Tumor Infiltrating Lymphocytes (TILs) are cytotoxic T-cells that are found in tumors. They serve to destroy cancer, or at least keep cancer at bay. Adoptive immunotherapy, Continue reading
Author Archives: Joseph Gulfo
arGENX – Immune Checkpoint Control of TNFR Superfamliy
A Dutch biotechnology company called arGENX raised $54 MM in an IPO (initial public offering) yesterday to advance its antibody pipeline. Its lead product, ARGX-110 is in late Phase 1 studies for hematologic malignancies. It is an immune checkpoint control modulator that acts on the CD70/CD27 axis, which is part of the TNFR superfamily, not the CD28/B7 superfamliy of co-stimulatory molecules. Continue reading
Cancer Immunotherapy Projections – Immune Checkpoint Inhibitors lead the way
The worldwide market for cancer immunotherapies is anticipated to grow from $1.1B in 2012 to $9B in 2022, that equals a 23/8% annual growth. Leading the growth are the immune checkpoint inhibitors.
Enhanced ADCC technologies to improve cancer cytotoxicity
Antibody Dependent Cell-Mediated Cytotoxicity (ADCC) is a process by which the Fab (variable region) of antibodies, produced by B-cells, first bind to antigens on target cells (cancer), and their Fc (constant regions) then bind white cells (macrophages, granulocytes, and NK – natural killer cells), which destroy the target cells. The antibodies opsonize the target and then attract white cells to destroy the target. Continue reading
PD-1 inhibitor approved in Asia
Ono Pharmaceuticals announced that nivolumab has been approved in Asia. It obtained the rights to nivolumab from Medarex in 2005. It is approved for use in patients with unresectable melanoma.
Targeted Nanoparticles for Cancer – optimizing physiochemical properties for enhanced tumor-killing
Last week, BIND Therapeutics and Amgen ended a collaboration on a targeted nanaoparticle that employed a proprietary cytotoxic compound from Amgen. However, BIND has several other programs (and partnerships with AstraZeneca, Roche, and Pfizer) that are proceeding in the clinic, which employ its Targeted Nanoparticle (TNP) technology. How does this work? Continue reading
Beleodaq, a new pan-HDAC inhibitor approved for peripheral T-cell lymphoma
HDAC inhibitors work by blocking Histone De-ACetylase enzyme, which removes acetyl groups from the proteins that encase DNA, that is histones. They are triggered by CpG sequences on DNA promoters; HDACs put chromatin in a configuration that favors LACK of transcription. So, blocking HDACs favors transcription – see prior post. Continue reading
Genentech Acquires Seragon – Selective Estrogen Receptor Degraders for breast cancer
Roche /Genentech announced that it acquired a company called Seragon for its new class of compound – SERD (selective Estrogen Receptor Degraders). Blocking estrogen production (aromatse inhibitors) and the binding to the estrogen receptor (tamoxifen) are mainstays of treatment for patients with ER (estrogen receptor) and PR (progesterone receptor) positive breast cancer. However, patients relapse subsequent to treatment with these agents. Continue reading
Bi-specific antibodies – matchmaking cancer and T-cells
Amgen reported encouraging data from a 189 patient phase 2 trial at this year’s ASCO meeting on blinatumomab in patients with Philadelphia Chromosome (9,22 translocation) negative relapsed/refractory B-precursor acute lymphoblastic leukemia (ALL) – see http://ecancer.org/conference/514-asco-2014/video/2913/blinatumomab-shown-to-be-beneficial-in-relapsed-refractory-b-precursor-acute-lymphoblastic-leukaemia.php. Continue reading
EGFRm+ non-small cell lung cancer – new treatments in development
For patients with activating mutations to the EGFR receptor kinase, small molecule specific inhibitors Iressa (gefintinib) or Tarceva (erlotinib) are administered as front-line treatments. But, non-small cell lung cancers develop resistance after about one year of treatment via a single recurrent missense mutation (T790M) to the tyrosine kinase. This is similar to resistance observed in patients with CML (Chronic Myeloid Leukemia) following treatment Gleevec (imatinib), which is mediated by a mutation to the Bcr-Abl transgene. Continue reading