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Journal articles on the topic 'Peripheral neuropathy, murine models, bortezomib, multiple myeloma'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

Berenson, James R., Ori Yellin, Ravi Patel, et al. "A Phase II Study of Pegylated Liposomal Doxorubicin, Bortezomib and Dexamethasone (DVD) for Patients with Previously Untreated Multiple Myeloma (MM)." Blood 114, no. 22 (2009): 4936. http://dx.doi.org/10.1182/blood.v114.22.4936.4936.

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Abstract Abstract 4936 Despite recent advances in the treatment of MM, the disease remains incurable and many of the most effective, newer combination therapies are accompanied by significant side effects that have a major negative impact on the patient's quality of life. Pegylated liposomal doxorubicin (PLD) and bortezomib have shown anti-MM efficacy in the laboratory and for the treatment of previously treated MM patients, leading to FDA approval for patients who have failed one prior therapy. Using our severe combined immunodeficiency-hu murine models of human MM, we have previously demonst

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2

Dave, Ami Atulkumar, Jaime K. Lewis, and Agne Paner. "Retrospective review of chronic pain causes and management in multiple myeloma patients." Journal of Clinical Oncology 38, no. 15_suppl (2020): e20552-e20552. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e20552.

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e20552 Background: The survival of patients with multiple myeloma has improved dramatically since the introduction of proteasome inhibitors such as bortezomib, which can have the adverse effect of peripheral neuropathy. This study retrospectively examines causes of chronic pain in myeloma patients and the modalities and duration of treatments used for pain control. Methods: Rush University Medical Center multiple myeloma patients who were diagnosed and treated between 2000-2019 were included. Outcome measures were abstracted from the medical record and included: classes of pain medication used

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3

Mavis, Cory, Juan Gu, Joseph Skitzki, Francisco Hernandez, and Myron S. Czuczman. "Ixazomib, An Investigational Orally Bioavailable Proteasome Inhibitor, Increases p21 Expression Inducing Caspase-Dependent Cell Death, Cell-Cycle Arrest, and In B-Cell Lymphoma Pre-Clinical Models." Blood 122, no. 21 (2013): 1828. http://dx.doi.org/10.1182/blood.v122.21.1828.1828.

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Abstract Pharmacological inhibition of the proteasome with bortezomib (BTZ) has translated into an improved clinical outcome in patients with multiple myeloma and mantle cell lymphoma. Despite the observed clinical activity, BTZ anti-tumor activity in B-cell lymphoma has been partially hindered by treatment-related toxicities (peripheral neuropathy) preventing further dose escalation and emergence of acquired resistance. To further develop therapeutic strategies targeting the proteasome system, we studied the anti-tumor activity and mechanisms-of-action of ixazomib (MLN2238), a reversible prot

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4

Uy, Geoffrey L., Matthew S. Holt, Nicholas M. Fisher, et al. "Bortezomib Alters Peripheral Blood Lymphocyte Subsets in Patients with Multiple Myeloma." Blood 106, no. 11 (2005): 2387. http://dx.doi.org/10.1182/blood.v106.11.2387.2387.

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Abstract Bortezomib (VELCADE®) is a potent inhibitor of the proteasome which exerts its antimyeloma effect in part by blocking the activation of NF-κB. As NF-κB is critical for lymphocyte development and survival, there is great interest in harnessing the potential immunomodulatory effects of bortezomib. In murine hematopoietic transplantation models, bortezomib inhibits in vitro mixed lymphocyte responses and promotes the apoptosis of alloreactive T cells protecting against acute graft-versus-host disease. However, no data exists on the in vivo effects of bortezomib on human T cells. To chara

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Zhou, Jialin, Hanheng Mai, Yunqing Liu, et al. "Genetic Insusceptibility Mediated Inflammation Contributes to Bortezomib-Induced Peripheral Neuropathy." Blood 144, Supplement 1 (2024): 1961. https://doi.org/10.1182/blood-2024-201966.

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Introduction: Chemotherapy-induced peripheral neuropathy (CIPN) is a disabling pain condition resulting from chemotherapy for cancer. CIPN-inducing drug bortezomib is widely used in multiple myeloma (MM) treatment. The pathogenesis of bortezomib-induced peripheral neuropathy (BIPN) is poorly understood. Our study reported here elucidates the murine transcriptomic modifications in oxaliplatin- and cisplatin-induced CIPN and whole exome sequencing (WES) features in MM patients with BIPN. Methods: RNA sequencing (RNA-seq) data of murine spinal cords were retrieved under the GEO accession numbers

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Anchoori, Ravi K., Vidyasagar Anchoori, Brandon Lam, et al. "Development and anticancer properties of Up284, a spirocyclic candidate ADRM1/RPN13 inhibitor." PLOS ONE 18, no. 6 (2023): e0285221. http://dx.doi.org/10.1371/journal.pone.0285221.

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Bortezomib has been successful for treatment of multiple myeloma, but not against solid tumors, and toxicities of neuropathy, thrombocytopenia and the emergence of resistance have triggered efforts to find alternative proteasome inhibitors. Bis-benzylidine piperidones such as RA190 covalently bind ADRM1/RPN13, a ubiquitin receptor that supports recognition of polyubiquitinated substrates of the proteasome and their subsequent deububiqutination and degradation. While these candidate RPN13 inhibitors (iRPN13) show promising anticancer activity in mouse models of cancer, they have suboptimal drug

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7

Kuhn, Deborah J., Sally A. Hunsucker, Qing Chen, Peter M. Voorhees, Marian Orlowski, and Robert Z. Orlowski. "Targeted inhibition of the immunoproteasome is a potent strategy against models of multiple myeloma that overcomes resistance to conventional drugs and nonspecific proteasome inhibitors." Blood 113, no. 19 (2009): 4667–76. http://dx.doi.org/10.1182/blood-2008-07-171637.

