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South San Francisco, CA, United States

Genentech Inc., is a biotechnology corporation which became a subsidiary of Roche in 2009. Genentech Research and Early Development operates as an independent center within Roche.As of August 2013, Genentech employed more than 12,300 people. In July 2014, Genentech announced its acquisition of Seragon for up to $1.725 billion. Wikipedia.

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Patent
Curis and Genentech | Date: 2017-02-22

Novel inhibitors of IAP that are useful as therapeutic agents for treating malignancies and have the general formula I:R and R are as described herein.


Patent
Genentech | Date: 2017-02-15

Methods for treating multiple sclerosis (MS) with a CD20 antibody using special dosing regimens and protocols are described. Articles of manufacture for use in such methods are also described.


Patent
Genentech | Date: 2017-03-15

The present invention concerns affinity matured CRIg variants. In particular, the invention concerns CRIg variants having increased binding affinity to C3b and retaining selective binding to C3b over C3.


Patent
Genentech and Hoffmann-La Roche | Date: 2017-09-20

Methods of identifying, diagnosing, and prognosing lupus, including certain subphenotypes of lupus, are provided, as well as methods of treating lupus, including certain subpopulations of patients. The methods are based on the identification of risk SNPs for the development of lupus (SLE), in particular the BLK region and the SNP rs922483. Other preferred risk regions are in the TNIP1, PRDM1, JAZF1, UHRF1BP 1, IL10, IFIH1, CFB, CLEC16A, IL12B and SH2B3 genes. Also provided are methods for identifying effective lupus therapeutic agents and predicting responsiveness to lupus therapeutic agents.


Patent
Genentech and Constellation Pharmaceuticals | Date: 2017-09-20

The present invention relates to compounds of formula (I): [INSERT FORMULA (1)] and to salts thereof, wherein R1, R2, Rc, and Rd have any of the values defined in the specification, and compositions and uses thereof. The compounds are useful as inhibitors of bromodomains. Also included are pharmaceutical compositions comprising a compound of formula (I) or a pharmaceutically acceptable salt thereof, and methods of using such compounds and salts in the treatment of various bromodomain-mediated disorders.


Ferrara N.,University of California at San Diego | Adamis A.P.,Genentech
Nature Reviews Drug Discovery | Year: 2016

The targeting of vascular endothelial growth factor A (VEGFA), a crucial regulator of both normal and pathological angiogenesis, has revealed innovative therapeutic approaches in oncology and ophthalmology. The first VEGFA inhibitor, bevacizumab, was approved by the US Food and Drug Administration in 2004 for the first-line treatment of metastatic colorectal cancer, and the first VEGFA inhibitors in ophthalmology, pegaptanib and ranibizumab, were approved in 2004 and 2006, respectively. To mark this tenth anniversary of anti-VEGFA therapy, we discuss the discovery of VEGFA, the successes and challenges in the development of VEGFA inhibitors and the impact of these agents on the treatment of cancers and ophthalmic diseases. © 2016 Macmillan Publishers Limited.


Polakis P.,Genentech
EMBO Journal | Year: 2012

Aberrant regulation of the Wnt signalling pathway has emerged as a prevalent theme in cancer biology. This chapter summarizes the research that provides a proof of concept for inhibiting Wnt signalling in cancer, the potential means by which this could be achieved, and some recent advances towards this goal. A brief discussion of molecular diagnostics and possible safety concerns is also provided. © 2012 European Molecular Biology Organization.


Polakis P.,Genentech
Cold Spring Harbor Perspectives in Biology | Year: 2012

Aberrant regulation of the Wnt signaling pathway is a prevalent theme in cancer biology. From the earliest observation that Wnt overexpression could lead to malignant transformation of mouse mammary tissue to the most recent genetic discoveries gleaned from tumor genome sequencing, the Wnt pathway continues to evolve as a central mechanism in cancer biology. This article summarizes the evidence supporting a role for Wnt signaling in human cancer. This includes a review of the genetic mutations affecting Wnt pathway components, as well as some of epigenetic mechanisms that alter expression of genes relevant to Wnt. I also highlight some research on the cooperativity of Wnt with other signaling pathways in cancer. Finally, some emphasis is placed on laboratory research that provides a proof of concept for the therapeutic inhibition of Wnt signaling in cancer. © 2012 Cold Spring Harbor Laboratory Press; all rights reserved.


To understand the genetic predisposition to selective immunoglobulin A deficiency (IgAD), we performed a genome-wide association study in 430 affected individuals (cases) from Sweden and Iceland and 1,090 ethnically matched controls, and we performed replication studies in two independent European cohorts. In addition to the known association of HLA with IgAD, we identified association with a nonsynonymous variant in IFIH1 (rs1990760G>A, P = 7.3 x 10(-10)) which was previously associated with type 1 diabetes and systemic lupus erythematosus. Variants in CLEC16A, another known autoimmunity locus, showed suggestive evidence for association (rs6498142C>G, P = 1.8 x 10(-7)), and 29 additional loci were identified with P < 5 x 10(-5). A survey in IgAD of 118 validated non-HLA autoimmunity loci indicated a significant enrichment for association with autoimmunity loci as compared to non-autoimmunity loci (P = 9.0 x 10(-4)) or random SNPs across the genome (P < 0.0001). These findings support the hypothesis that autoimmune mechanisms may contribute to the pathogenesis of IgAD.


Zhang Z.,Genentech
Nature Genetics | Year: 2012

A new exome sequencing study of individuals with hepatocellular carcinoma (HCC) reveals imprints of mutagenic exposure and identifies new genes contributing to tumorigenesis. This work joins several recent publications reporting whole-genome, exome and RNA sequencing in HCC, which together provide a comprehensive genomic landscape and new insights into the etiology of liver cancer. © 2012 Nature America, Inc. All rights reserved.

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