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Journal articles on the topic 'Lenalidomide and pomalidomide'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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1

Lopez-Girona, Antonia, Derek Mendy, Karen Miller, et al. "Direct Binding with Cereblon Mediates the Antiproliferative and Immunomodulatory Action of Lenalidomide and Pomalidomide." Blood 118, no. 21 (2011): 738. http://dx.doi.org/10.1182/blood.v118.21.738.738.

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Abstract Abstract 738 Thalidomide, lenalidomide and pomalidomide are therapeutically active in a number of hematological malignant and premalignant conditions including myelodysplastic syndromes, multiple myeloma, and lymphomas. Clinical efficacy is ascribed to a complement of overlapping activities including direct antitumor effects, immune system activation and inhibition of stromal support of tumor growth. Thalidomide has previously been shown to bind cereblon (CRBN) a protein required for the teratogenic effects of thalidomide in zebrafish and chicken embryos (Ito et al). CRBN forms an ubi

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2

Lacy, Martha Q., and Arleigh R. McCurdy. "Pomalidomide." Blood 122, no. 14 (2013): 2305–9. http://dx.doi.org/10.1182/blood-2013-05-484782.

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Abstract This spotlight review focuses on the second-generation immunomodulatory drug pomalidomide, which was recently approved by the US Food and Drug Administration. This drug was approved for patients with multiple myeloma who have received at least 2 prior therapies, including lenalidomide and bortezomib, and have demonstrated disease progression on or within 60 days of completion of the last therapy. This review focuses on the clinical trial data that led to approval and provides advice for treating physicians who are now prescribing this drug for patients.

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3

Sinha, Shirshendu, Shaji Kumar, Suzanne Hayman, et al. "Response to Salvage Therapies and Outcome of Patients with Multiple Myeloma Relapsing After Pomalidomide Therapy." Blood 116, no. 21 (2010): 1965. http://dx.doi.org/10.1182/blood.v116.21.1965.1965.

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Abstract Abstract 1965 Background: Pomalidomide is an immunomodulatory compound to be used for heavily pre-treated patients with relapse and refractory multiple myeloma and has shown considerable efficacy in recent clinical trials. It is not clear how patients may respond to other therapies, once the disease becomes refractory to pomalidomide. We examined this question among a cohort of patients receiving pomalidomide therapy in phase 2 clinical trials. Methods: Patients enrolled in an ongoing phase 2 clinical trial of pomalidomide (2-4 mg daily) along with dexamethasone (40 mg weekly), in rel

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4

Kastritis, Efstathios, Maria Roussou, Maria Gavriatopoulou, et al. "Impact of last lenalidomide dose, duration, and IMiD-free interval in patients with myeloma treated with pomalidomide/dexamethasone." Blood Advances 3, no. 23 (2019): 4095–103. http://dx.doi.org/10.1182/bloodadvances.2019000539.

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Key Points There was no significant difference in response rates, PFS, or OS among patients that developed resistance to different lenalidomide doses. Longer duration of prior lenalidomide and a longer lenalidomide-free interval are associated with better outcomes with pomalidomide.

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5

Bartlett, J. B., L. Wu, M. Adams, P. Schafer, G. Muller, and D. Stirling. "Lenalidomide and pomalidomide strongly enhance tumor cell killing in vitro during antibody-dependent cellular cytotoxicity (ADCC) mediated by trastuzumab, cetuximab and rituximab." Journal of Clinical Oncology 25, no. 18_suppl (2007): 3023. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.3023.

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3023 Background: Potential mechanisms of action of lenalidomide and pomalidomide (CC-4047) include anti-angiogenic, anti- proliferative and immunomodulatory activities, e.g., enhancement of T cell and NK cell function. Both drugs appear to enhance T cell activation and Th1-type cytokines in cancer patients. Also, both drugs have been shown to enhance rituximab-mediated protection in a mouse lymphoma model. Methods: We have utilized an in vitro ADCC system to assess the ability of these drugs to enhance human NK cell function in response to the approved therapeutic antibodies trastuzumab, cetux

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6

Rekhtina, I. G., and L. P. Mendeleeva. "Efficiency of pomalidomide therapy in patients with multiple myeloma refractory to lenalidomide." Oncohematology 14, no. 1 (2019): 8–13. http://dx.doi.org/10.17650/1818-8346-2019-14-1-8-13.

