topline registrational data from either the CARDINAL study of bardoxolone in patients with Alport syndrome or the MOXIe study of omaveloxolone in patients with Friedrich’s ataxia.

Nik Kiran

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