Summit, NJ, United States
Summit, NJ, United States

Celgene Corporation is an American biotechnology company that manufactures drug therapies for cancer and inflammatory disorders. It is incorporated in Delaware and headquartered in Summit, New Jersey. The company's major products are Thalomid , which is approved for the acute treatment of the cutaneous manifestations of moderate to severe erythema nodosum leprosum , as well as in combination with dexamethasone for patients with newly diagnosed multiple myeloma, and Revlimid , for which the company has received FDA and EMA approval in combination with dexamethasone for the treatment of multiple myeloma patients who have received at least one prior therapy. Revlimid is also approved in the United States for the treatment of patients with transfusion-dependent anemia due to Low- or Intermediate-1-risk Myelodysplastic syndromes associated with a deletion 5q cytogenetic abnormality with or without additional cytogenetic abnormalities. Both Thalomid and Revlimid are sold through proprietary risk-management distribution programs to ensure safe and appropriate use of these pharmaceuticals. Vidaza is approved for the treatment of patients with MDS. Celgene also receives royalties from Novartis Pharma AG on sales of the entire Ritalin family of drugs, which are widely used to treat Attention Deficit Hyperactivity Disorder .Celgene Cellular Therapeutics, a subsidiary, is a public cord blood bank. Wikipedia.


Time filter

Source Type

Methods of treating, preventing or managing mantle cell lymphomas are disclosed. The methods encompass the administration of an immunomodulatory compound of the invention known as Revlimid or lenalidomide. The invention further relates to methods of treatment using this compound with chemotherapy, radiation therapy, hormonal therapy, biological therapy or immunotherapy. Pharmaceutical compositions and single unit dosage forms suitable for use in the methods of the invention are also disclosed.


Patent
Celgene | Date: 2016-06-24

The present invention provides compounds, pharmaceutically acceptable compositions thereof, and methods of using the same.


Patent
Celgene | Date: 2016-11-17

The present invention relates generally to compositions and methods for treating cancer and neoplastic diseases. Provided herein are substituted imidazole-pyridine derivative compounds and pharmaceutical compositions comprising said compounds. The subject compounds and compositions are useful for inhibition of histone demethylase enzymes. Furthermore, the subject compounds and compositions are useful for the treatment of cancer, such as prostate cancer, breast cancer, bladder cancer, lung cancer and/or melanoma and the like.


Patent
Celgene | Date: 2016-09-28

Provided herein are compositions, methods and uses involving antibodies that specifically bind to Programmed Death-1 (PD-1) and modulate the expression and/or activity of PD-1.


Patent
Celgene | Date: 2016-04-15

The present invention relates to substituted heterocyclic derivative compounds, compositions comprising said compounds, and the use of said compounds and compositions for epigenetic regulation by inhibition of bromodomain-mediated recognition of acetyl lysine regions of proteins, such as histones. Said compositions and methods are useful for the treatment of cancer and neoplastic disease.


Patent
Celgene | Date: 2016-12-12

Provided herein are isoindoline compounds, pharmaceutical compositions comprising one or more of such compounds, and methods of their use for treating, preventing, or managing various diseases.


Pharmaceutical compositions and single unit dosage forms of Compound A (3-(5-amino-2-methyl-4-oxo-4H-quinazolin-3-yl)-piperidine-2,6-dione), or an enantiomer or a mixture of enantiomers thereof, a pharmaceutically acceptable salt, solvate, hydrate, co-crystal, clathrate, or polymorph thereof, are provided herein. Also provided are methods of treating, managing, or preventing cancer using the dosage forms described herein.


Patent
Celgene | Date: 2017-03-22

The present invention provides a salt form, and compositions thereof, useful as an inhibitor of one or more protein kinases and which exhibits desirable characteristics for the same.


Provided herein, for example, are methods generally relating to the expansion and/or regeneration of central nervous system (CNS) cells, such as nerve cells, astrocytes and oligodendrocytes, using an activator of cereblon (CRBN), such as an inhibitor of a CRBN substrate or downstream protein. Also provided herein, for example, are methods related to the expansion of neural stem cells, neural progenitor cells, or neural precursor cells and/or differentiation of these cells into CNS cells using a BRD7 antagonist, Ikaros antagonist, or CRBN activator. In certain embodiments, the methods further comprise differentiation of certain stem cells into the neural stem cells, neural progenitor cells, or neural precursor cells using a BRD7 antagonist, Ikaros antagonist, or CRBN activator. Also provided herein, for example, are methods of preventing or treating a CNS cell defective disease, disorder or condition, or a symptom thereof, using a BRD7 antagonist, Ikaros antagonist, or CRBN activator.


Chamberlain P.P.,Celgene
Nature Structural and Molecular Biology | Year: 2014

The Cul4-Rbx1-DDB1-Cereblon E3 ubiquitin ligase complex is the target of thalidomide, lenalidomide and pomalidomide, therapeutically important drugs for multiple myeloma and other B-cell malignancies. These drugs directly bind Cereblon (CRBN) and promote the recruitment of substrates Ikaros (IKZF1) and Aiolos (IKZF3) to the E3 complex, thus leading to substrate ubiquitination and degradation. Here we present the crystal structure of human CRBN bound to DDB1 and the drug lenalidomide. A hydrophobic pocket in the thalidomide-binding domain (TBD) of CRBN accommodates the glutarimide moiety of lenalidomide, whereas the isoindolinone ring is exposed to solvent. We also solved the structures of the mouse TBD in the apo state and with thalidomide or pomalidomide. Site-directed mutagenesis in lentiviral-expression myeloma models showed that key drug-binding residues are critical for antiproliferative effects.

Loading Celgene collaborators
Loading Celgene collaborators