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Abstract Proteasome inhibition is a validated strategy for therapy of multiple myeloma, but this disease remains challenging as relapses are common, and often associated with increasing chemoresistance. Moreover, nonspecific proteasome inhibitors such as bortezomib can induce peripheral neuropathy and other toxicities that may compromise the ability to deliver therapy at full doses, thereby decreasing efficacy. One novel approach may be to target the immunoproteasome, a proteasomal variant found predominantly in cells of hematopoietic origin that differs from the constitutive proteasome found

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8

Ikeda, Hiroshi, Teru Hideshima, Mariateresa Fulciniti та ін. "PI3K/p110δ is a novel therapeutic target in multiple myeloma". Blood 116, № 9 (2010): 1460–68. http://dx.doi.org/10.1182/blood-2009-06-222943.

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In this study, we demonstrate expression and examined the biologic sequelae of PI3K/p110δ signaling in multiple myeloma (MM). Knockdown of p110δ by small interfering RNA caused significant inhibition of MM cell growth. Similarly, p110δ specific small molecule inhibitor CAL-101 triggered cytotoxicity against LB and INA-6 MM cell lines and patient MM cells, associated with inhibition of Akt phosphorylation. In contrast, CAL-101 did not inhibit survival of normal peripheral blood mononuclear cells. CAL-101 overcame MM cell growth conferred by interleukin-6, insulin-like growth factor-1, and bone

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Steinberg, Jeffrey A., Jing Shen, Eric Sanchez, et al. "Alpha Lipoic Acid (ALA) Inhibits the Anti-Myeloma Effects of Bortezomib." Blood 114, no. 22 (2009): 3832. http://dx.doi.org/10.1182/blood.v114.22.3832.3832.

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Abstract Abstract 3832 Poster Board III-768 Introduction ALA is an antioxidant often used in the management of peripheral neuropathy (PN) for patients with multiple myeloma (MM). A clinical trial evaluating ALA in diabetic neuropathy showed this drug to be effective for patients with both somatic and autonomic neuropathies. It also normalized the endoneural blood flow, reduced oxidative stress and improved vascular dysfunction. Bortezomib (Velcade®), the first-in-class proteasome inhibitor (PI), which is approved for the treatment of patients with MM, may cause PN. As a result, patients are of

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10

Moreau, Philippe, Asher A. Chanan-Khan, Andrew W. Roberts, et al. "Venetoclax Combined with Bortezomib and Dexamethasone for Patients with Relapsed/Refractory Multiple Myeloma." Blood 128, no. 22 (2016): 975. http://dx.doi.org/10.1182/blood.v128.22.975.975.

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Abstract Background: BCL-2 and MCL-1 promote multiple myeloma (MM) cell survival. Venetoclax (VEN) is a potent, selective, orally bioavailable small-molecular inhibitor of BCL-2. When combined with bortezomib, which can inhibit MCL-1, VEN can enhance the activity of bortezomib in MM cell lines and xenograft models. Methods: In this Phase 1b, open label, dose escalation study, patients with relapsed/refractory (R/R) MM received daily VEN (50 - 1200 mg per designated dose cohort) with bortezomib and dexamethasone. The objectives of the study were to assess the safety, pharmacokinetics, maximum t

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Ricci, Deborah S., Reyna Favis, Yu Sun, et al. "Pharmacogenomic (PGx) Analysis of Bortezomib-Associated Peripheral Neuropathy in the Phase 3 VISTA Trial of Bortezomib Plus Melphalan–Prednisone Versus Melphalan–Prednisone in Multiple Myeloma." Blood 114, no. 22 (2009): 3875. http://dx.doi.org/10.1182/blood.v114.22.3875.3875.

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Abstract Abstract 3875 Poster Board III-811 We investigated genotyping of 172 candidate gene loci (2016 SNPs) related to hereditary neuropathy, energy production and fast axonal transport, nociception and pain transmission, mitochondria, neurogenesis, neuroprotection, immune function, and bortezomib (Velcade®) mechanism of action. Our aim was to identify predictive classifiers for peripheral neuropathy (PN) in multiple myeloma (MM) following treatment with bortezomib in the phase 3 VISTA trial of bortezomib plus melphalan–prednisone (VMP, N=344) vs MP (N=338) in previously untreated MM patient

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12

Schueler, Julia B., Dagmar Wider, Kerstin Klingner, et al. "Novel Patient Derived Multiple Myeloma Model Reflects Sensitivity Towards Anticancer Treatment in Multiple Myeloma Patients." Blood 126, no. 23 (2015): 3004. http://dx.doi.org/10.1182/blood.v126.23.3004.3004.

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Abstract Background Appropriate animal models for hematological malignancies are highly attractive, because they allow the study of the tumor biology and underlying disease mechanisms. They also constitute a major prerequisite for rapid bench-to-bedside translation of investigational anticancer therapies. To validate our multiple myeloma patient (pt)-derived xenograft (MM PDX) model (Schueler et al, Expert Opin Biol Ther, 2013), we systematically analyzed a panel of MM PDX with regard to their sensitivity towards standard of care treatment and compared these data with the pts' clinical outcome

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13

Magrangeas, Florence, Rowan Kuiper, Hervé Avet-loiseau, et al. "A Genome Wide Association Study Reveals Genetic Predisposition for Bortezomib-Induced Peripheral Neuropathy in Multiple Myeloma By Variation in the PREP1-Cbs Locus." Blood 124, no. 21 (2014): 2057. http://dx.doi.org/10.1182/blood.v124.21.2057.2057.

