Abingdon, United Kingdom
Abingdon, United Kingdom

Vertex Pharmaceuticals is an American Pharmaceutical company based in South Boston, Massachusetts. Vertex was founded in 1989 by Joshua Boger and Kevin J. Kinsella. Vertex was one of the first biotech firms to use an explicit strategy of rational drug design rather than combinatorial chemistry. By 2004, its product pipeline focused on viral infections, inflammatory and autoimmune disorders, and cancer. It maintains headquarters in South Boston, Massachusetts, and two research facilities, in San Diego, California, and Oxford, England. The company's beginnings were profiled by Barry Werth in the 1994 book The Billion-Dollar Molecule and its further development in his 2014 book, The Antidote: Inside the World of New Pharma. In 2009, the company had about 1,800 employees, including 1,200 in the Boston area.In January of 2014, Vertex completed its move from Cambridge, Massachusetts to South Boston, Massachusetts, and took residence in a new, $800 million complex. Located on the South Boston waterfront, it will mark the first time in the company's history that all of the roughly 1,200 Vertex employees in the Greater Boston area will be working together. Wikipedia.


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Patent
Vertex Pharmaceuticals | Date: 2016-08-31

The present invention relates to pharmaceutical compositions comprising a solid dispersion of N-[2,4-Bis(1,1-dimethylethyl)-5-hydroxyphenyl]-1,4-dihydro-4-oxoquinoline-3-carboxamide, methods of manufacturing pharmaceutical compositions of the present invention, and methods of administering pharmaceutical compositions of the present invention.


Patent
Vertex Pharmaceuticals | Date: 2016-11-22

The present invention relates to the novel regioselective syntheses of 2,4-disubstituted pyrimidines through sequential nucleophilic aromatic substitutions.


Patent
Vertex Pharmaceuticals | Date: 2017-03-15

The present invention relates to processes and intermediates for the preparation of compounds useful as inhibitors of Janus kinases (JAK).


Patent
Vertex Pharmaceuticals | Date: 2017-03-08

The present invention relates to pharmaceutical compositions comprising a compound of Formula I in combination with one or both of a Compound of Formula II and/or a Compound of Formula III. The invention also relates to solid forms and to pharmaceutical formulations thereof, and to methods of using such compositions in the treatment of CFTR mediated diseases, particularly cystic fibrosis.


A pharmaceutical composition comprising Compound 1, (3-(6-(1-(2,2-difluorobenzo[d][1,3]dioxol-5-yl)cyclopropanecarboxamido)-3-methylpyridin-2-yl)benzoic acid), and at least one excipient selected from: a filler, a diluent, a disintegrant, a surfactant, a binder, a glidant and a lubricant, the composition being suitable for oral administration to a patient in need thereof to treat a CFTR mediated disease such as Cystic Fibrosis. Methods for treating a patient in need thereof include administering an oral pharmaceutical formulation of Compound 1 to the patient.


Patent
Vertex Pharmaceuticals | Date: 2017-03-15

Methods of inhibiting the replication of influenza viruses in a biological sample or patient, of reducing the amount of influenza viruses in a biological sample or patient, and of treating influenza in a patient, comprises administering to said biological sample or patient an effective amount of a compound represented by Structural Formula (I):IA) are as described herein. A compound is represented by Structural Formula (IA) or a pharmaceutically acceptable salt thereof, wherein the values of Structural Formula (IA) are as described herein. A pharmaceutical composition comprises an effective amount of such a compound or pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier, adjuvant or vehicle.


Patent
Vertex Pharmaceuticals | Date: 2017-03-29

Methods of inhibiting the replication of influenza viruses in a biological sample or patient, of reducing the amount of influenza viruses in a biological sample or patient, and of treating influenza in a patient, comprises administering to said biological sample or patient an effective amount of a compound represented by Structural Formula (I):I) are as described herein. A compound is represented by Structural Formula (I) or a pharmaceutically acceptable salt thereof, wherein the values of Structural Formula (I) are as described herein. A pharmaceutical composition comprises an effective amount of such a compound or pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier, adjuvant or vehicle.


The present invention features compositions comprising a plurality of therapeutic agents wherein the presence of one therapeutic agent enhances the properties of at least one other therapeutic agent. In one embodiment, the therapeutic agents are cystic fibrosis transmembrane conductance regulators (CFTR) such as a CFTR corrector or CFTR potentiator for the treatment of CFTR mediated diseases such as cystic fibrosis. Methods and kits thereof are also disclosed.


In patients with genotype 1 chronic hepatitis C infection, telaprevir (TVR) in combination with peginterferon and ribavirin (PR) significantly increased sustained virologic response (SVR) rates compared with PR alone. However, genotypic changes could be observed in TVR-treated patients who did not achieve an SVR. Population sequence analysis of the NS3•4A region was performed in patients who did not achieve SVR with TVR-based treatment. Resistant variants were observed after treatment with a telaprevir-based regimen in 12% of treatment-naïve patients (ADVANCE; T12PR arm), 6% of prior relapsers, 24% of prior partial responders, and 51% of prior null responder patients (REALIZE, T12PR48 arms). NS3 protease variants V36M, R155K, and V36M+R155K emerged frequently in patients with genotype 1a and V36A, T54A, and A156S/T in patients with genotype 1b. Lower-level resistance to telaprevir was conferred by V36A/M, T54A/S, R155K/T, and A156S variants; and higher-level resistance to telaprevir was conferred by A156T and V36M+R155K variants. Virologic failure during telaprevir treatment was more common in patients with genotype 1a and in prior PR nonresponder patients and was associated with higher-level telaprevir-resistant variants. Relapse was usually associated with wild-type or lower-level resistant variants. After treatment, viral populations were wild-type with a median time of 10 months for genotype 1a and 3 weeks for genotype 1b patients. A consistent, subtype-dependent resistance profile was observed in patients who did not achieve an SVR with telaprevir-based treatment. The primary role of TVR is to inhibit wild-type virus and variants with lower-levels of resistance to telaprevir. The complementary role of PR is to clear any remaining telaprevir-resistant variants, especially higher-level telaprevir-resistant variants. Resistant variants are detectable in most patients who fail to achieve SVR, but their levels decline over time after treatment.


Nugent W.A.,Vertex Pharmaceuticals
Angewandte Chemie - International Edition | Year: 2012

When a research area "goes viral", the event typically occurs in conjunction with a major change in "conventional wisdom". In retrospect, the literature often contains earlier hints that the original judgment was not correct. These antecedents are referred to as "Black Swan" events. The picture shows research on homogeneous gold catalysis "going viral". Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

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