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Currently, there has been a marked increase in the number of opportunities for relapsed and refractory multiple myeloma treatment due toemergence of new target drugs. These include pomalidomide, a 3rd generation immunomodulator capable of treating double refractory multiple myeloma (to lenalidomide and bortezomib). Efficacy and safety of pomalidomide combined with low doses of dexamethasone have beenestablished in MM-003 and STRATUS trials. The summary presents the data on opportunities to further enhance the efficacy of pomalidomide combined with other antitumor drugs in patients with relapse

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7

Siegel, David S., Gary J. Schiller, Christy Samaras, et al. "Pomalidomide, dexamethasone, and daratumumab in relapsed refractory multiple myeloma after lenalidomide treatment." Leukemia 34, no. 12 (2020): 3286–97. http://dx.doi.org/10.1038/s41375-020-0813-1.

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AbstractPatients with multiple myeloma who have relapsed after or become refractory to lenalidomide in early treatment lines represent a clinically important population in need of effective therapies. The safety and efficacy of pomalidomide, low-dose dexamethasone, and daratumumab was evaluated in lenalidomide-pretreated patients with relapsed or refractory multiple myeloma (RRMM) after one to two prior treatment lines in the phase 2 MM-014 study. Patients received pomalidomide 4 mg daily from days 1–21 and dexamethasone 40 mg weekly (28-day cycles). Daratumumab 16 mg/kg was administered per l

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8

Phan, Vien, Tomoki Ito, Muneo Inaba, et al. "Immunomodulatory drugs suppress Th1-inducing ability of dendritic cells but enhance Th2-mediated allergic responses." Blood Advances 4, no. 15 (2020): 3572–85. http://dx.doi.org/10.1182/bloodadvances.2019001410.

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Abstract Immunomodulatory drugs (IMiDs), lenalidomide and pomalidomide, are widely used treatments for multiple myeloma; however, they occasionally lead to episodes of itchy skin and rashes. Here, we analyzed the effects of IMiDs on human myeloid dendritic cells (mDCs) as major regulators of Th1 or Th2 responses and the role they play in allergy. We found that lenalidomide and pomalidomide used at clinical concentrations did not affect the survival or CD86 and OX40-ligand expression of blood mDCs in response to lipopolysaccharide (LPS) and thymic stromal lymphopoietin (TSLP) stimulation. Both

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9

Leleu, Xavier, Michel Attal, Bertrand Arnulf, et al. "Pomalidomide plus low-dose dexamethasone is active and well tolerated in bortezomib and lenalidomide–refractory multiple myeloma: Intergroupe Francophone du Myélome 2009-02." Blood 121, no. 11 (2013): 1968–75. http://dx.doi.org/10.1182/blood-2012-09-452375.

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Key Points Combination of pomalidomide with dexamethasone is highly active and can salvage end stage myeloma refractory to lenalidomide and bortezomib. Current data suggest pomalidomide 4 mg/day on days 1 to 21 per 28-days cycle with dexmethasone should be studied in future phase 3 trials.

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10

Bolzoni, Marina, Manuela Abeltino, Paola Storti, et al. "The Immunomodulatory Drugs Lenalidomide and Pomalidomide Inhibit Multiple Myeloma-Induced Osteoclast Formation and RANKL/OPG Ratio In Myeloma Microenvironment Targeting the Expression of Adhesion Molecules." Blood 116, no. 21 (2010): 448. http://dx.doi.org/10.1182/blood.v116.21.448.448.