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Abstract Introduction: Bortezomib has become an important part of myeloma therapy, despite the occurrence of toxicities such as bortezomib induced peripheral neuropathy (BiPN). Since effective prophylactic treatment is lacking, onset of BiPN can only be remedied by dose reduction or stop of treatment. Here, using a genome-wide genotyping method, we investigated the potential genetic predisposition to BiPN in MM patients who received bortezomib-dexamethasone (VD) induction therapy prior to autologous stem-cell transplantation (ASCT). Methods: We performed a genome-wide association study using t

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14

Mereu, Elisabetta, Damiano Abbo, Tina Paradzik, et al. "Euchromatic Histone Lysine Methyltransferase 2 Inhibition Enhances Carfilzomib Sensitivity and Overcomes Drug Resistance in Multiple Myeloma Cell Lines." Cancers 15, no. 8 (2023): 2199. http://dx.doi.org/10.3390/cancers15082199.

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Proteasome inhibitors (PIs) are extensively used for the therapy of multiple myeloma. However, patients continuously relapse or are intrinsically resistant to this class of drugs. In addition, adverse toxic effects such as peripheral neuropathy and cardiotoxicity could arise. Here, to identify compounds that can increase the efficacy of PIs, we performed a functional screening using a library of small-molecule inhibitors covering key signaling pathways. Among the best synthetic lethal interactions, the euchromatic histone-lysine N-methyltransferase 2 (EHMT2) inhibitor UNC0642 displayed a coope

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15

Bagal, Bhausaheb, Anant Gokarn, Avinash Bonda, et al. "Bortezomib in Combination with Cyclophosphamide and G-CSF for Hematopoietic Stem Cell Mobilization in Patients with Multiple Myeloma." Blood 132, Supplement 1 (2018): 2067. http://dx.doi.org/10.1182/blood-2018-99-116886.

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Abstract Background: Proteasome inhibitors (PI) have become integral part of front-line treatment of multiple myeloma. Murine model experiments have shown mobilization of hematopoietic stem cells from bone marrow to peripheral blood after PI administration via down regulation of very late antigen 4 (VLA-4) which mediate adherence of hematopoietic stem cells to the bone marrow microenvironment via interaction with vascular cell adhesion molecule (VCAM-1). Human studies with bortezomib in combination with G-CSF for mobilization have yielded encouraging results with no additional toxicity and no

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Voorhees, Peter M., Cristina Gasparetto, Keren Osman, et al. "Results of a Phase I Study of Vorinostat In Combination with Pegylated Liposomal Doxorubicin and Bortezomib In Patients with Relapsed/Refractory Multiple Myeloma." Blood 116, no. 21 (2010): 1955. http://dx.doi.org/10.1182/blood.v116.21.1955.1955.

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Abstract Abstract 1955 Introduction: The histone deacetylase inhibitor vorinostat has additive to synergistic activity in combination with anthracyclines and proteasome inhibitors in preclinical models of multiple myeloma (MM). We therefore sought to evaluate the safety of vorinostat in combination with pegylated liposomal doxorubicin (PLD) and bortezomib in patients with relapsed and/or refractory MM. Patients and Methods: Treatment consisted of PLD 30mg/m2 on D4, bortezomib 1.3mg/m2 on D1,4,8,11 and escalating doses of vorinostat from either D4-11 or D1-14 of a 3-week cycle. Dose escalation

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Sanchez, Larysa, Xavier Leleu, Jennifer Beaumont, et al. "Peripheral Neuropathy Symptoms, Pain and Functioning in Relapsed or Refractory Multiple Myeloma Patients Treated with Selinexor, Bortezomib, and Dexamethasone." Blood 136, Supplement 1 (2020): 39–41. http://dx.doi.org/10.1182/blood-2020-141319.

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Introduction: The BOSTON study is a Phase 3 trial comparing the novel triplet regimen of once weekly oral selinexor with once weekly bortezomib and dexamethasone (SVd) versus standard twice weekly Vd in patients with multiple myeloma (MM) after 1-3 prior therapies. The SVd regimen conferred a 47% increase in median progression-free survival (PFS) and time to next therapy (TTNT), higher overall response rates (ORR) and deeper responses compared to Vd. Furthermore, this is the first trial of a bortezomib-based triplet therapy (i.e., SVd) that showed lower rates of overall and Grade ≥2 peripheral

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Ahn, Won-Gyun, Yeejin Jeon, Yeong-In Yang, et al. "Abstract 416: A novel non-covalent and rapidly reversible proteasome inhibitor for multiple myeloma and various solid cancers." Cancer Research 82, no. 12_Supplement (2022): 416. http://dx.doi.org/10.1158/1538-7445.am2022-416.

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Abstract The existing proteasome inhibitors, such as bortezomib and ixazomib, are effective in multiple myeloma, but have little activity against solid tumors. These are covalent boronic acid-based compounds and are associated with undesired side effects, mainly hematologic toxicity and peripheral neuropathy. A variety of improved covalent proteasome inhibitors have been developed, but lack of oral availability and low distribution in tumors make them ineffective in solid tumors. In addition, they still have a narrow therapeutic window due to unexpected adverse effects such as cardiac and pulm

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Flint, Oliver P., Jae Kwagh, Faye Wang, et al. "Tanespimycin Prevents Bortezomib Toxicity and Preserves Neuronal Morphology in Primary Rat Dorsal Root Ganglion Cultures." Blood 114, no. 22 (2009): 2847. http://dx.doi.org/10.1182/blood.v114.22.2847.2847.

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Abstract Abstract 2847 Poster Board II-823 INTRODUCTION: Tanespimycin, an inhibitor of Hsp90, is in phase 3 clinical trials in combination with bortezomib in patients with relapsed/refractory multiple myeloma (MM). The combination of tanespimycin and bortezomib produces synergistic antitumor activity and enhanced proteasome inhibition in primary MM cells (Mitsiades, Blood, 2006). In a phase 1/2 study in 72 patients with relapsed/refractory myeloma, tanespimycin + bortezomib produced durable responses in patients including bortezomib-refractory patients. Bortezomib-induced peripheral neuropathy

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Raje, Noopur, Edward Anthony Faber, Paul G. Richardson, et al. "Phase 1 Study of Tabalumab, a Human Anti-BAFF Antibody and Bortezomib in Patients with Previously-Treated Multiple Myeloma." Blood 120, no. 21 (2012): 447. http://dx.doi.org/10.1182/blood.v120.21.447.447.

