Jonathan Hebb
Stanford University
7 Papers
214 Citations
Jonathan Hebb is an academic researcher from Stanford University. The author has contributed to research in topics: Immunotherapy & CD137. The author has an hindex of 5, co-authored 7 publications. Previous affiliations of Jonathan Hebb include Dalhousie University.
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Papers
Targeting CD137 enhances the efficacy of cetuximab
Holbrook E Kohrt,A. Dimitrios Colevas,Roch Houot,Roch Houot,Kipp Weiskopf,Matthew J. Goldstein,Peder Lund,Antonia Ms Mueller,Idit Sagiv-Barfi,Aurélien Marabelle,Aurélien Marabelle,Ruth R Lira,Emily Troutner,Lori Richards,Amanda Rajapaska,Jonathan Hebb,Cariad Chester,Erin Waller,Anton Ostashko,Wen-Kai Weng,Lieping Chen,Debra K. Czerwinski,Yang Xin Fu,John B. Sunwoo,Ronald Levy +24 more
TL;DR: It is found that isolated human NK cells substantially increased expression of CD137 when exposed to cetuximab-coated, EGFR-expressing HN and CRC cell lines, and activation ofCD137 with an agonistic mAb enhanced NK cell degranulation and cytotoxicity.
Administration of low-dose combination anti-CTLA4, anti-CD137, and anti-OX40 into murine tumor or proximal to the tumor draining lymph node induces systemic tumor regression.
Jonathan Hebb,Jonathan Hebb,Adriane Mosley,Felipe Vences-Catalán,Narendiran Rajasekaran,Narendiran Rajasekaran,Anna Rosén,Peter Ellmark,Dean W. Felsher +8 more
TL;DR: Overall intratumoral or peri-tDLN administration of the novel combination of anti-CTLA4, anti-CD137, and anti-OX40, all agents in the clinic or clinical trials, demonstrates potent systemic anti-tumor effects and is promising for future clinical development via both these safe and highly efficacious routes of administration.
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Three BTK-Specific Inhibitors, in Contrast to Ibrutinib, Do Not Antagonize Rituximab-Dependent NK-Cell Mediated Cytotoxicity
Narendiran Rajasekaran,Mohith Sadaram,Jonathan Hebb,Idit Sagiv-Barfi,Sid Ambulkar,Amanda Rajapaksa,Serena Chang,Cariad Chester,Erin Waller,Lai Wang,Brian J. Lannutti,Dave Johnson,Ronald Levy,Holbrook E Kohrt +13 more
TL;DR: The BTK inhibitor, ibrutinib is FDA-approved in MCL and CLL, with activity in the majority of CD20+ B-cell malignancies, and is clinically effective as monotherapy and in combination with rituximab despite inhibition of ADCC in vitro and in vivo murignancies.
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Obinutuzumab (GA101) Is Less Prone to Antagonism of Immune Effector Function By Ibrutinib Than Rituximab in Vitro and in Vivo
Sylvia Herter,Idit Sagiv-Barfi,Cariad Chester,Mohith Sadaram,Jonathan Hebb,Debra K. Czerwinski,Narendiran Rajasekaran,Marina Bacac,Pablo Umana,Ronald Levy,Christian Klein,Holbrook E Kohrt +11 more
TL;DR: Surprisingly, the inhibitory effect of ibrutinib on the immune effector mediated activity of obinutuzumab is not observed when compared to rituximab.
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Abstract 2941: Local tumor irradiation combined with α-PDL-1 immune checkpoint inhibition results in local and systemic anti-tumor responses: Successful translation of a mouse model to a human case series
Idit Sagiv-Barfi,Amanda Rajapaksa,Debra K. Czerwinski,Serena Chang,Jonathan Hebb,Cariad Chester,Erin Waller,Gregg Fine,Daniel S. Chen,Marcin Kowanetz,Bryan Irving,Ronald Levy,Holbrook E Kohrt +12 more
TL;DR: The magnitude of the immune response and abscopal response rate in mice and humans provides proof-of-concept that anti-PD-L1 may be an equally if not more potent combination immunotherapy with radiation compared to the authors' experience with CpG and/or anti-CTLA4.
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