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Covalent and allosteric inhibitors of the ATPase VCP/p97 induce cancer cell death

Nature chemical biology, 2013-09, Vol.9 (9), p.548-556

2013

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Decline in self-renewal factors contributes to aging of the stem cell niche in the Drosophila testis

Cell stem cell, 2007-10, Vol.1 (4), p.470-478

2007

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Tumor-specific activation of an EGFR-targeting probody enhances therapeutic index

Science translational medicine, 2013-10, Vol.5 (207), p.207ra144

2013

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HIM-8 Binds to the X Chromosome Pairing Center and Mediates Chromosome-Specific Meiotic Synapsis

Cell, 2005-12, Vol.123 (6), p.1051-1063

2005

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Efficiency of spermatogonial dedifferentiation during aging

PloS one, 2012-03, Vol.7 (3), p.e33635-e33635

2012

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P946: TOCILIZUMAB PRE‐TREATMENT SIGNIFICANTLY REDUCES THE INCIDENCE OF CYTOKINE RELEASE SYNDROME IN PATIENTS WITH RELAPSED/REFRACTORY MULTIPLE MYELOMA (RRMM) WHO RECEIVE CEVOSTAMAB

HemaSphere, 2023-08, Vol.7 (S3), p.e75458a8-n/a

2023

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Stem Cell Dynamics in Response to Nutrient Availability

Current biology, 2010-12, Vol.20 (23), p.2100-2105

2010

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Pretreatment with Tocilizumab Prior to the CD3 Bispecific Cevostamab in Patients with Relapsed/Refractory Multiple Myeloma (RRMM) Showed a Marked Reduction in Cytokine Release Syndrome Incidence and Severity

Blood, 2022-11, Vol.140 (Supplement 1), p.1363-1365

2022

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Bcl-2, Bcl-xL, and Bcl-w are not equivalent targets of ABT-737 and navitoclax (ABT-263) in lymphoid and leukemic cells

Blood, 2012-06, Vol.119 (24), p.5807-5816

2012

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Enduring Responses after 1-Year, Fixed-Duration Cevostamab Therapy in Patients with Relapsed/Refractory Multiple Myeloma: Early Experience from a Phase I Study

Blood, 2022-11, Vol.140 (Supplement 1), p.4415-4417

2022

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P-012: Cevostamab is efficacious and well tolerated in patients aged < 65 and ≥65 years with relapsed/refractory multiple myeloma (RRMM)

Clinical lymphoma, myeloma and leukemia, 2022-08, Vol.22, p.S42-S43

2022

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Preliminary single-dose clinical pharmacokinetics of an anti–PD-L1 Probody therapeutic (Pb-Tx) in cancer patients

Journal of clinical oncology, 2018-05, Vol.36 (15_suppl), p.e14558-e14558

2018

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Conditional PD-1/PD-L1 Probody Therapeutics Induce Comparable Antitumor Immunity but Reduced Systemic Toxicity Compared with Traditional Anti-PD-1/PD-L1 Agents

Cancer immunology research, 2021-12, Vol.9 (12), p.1451-1464

2021

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PROCLAIM-001: A first-in-human trial to assess tolerability of the protease-activatable anti-PD-L1 Probody CX-072 in solid tumors and lymphomas

Journal of clinical oncology, 2017-05, Vol.35 (15_suppl), p.TPS3107-TPS3107

2017

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Abstract 2665: Transforming Notch ligands into tumor-antigen targets: A Probody-Drug Conjugate (PDC) targeting Jagged 1 and Jagged 2

Cancer research (Chicago, Ill.), 2014-10, Vol.74 (19_Supplement), p.2665-2665

2014

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Abstract C158: Tumor-specific inhibition of jagged-dependent notch signaling using a Probody™ therapeutic

Molecular cancer therapeutics, 2013-11, Vol.12 (11_Supplement), p.C158-C158

2013

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Abstract A081: A PD-L1-targeted Probody provides antitumor efficacy while minimizing induction of systemic autoimmunity

Cancer immunology research, 2016-01, Vol.4 (1_Supplement), p.A081-A081

2016

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Characterization of germline stem cell behavior during aging in Drosophila melanogaster

Wong, Chihunt

2010

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HIM-8 binds to the X chromosome pairing center and mediateschromosome-specific meiotic synapsis

Cell, 2005-06, Vol.123

2005

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Bcl-2, Bcl-x(L), and Bcl-w are not equivalent targets of ABT-737 and navitoclax (ABT-263) in lymphoid and leukemic cells

Blood, 2012-06, Vol.119 (24), p.5807

2012

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Covalent and allosteric inhibitors of the ATPase VCP/p97 induce cancer cell death

Decline in self-renewal factors contributes to aging of the stem cell niche in the Drosophila testis

Tumor-specific activation of an EGFR-targeting probody enhances therapeutic index

HIM-8 Binds to the X Chromosome Pairing Center and Mediates Chromosome-Specific Meiotic Synapsis

Efficiency of spermatogonial dedifferentiation during aging

P946: TOCILIZUMAB PRE‐TREATMENT SIGNIFICANTLY REDUCES THE INCIDENCE OF CYTOKINE RELEASE SYNDROME IN PATIENTS WITH RELAPSED/REFRACTORY MULTIPLE MYELOMA (RRMM) WHO RECEIVE CEVOSTAMAB

Stem Cell Dynamics in Response to Nutrient Availability

Pretreatment with Tocilizumab Prior to the CD3 Bispecific Cevostamab in Patients with Relapsed/Refractory Multiple Myeloma (RRMM) Showed a Marked Reduction in Cytokine Release Syndrome Incidence and Severity

Bcl-2, Bcl-xL, and Bcl-w are not equivalent targets of ABT-737 and navitoclax (ABT-263) in lymphoid and leukemic cells

Enduring Responses after 1-Year, Fixed-Duration Cevostamab Therapy in Patients with Relapsed/Refractory Multiple Myeloma: Early Experience from a Phase I Study

Cevostamab Monotherapy Continues to Show Clinically Meaningful Activity and Manageable Safety in Patients with Heavily Pre-Treated Relapsed/Refractory Multiple Myeloma (RRMM): Updated Results from an Ongoing Phase I Study

P-012: Cevostamab is efficacious and well tolerated in patients aged < 65 and ≥65 years with relapsed/refractory multiple myeloma (RRMM)

Preliminary single-dose clinical pharmacokinetics of an anti–PD-L1 Probody therapeutic (Pb-Tx) in cancer patients

Conditional PD-1/PD-L1 Probody Therapeutics Induce Comparable Antitumor Immunity but Reduced Systemic Toxicity Compared with Traditional Anti-PD-1/PD-L1 Agents

PROCLAIM-001: A first-in-human trial to assess tolerability of the protease-activatable anti-PD-L1 Probody CX-072 in solid tumors and lymphomas

Abstract 2665: Transforming Notch ligands into tumor-antigen targets: A Probody-Drug Conjugate (PDC) targeting Jagged 1 and Jagged 2

Abstract C158: Tumor-specific inhibition of jagged-dependent notch signaling using a Probody™ therapeutic

Abstract A081: A PD-L1-targeted Probody provides antitumor efficacy while minimizing induction of systemic autoimmunity

Characterization of germline stem cell behavior during aging in Drosophila melanogaster

HIM-8 binds to the X chromosome pairing center and mediateschromosome-specific meiotic synapsis

Bcl-2, Bcl-x(L), and Bcl-w are not equivalent targets of ABT-737 and navitoclax (ABT-263) in lymphoid and leukemic cells

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