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Abstract Abstract 447 Background: Tabalumab, a human mAb that neutralizes membrane-bound and soluble B cell activating factor (BAFF), has demonstrated both anti-myeloma activity and osteoclastogenesis inhibition in xenograft models of multiple myeloma (MM). We initially conducted a Phase 1 study with the combination of tabalumab and bortezomib in previously-treated MM patients who were not refractory to bortezomib. The results from the dose escalation (Part A) have been previously reported, where a tabalumab dose of 100 mg was selected based on several factors, most notably the stabilization o

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Jakubowiak, Andrzej J., Don M. Benson, William Bensinger, et al. "Elotuzumab In Combination with Bortezomib In Patients with Relapsed/Refractory Multiple Myeloma: Updated Results of a Phase 1 Study." Blood 116, no. 21 (2010): 3023. http://dx.doi.org/10.1182/blood.v116.21.3023.3023.

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Abstract Abstract 3023 Background: Elotuzumab is a humanized monoclonal IgG1 antibody directed against a cell surface glycoprotein, CS1, which is highly and uniformly expressed in multiple myeloma (MM). Elotuzumab induces dose-dependent antibody-dependent cellular cytotoxicity (ADCC) against MM cell lines. In vitro pretreatment with bortezomib enhanced elotuzumab-mediated autologous ADCC, and in a murine xenograft model of MM the combination of elotuzumab and bortezomib exhibited synergistic antimyeloma activity. We present updated results of a phase 1 study that evaluated the maximum tolerate

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Ghobrial, Irene, Abdel Kareem A. Azab, Jacob P. Laubach, et al. "Phase I Trial of Plerixafor and Bortezomib as a Chemosensitization Strategy In Relapsed or Relapsed/Refractory Multiple Myeloma." Blood 116, no. 21 (2010): 1943. http://dx.doi.org/10.1182/blood.v116.21.1943.1943.

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Abstract Abstract 1943 Introduction: Plerixafor (Mozobil®), a potent CXCR4 inhibitor, is approved in combination with G-CSF to mobilize hematopoietic stem cells (HSCs) for autologous transplantation in multiple myeloma (MM) and non Hodgkin's lymphoma (NHL). Another area of investigation consists of exploring whether disruption of the CXCR4 pathway by plerixafor could potentiate the effect of chemotherapy in active disease. This study aimed to establish the maximum tolerated dose (MTD) of plerixafor in combination with bortezomib in patients who have active relapse/refractory MM. This was infor

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Rosiñol, Laura, Albert Oriol, Maria Victoria Mateos, et al. "Phase II Pethema Trial of Alternating Bortezomib and Dexamethasone As Induction Regimen Before Autologous Stem-Cell Transplantation in Younger Patients With Multiple Myeloma: Efficacy and Clinical Implications of Tumor Response Kinetics." Journal of Clinical Oncology 25, no. 28 (2007): 4452–58. http://dx.doi.org/10.1200/jco.2007.12.3323.

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PurposeThis is the first study in which bortezomib and dexamethasone were administered on an alternating basis as up-front therapy in multiple myeloma (MM). We investigated the efficacy and kinetics of response to each drug and safety.Patients and MethodsPatients with newly diagnosed MM who were less than 66 years old were treated with bortezomib at 1.3 mg/m2on days 1, 4, 8, and 11 (cycles 1, 3, and 5) and dexamethasone 40 mg orally on days 1 through 4, 9 to 12, and 17 to 20 (cycles 2, 4, and 6), followed by autologous stem-cell transplantation (ASCT). Responses were evaluated by modified Euro

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Rowley, Scott D., David Siegel, Michele L. Donato, et al. "Combination Melphalan and Bortezomib Conditioning with Autologous Hematopoietic Stem Cell Support in Patients with Advanced Multiple Myeloma. A Phase I/II Study." Blood 114, no. 22 (2009): 1214. http://dx.doi.org/10.1182/blood.v114.22.1214.1214.

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Abstract Abstract 1214 Poster Board I-236 Bortezomib is an active agent in the treatment of multiple myeloma (MM) and shows additive or synergistic effects when combined with various chemotherapeutics in pre-clinical and clinical models. We are conducting a phase I/II clinical study of bortezomib with dose-intense melphalan with autologous peripheral blood stem cell transplantation (PBSCT) in patients (pts) with disease progression or less than partial response after a prior PBSCT (tandem transplant). Primary exclusion criteria are active infection at time of PBSCT, cardiac amyloid deposition,

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Weber, Donna M., Sundar Jagannath, Amitabha Mazumder, et al. "Phase I Trial of Oral Vorinostat (Suberoylanilide Hydroxamic Acid, SAHA) in Combination with Bortezomib in Patients with Advanced Multiple Myeloma." Blood 110, no. 11 (2007): 1172. http://dx.doi.org/10.1182/blood.v110.11.1172.1172.

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Abstract Background: Vorinostat is a histone deacetylase inhibitor that has demonstrated antiproliferative and proapoptotic activity alone and in combination with the proteasome inhibitor bortezomib in preclinical multiple myeloma (MM) models. In a Phase I study, vorinostat also demonstrated modest single agent activity in patients (pts) with relapsed or refractory MM. Patients and Methods: We conducted a Phase I trial of oral vorinostat (200 mg bid or 400 mg daily × 14 days (d1–14) in combination with bortezomib 0.7 or 0.9 mg/m2 i.v. on d 4, 8, 11 and 15 or 0.9, 1.1, or 1.3 mg/m2 i.v. on d 1,

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Bahlis, Nizar J., Rami Kotb, Michael Sebag, et al. "Selinexor in Combination with Bortezomib and Dexamethasone (SdB) Demonstrates Significant Activity in Patients with Refractory Multiple Myeloma (MM) Including Proteasome-Inhibitor Refractory Patients: Results of the Phase I Stomp Trial." Blood 128, no. 22 (2016): 977. http://dx.doi.org/10.1182/blood.v128.22.977.977.

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Abstract Introduction - Selinexor is a first-in-class Selective Inhibitor of Nuclear Export (SINE) compound that binds and inactivates Exportin 1 (XPO1). Selinexor with low dose dexamethasone (dex) has demonstrated potent anti-cancer activity in patients with heavily pretreated MM. While the development of proteasome inhibitors (PIs) has transformed the treatment of MM, acquired resistance to PIs limit their efficacy. Preclinical studies have shown that selinexor, when combined with bortezomib, can restore sensitivity of bortezomib-resistant MM to this drug, inducing tumor growth inhibition an

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Martin, Thomas G., Sumeet Panjabi, Jiandong Kerr, Michael G. Martin, and Mark S. Walker. "Association Of Treatment Induced Peripheral Neuropathy (TIPN) With Treatment Patterns and Outcomes In Patients (pts) With Newly Diagnosed Multiple Myeloma (NDMM)." Blood 122, no. 21 (2013): 1750. http://dx.doi.org/10.1182/blood.v122.21.1750.1750.

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Abstract Background Peripheral neuropathy (PN) is associated with multiple myeloma (MM) and often exacerbated by anti-MM treatments. TIPN poses significant morbidity and may result in therapy modifications. The impact of TIPN on treatment patterns and outcomes is not well studied in “real world” settings. We examined the association between TIPN in NDMM with treatment changes and efficacy outcomes in community oncology practices. Methods This was a retrospective review of clinical practice data from 12 US practices. Included pts had NDMM between 1/1/2008 and 7/1/2010, received anti-MM therapy

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Kohler, Siegfried, Stefanie Märschenz, Ulrike Grittner, Tobias Alexander, Falk Hiepe, and Andreas Meisel. "Bortezomib in antibody-mediated autoimmune diseases (TAVAB): study protocol for a unicentric, non-randomised, non-placebo controlled trial." BMJ Open 9, no. 1 (2019): e024523. http://dx.doi.org/10.1136/bmjopen-2018-024523.

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IntroductionThe clinical characteristics of autoantibody-mediated autoimmune diseases are diverse. Yet, medical treatment and the associated complications are similar, that is, the occurrence of long-term side effects and the problem that a significant proportion of patients are non-responders. Therefore, new therapeutic options are needed. Bortezomib, a proteasome inhibitor, is effective in the treatment of multiple myeloma and data from experimental models and case reports suggest an effect in the treatment of autoantibody-mediated autoimmunity. In our study, we will determine the effect of

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Rosiñol, L., A. Oriol, M. Mateos, et al. "Final results of a phase II PETHEMA trial of alternating bortezomib and dexamethasone as induction regimen prior autologous stem cell transplantation (ASCT) in younger patients with multiple myeloma (MM): Efficacy and clinical implications of tumor response." Journal of Clinical Oncology 25, no. 18_suppl (2007): 8024. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.8024.

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8024 Background: Dexamethasone-based combinations are the standard induction regimens for younger patients with MM prior ASCT. This is the first study in which bortezomib and dexamethasone were administered on an alternating basis. Aims: efficacy and kinetics of response. Methods: patients with newly diagnosed MM under the age of 66 years were treated with bortezomib at 1.3 mg/m2 on days 1, 4, 8 and 11 (cycles 1, 3, 5) and dexamethasone 40 mg p.o. on days 1–4, 9–12 and 17–20 (cycles 2, 4 and 6), followed by ASCT with melphalan-200. Responses were evaluated by the EBMT criteria but a VGPR was i

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Voorhees, Peter M., Cristina Gasparetto, Kristy L. Richards, et al. "Vorinostat in Combination with Pegylated Liposomal Doxorubicin and Bortezomib for Patients with Relapsed/Refractory Multiple Myeloma: Results of a Phase I Study." Blood 114, no. 22 (2009): 306. http://dx.doi.org/10.1182/blood.v114.22.306.306.

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Abstract Abstract 306 Introduction: Histone deacetylase inhibitors potentiate the efficacy of anthracyclines and proteasome inhibitors in preclinical models of multiple myeloma (MM). We therefore conducted a phase I clinical trial to evaluate the safety of the histone deacetylase inhibitor, vorinostat, in combination with pegylated liposomal doxorubicin (PLD) and bortezomib for patients with relapsed/refractory MM. Patients and Methods: Patients received bortezomib at 1.3mg/m2 on days 1, 4, 8, and 11; PLD at 30mg/m2 on day 4, and escalating doses of vorinostat (200 to 400mg once daily) on days

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Ghobrial, Irene M., Ranjit Banwait, Abdel Kareem Azab, et al. "Phase I Trial of Plerixafor and Bortezomib As a Chemosensitization Strategy in Relapsed or Relapsed/Refractory Multiple Myeloma." Blood 118, no. 21 (2011): 1874. http://dx.doi.org/10.1182/blood.v118.21.1874.1874.

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Abstract Abstract 1874 INTRODUCTION: This study aimed to determine the safety and activity of plerixafor (CXCR4 inhibitor) in combination with bortezomib as a chemosensitization strategy in multiple myeloma (MM). This was based on our preclinical studies showing that plerixafor (Mozobil, Genzyme Corporation, MA) induces de-adhesion of MM cells and sensitization to bortezomib in preclinical animal models. METHODS: Eligibility criteria included: 1) patients with relapsed or relapsed/refractory MM with 1–5 prior lines of therapy including bortezomib (unless patients were refractory to bortezomib)

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Ghobrial, Irene M., Kenneth Shain, Courtney Hanlon, et al. "Phase I/II Trial of Plerixafor and Bortezomib As a Chemosensitization Strategy In Relapsed Or Relapsed/Refractory Multiple Myeloma." Blood 122, no. 21 (2013): 1947. http://dx.doi.org/10.1182/blood.v122.21.1947.1947.

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Abstract Introduction This study aimed to determine the safety and activity of plerixafor (CXCR4 inhibitor) in combination with bortezomib as a chemosensitization strategy in multiple myeloma (MM). The phase I portion of this study was to determine the maximum tolerated dose (MTD). The phase II portion was designed to assess the toxicity profile and the proportion of overall confirmed response (CR + PR). This was based on preclinical studies demonstrating that plerixafor (Mozobil, Sanofi Corporation, MA) induces de-adhesion of MM cells and sensitization to bortezomib in preclinical animal mode

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Ghobrial, Irene M., Jacob P. Laubach, Kenneth H. Shain, et al. "Phase I/II Trial of Plerixafor and Bortezomib As a Chemosensitization Strategy in Relapsed or Relapsed/Refractory Multiple Myeloma." Blood 124, no. 21 (2014): 5777. http://dx.doi.org/10.1182/blood.v124.21.5777.5777.

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Abstract INTRODUCTION: This study aimed to determine the safety and activity of plerixafor (CXCR4 inhibitor) in combination with bortezomib as a chemosensitization strategy in multiple myeloma (MM). The phase I portion of this study was to determine the maximum tolerated dose (MTD). The phase II portion was designed to assess the toxicity profile and the proportion of overall confirmed response (CR + PR). This was based on preclinical studies demonstrating that plerixafor (Mozobil, Sanofi Corporation, MA) induces de-adhesion of MM cells and sensitization to bortezomib in preclinical animal mod

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Ghobrial, Irene M., Nikhil C. Munshi, Brianna N. Harris, et al. "A Phase I Safety Study of Enzastaurin Plus Bortezomib in the Treatment of Relapsed or Refractory Multiple Myeloma." Blood 114, no. 22 (2009): 1870. http://dx.doi.org/10.1182/blood.v114.22.1870.1870.

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Abstract Abstract 1870 Poster Board I-895 Background: Enzastaurin is an oral serine/threonine kinase inhibitor that targets the PKC and PI3K/AKT pathways. Enzastaurin has demonstrated activity in preclinical models of multiple myeloma (MM), and clinical studies suggest activity and a favorable safety profile in a variety of hematological cancers. Enzastaurin has also demonstrated in-vitro synergy with bortezomib. Objectives: This phase I, open-label, multicenter, dose-escalation study was initiated to identify the recommended doses of enzastaurin and bortezomib in combination for phase II stud

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Jakubowiak, Andrzej J., William Bensinger, David Siegel, et al. "Phase 1/2 Study of Elotuzumab in Combination with Bortezomib in Patients with Multiple Myeloma with One to Three Prior Therapies: Interim Results." Blood 114, no. 22 (2009): 3876. http://dx.doi.org/10.1182/blood.v114.22.3876.3876.

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Abstract Abstract 3876 Poster Board III-812 Background Elotuzumab is a humanized monoclonal IgG1 antibody directed against CS1, a cell surface glycoprotein, which is highly and uniformly expressed in multiple myeloma (MM). In mouse xenograft models of MM, elotuzumab demonstrated significantly enhanced anti-tumor activity when combined with bortezomib compared to bortezomib alone (Van Rhee et al., Mol. Cancer Ther., in press, 2009). This phase 1/2 trial will determine the maximum tolerated dose (MTD), overall safety, pharmacokinetics (PK) and clinical response of elotuzumab in combination with

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White, Darrell, Brea Lipe, Mercedes Gironella Mesa, et al. "Iberdomide, bortezomib, and dexamethasone (IberVd) in transplant-ineligible (TNE) newly diagnosed multiple myeloma (NDMM): Updated results from the CC-220-MM-001 trial." Journal of Clinical Oncology 43, no. 16_suppl (2025): 7532. https://doi.org/10.1200/jco.2025.43.16_suppl.7532.

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7532 Background: Lenalidomide (LEN), bortezomib (BORT), and dexamethasone (DEX) are recommended for NDMM. Iberdomide (IBER), an oral CELMoD agent, has stronger tumoricidal and immune-stimulatory effects than LEN and shows synergy with DEX and BORT in preclinical models. IberVd has shown meaningful efficacy and safety in patients (pts) with TNE NDMM in the ongoing phase 1/2 CC-220-MM-001 trial (NCT02773030). Here we report updated results with longer follow-up from the IberVd dose-expansion cohort. Methods: Eligible pts had untreated NDMM and were TNE or deferred. Oral IBER was given on days (D

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Richardson, P. G., A. Chanan-Khan, S. Lonial, et al. "Tanespimycin plus bortezomib in patients with relapsed and refractory multiple myeloma: Final results of a phase I/II study." Journal of Clinical Oncology 27, no. 15_suppl (2009): 8503. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.8503.

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8503 Background: Tanespimycin (Tan) disrupts HSP90, a key molecular chaperone for signal transduction proteins critical to myeloma (MM) growth, survival and drug resistance. Preclinical data show anti-tumor synergy between Tan and bortezomib (Bz) and suggest Tan may be neuroprotective, including reversibility of Bz-induced peripheral neuropathy (PN). A phase I study of single agent Tan in advanced MM showed favorable tolerability and modest activity. Methods: 72 patients (pts) with relapsed/refractory MM received 0.7 - 1.3 mg/m2 Bz as IVB followed by 1-hr infusion of 100 -340 mg/m2 Tan on days

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Das, Deepika Sharma, Durgadevi Ravillah, Arghya Ray, et al. "Synergistic Anti-Myeloma Activity of a Proteasome Inhibitor Marizomib and IMiD® Immunomodulatory Drug Pomalidomide." Blood 124, no. 21 (2014): 2099. http://dx.doi.org/10.1182/blood.v124.21.2099.2099.

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Abstract Background and Rationale: Proteasome inhibitor bortezomib is an effective therapy for the treatment of relapsed and refractory multiple myeloma (RRMM); however, prolonged treatment can be associated with toxicity, peripheral neuropathy and drug resistance. Our earlier studies showed that a novel proteasome inhibitor marizomib is distinct from bortezomib in its chemical structure, mechanisms of action, and effects on proteasomal activities (Chauhan et al., Cancer Cell 2005, 8:407-419). We also showed that marizomib triggers synergistic anti-MM activity in combination with lenalidomide

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Raje, Noopur, Dan T. Vogl, Parameswaran N. Hari, et al. "ACY-1215, a Selective Histone Deacetylase (HDAC) 6 Inhibitor: Interim Results Of Combination Therapy With Bortezomib In Patients With Multiple Myeloma (MM)." Blood 122, no. 21 (2013): 759. http://dx.doi.org/10.1182/blood.v122.21.759.759.

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Abstract Background Although non-selective HDAC inhibitors are active in MM, combination therapy is limited by significant adverse effects (AEs) including severe fatigue, gastrointestinal toxicity, and myelosuppression. ACY-1215 is the first-in-class selective oral HDAC6 inhibitor that inhibits the aggresome/autophagy pathway, an alternate pathway to proteasome clearance of misfolded proteins. ACY-1215 has demonstrated potent synergy with bortezomib preclinically in cell and animal models of MM (Santo, Blood, 119(1):2527). Methods ACY-100 is a three part single arm, open label study with cohor

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Rozic, Gabriela, Paukov Lena, Jana Jakubikova, et al. "STK405759 As a Novel Tubulin Active Agent for Multiple Myeloma Therapy." Blood 126, no. 23 (2015): 5348. http://dx.doi.org/10.1182/blood.v126.23.5348.5348.

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Abstract Background: Despite advances in treatment, multiple myeloma (MM) remains incurable due to development of drug resistance in the bone marrow microenvironment. Microtubules (MTs) are dynamic protein biopolymers formed through polymerization of heterodimers of α- and β-tubulins. Disruption of microtubules induces cell cycle arrest in G2-M phase and formation of abnormal mitotic spindles. MTs are also involved in many processes in interphase cells, including intracellular trafficking, cell motility and angiogenesis. The important functions of MT in the cells make them an attractive target

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Moreau, Philippe, Thierry Facon, Cyrille Touzeau, et al. "Phase 1b Dose Escalation Study Of Oral Quisinostat, a Histone Deacetylase Inhibitor (HDACi), In Combination With Velcade (Bortezomib) and Dexamethasone For Patients With Relapsed Multiple Myeloma (MM)." Blood 122, no. 21 (2013): 1932. http://dx.doi.org/10.1182/blood.v122.21.1932.1932.

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Abstract Background HDACi inhibits aggresome function by acetylation of the tubulin-dynein complex that transports unfolded proteins via aggresomes to lysosomes for degradation, thereby serving as a mechanism for reversal of resistance to proteasome inhibitors. In vivo data have shown that quisinostat, a new oral pan HDACi, has a synergistic activity with bortezomib in preclinical models of MM. Methods Patients were treated with: quisinostat (Q) at escalated doses from 6 to 8 to 10 to 12 mg on days 1, 3, and 5 weekly, subcutaneous VELCADE (V) at 1.3 mg/m2 on days 1, 4, 8, and 11 of a 3-week cy

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Huang, Xiangao, Kathryn Bailey, Maurizio Di Liberto, et al. "Induction of Sustained Early G1 Arrest by Selective Inhibition of CDK4 and CDK6 Primes Myeloma Cells for Synergistic Killing by Proteasome Inhibitors Carfilzomib and PR-047." Blood 112, no. 11 (2008): 3670. http://dx.doi.org/10.1182/blood.v112.11.3670.3670.

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Abstract Targeting the cell cycle in combination with cytotoxic killing is a rational approach to cancer therapy. Dysregulation of the cyclin-dependent kinases CDK4 and CDK6 precedes uncontrolled proliferation of myeloma cells in vivo, in particular during relapse and drug resistance. This finding reinforces the critical importance of targeting CDK4/6 in myeloma, but success with broad-spectrum CDK inhibitors has been modest. Using the only known selective inhibitor of CDK4/6, PD 0332991, we have developed a novel approach to prime chemoresistant myeloma cells for synergistic killing by divers

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Richardson, Paul G., Akshanth R. Polepally, Monica Motwani, et al. "A Phase 1b, Open-Label Study of Eftozanermin Alfa in Combination with Bortezomib and Dexamethasone in Patients with Relapsed or Refractory Multiple Myeloma." Blood 136, Supplement 1 (2020): 16–17. http://dx.doi.org/10.1182/blood-2020-137037.

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Background Many patients (pts) with multiple myeloma (MM) will relapse after treatment or become refractory to all therapies currently available. For these pts, the prognosis is poor and there is a clear unmet need to identify agents with novel mechanisms of action. The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) pathway has a distinct role in the induction of apoptosis in tumor cells, and activating this pathway could represent an attractive therapeutic approach. Early generation TRAIL receptor agonists had minimal efficacy in pts with MM, which may be due to suboptimal TR

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Bai, Yan, Yuhuan Gao, Lihong Liu, et al. "Clinical Efficacy and Safety Evaluation of Isazomib Based Combination Regimen for Multiple Myeloma First-Line Therapy." Blood 144, Supplement 1 (2024): 7029. https://doi.org/10.1182/blood-2024-205537.

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INTRODUCTION Multiple myeloma (MM) is a hematological malignancy characterized by abnormal clonal proliferation of plasma cells in the bone marrow, resulting in uncontrolled growth and secretion of large amounts of monoclonal immunoglobulin. Currently, Isazomib-based combination regimens are primarily utilized as second and third-line therapies following Bortezomib treatment. Despite demonstrating significant advantages in clinical efficacy and safety, adverse reactions caused by Bortezomib still occur, necessitating further clinical studies. AIM The aim of this study was to assess the clinica

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Di Liberto, Maurizio, Xiangao Huang, Jamieson Bretz, et al. "Induction of Metabolic Impairment In Prolonged Early G1 Arrest Induced by CDK4/CDK6 Inhibition Sensitizes Myeloma Cells for Proteasome Inhibitor Killing During Subsequent S Phase Synchronization." Blood 116, no. 21 (2010): 2989. http://dx.doi.org/10.1182/blood.v116.21.2989.2989.

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Abstract Abstract 2989 Sequential drug combination is a rational approach to maximize tumor killing and minimize side effects in cancer therapy. However, this is rarely achieved because the mechanism of drug action is often incompletely understood and the cell cycle specificity of individual drugs unknown. Dysregulation of cyclin-dependent kinase (CDK)4 and CDK6 is common in human cancer and precedes unrestrained proliferation of tumor cells in multiple myeloma (MM) patients, especially during refractory relapse. This highlights the critical importance of targeting CDK4/CDK6 in MM. We have now

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Nooka, Ajay K., Jonathan L. Kaufman, Madhusmita Behera, et al. "The Improved Efficacy of Bortezomib Containing Induction Regimens (BCIR) Versus Non-Bortezomib Containing Induction Regimens (NBCIR) in Transplant-Eligible Patients with Multiple Myeloma (MM): Meta-Analysis of Phase III Randomized Controlled Trials (RCTs),." Blood 118, no. 21 (2011): 3994. http://dx.doi.org/10.1182/blood.v118.21.3994.3994.

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Abstract Abstract 3994 Introduction: Patients with MM undergoing autologous stem cell transplant (ASCT) achieving complete response (CR) or very good partial response (VGPR) have prolonged progression free survival (PFS) and overall survival (OS) compared to the patients that achieve <VGPR prior to ASCT (Lahuerta JJ et al., 2008; Moreau P et al., 2011). Therefore it is of profound significance to attain the best response with induction therapies to obtain the better long-term outcomes. The response rates have significantly improved since the introduction of bortezomib, a proteasome inhibito

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Kirk, Christopher J., Mark K. Bennett, Tonia J. Buchholz, et al. "Pharmacokinetics, Pharmacodynamics and Anti-Tumor Efficacy of PR-171, a Novel Inhibitor of the 20S Proteasome." Blood 106, no. 11 (2005): 609. http://dx.doi.org/10.1182/blood.v106.11.609.609.

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Abstract Clinical studies using the boronic acid-based proteasome inhibitor bortezomib (VelcadeTM) have validated the proteasome as a therapeutic intervention point for the treatment of multiple myeloma and non-Hodgkin’s Lymphoma. Despite encouraging clinical response rates with this drug, significant toxicities, including neutropenia, thrombocytopenia and peripheral neuropathy have restricted the intensity of bortezomib dosing. PR-171 is a novel peptide epoxyketone inhibitor that selectively and irreversibly inhibits the chymotryptic subunit of the 20S proteasome. We have characterized the ph

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Alsina, Melissa, Suzanne Trudel, Marcy Vallone, Christopher Molineaux, Lori Kunkel, and Andre Goy. "Phase 1 Single Agent Antitumor Activity of Twice Weekly Consecutive Day Dosing of the Proteasome Inhibitor Carfilzomib (PR-171) in Hematologic Malignancies." Blood 110, no. 11 (2007): 411. http://dx.doi.org/10.1182/blood.v110.11.411.411.

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Abstract Carfilzomib (CFZ) is a structurally- and mechanistically-novel proteasome inhibitor of peptide epoxyketone class that exhibits a high level of selectivity for the unique N-terminal threonine active sites within the proteasome. CFZ is similar to bortezomib (BTZ,Velcade®), in that it is a potent inhibitor of the proteasome chymotrypsin-like activity, but unlike BTZ, CFZ has shown minimal cross-reactivity with the other catalytic sites within the proteasome or across other protease classes. Preclinical human tumor xenograft models indicated that consecutive day (D1, D2) dosing resulting

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Di Liberto, Maurizio, Xiangao Huang, Rediet Zewdu, et al. "Selective inhibition of CDK4/CDK6 sensitizes bone marrow myeloma cells for killing by proteasome inhibitors carfilzomib and PR-047 through cell cycle-dependent expression of pro-apoptotic Noxa and Bim." Blood 114, no. 22 (2009): 2854. http://dx.doi.org/10.1182/blood.v114.22.2854.2854.

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Abstract Abstract 2854 Poster Board II-830 Targeting the cell cycle in combination with cytotoxic killing is a rational approach to cancer therapy. Progression in multiple myeloma (MM) stems from both loss of apoptotic control in the bone marrow (BM) microenvironment and dysregulation of the cyclindependent kinases (CDK)4 and CDK6, which precedes uncontrolled proliferation of myeloma cells in vivo in particular during relapse. This reinforces the critical importance of targeting CDK4/CDK6 in MM. Through selective and reversible inhibition of CDK4/CDK6 with PD 0332991, the only known CDK4/6-spe

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Nadiminti, Kalyan, Christopher Strouse, Praveen Vikas, et al. "Early Intensive Therapy in Multiple Myeloma Using Tandem Transplantation with Novel Conditioning and Two Years Maintenance: A Single Institution Experience." Blood 132, Supplement 1 (2018): 2152. http://dx.doi.org/10.1182/blood-2018-99-113890.

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Abstract Introduction The role of early intensive treatment of multiple myeloma, including tandem autologous stem cell transplantation( ASCT) with bortezomib, thalidomide, dexamethasone( VDT) and melphalan 200mg/m2 as a preparative regimen, followed by 2 years of combination agent maintenance therapy, is being studied. We sought to analyze a cohort of patients who received early intensive treatment at the University of Iowa between 2012 and 2016. Patients and Methods All consecutive patients who received early( < 12 months since diagnosis) tandem ASCT and have completed at least 2 years of

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