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Abstract Abstract 448 The increase of osteoclast formation and activation occurring into the bone marrow (BM) area of myeloma cells infiltration is the hallmark of multiple myeloma (MM). The increase of the RANKL/OPG ratio in BM stromal cells (BMSCs) and osteoprogenitor cells, induced by MM cells through the cell-to-cell contact, is critically involved in MM-induced osteoclast formation. In addition, MM cells also up-regulate RANKL expression and secretion by activated T in the MM BM microenvironment. Soluble factors such as CCL3/MIP-1α, IL-3 and IL-7 produced by MM cells contribute to the inc

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11

Gemechu, Yohannes, David Millrine, Shigeru Hashimoto, et al. "Humanized cereblon mice revealed two distinct therapeutic pathways of immunomodulatory drugs." Proceedings of the National Academy of Sciences 115, no. 46 (2018): 11802–7. http://dx.doi.org/10.1073/pnas.1814446115.

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Immunomodulatory drugs (IMiDs), including thalidomide derivatives such as lenalidomide and pomalidomide, offer therapeutic benefit in several hematopoietic malignancies and autoimmune/inflammatory diseases. However, it is difficult to study the IMiD mechanism of action in murine disease models because murine cereblon (CRBN), the substrate receptor for IMiD action, is resistant to some of IMiDs therapeutic effects. To overcome this difficulty, we generated humanized cereblon (CRBNI391V) mice thereby providing an animal model to unravel complex mechanisms of action in a murine physiological setu

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12

Mark, Tomer M., Peter A. Forsberg, Adriana C. Rossi, et al. "Phase 2 study of clarithromycin, pomalidomide, and dexamethasone in relapsed or refractory multiple myeloma." Blood Advances 3, no. 4 (2019): 603–11. http://dx.doi.org/10.1182/bloodadvances.2018028027.

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Abstract The addition of clarithromycin enhances the efficacy of lenalidomide plus dexamethasone in treatment-naive multiple myeloma (MM). We conducted a phase 2 trial to evaluate the safety and efficacy of clarithromycin, pomalidomide, and dexamethasone (ClaPd) in relapsed or refractory multiple myeloma (RRMM) with prior lenalidomide exposure. One hundred twenty patients with a median of 5 prior lines of therapy received clarithromycin 500 mg orally twice daily, pomalidomide 4 mg orally on days 1 to 21, and dexamethasone 40 mg orally on days 1, 8, 15, and 22 of a 28-day cycle. The overall res

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13

Zhu, Yuan Xiao, Esteban Braggio, Chang-Xin Shi, et al. "Cereblon expression is required for the antimyeloma activity of lenalidomide and pomalidomide." Blood 118, no. 18 (2011): 4771–79. http://dx.doi.org/10.1182/blood-2011-05-356063.

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Abstract The precise molecular mechanism of action and targets through which thalidomide and related immunomodulatory drugs (IMiDs) exert their antitumor effects remains unclear. We investigated the role of cereblon (CRBN), a primary teratogenic target of thalidomide, in the antimyeloma activity of IMiDs. CRBN depletion is initially cytotoxic to human myeloma cells, but surviving cells with stable CRBN depletion become highly resistant to both lenalidomide and pomalidomide, but not to the unrelated drugs bortezomib, dexamethasone, and melphalan. Acquired deletion of CRBN was found to be the pr

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14

Larocca, Alessandra, Vittorio Montefusco, Sara Bringhen, et al. "Pomalidomide, cyclophosphamide, and prednisone for relapsed/refractory multiple myeloma: a multicenter phase 1/2 open-label study." Blood 122, no. 16 (2013): 2799–806. http://dx.doi.org/10.1182/blood-2013-03-488676.

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15

Mark, Tomer M., Melissa Rodriguez, Manan Shah, et al. "ClaPD (Clarithromycin/[Biaxin®], Pomalidomide, Dexamethasone) Therapy in Relapsed or Refractory Multiple Myeloma." Blood 118, no. 21 (2011): 635. http://dx.doi.org/10.1182/blood.v118.21.635.635.

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Abstract Abstract 635 Background: The addition of clarithromycin has been reported to enhance anti-myeloma activity of lenalidomide+dexamethasone in the upfront treatment of multiple myeloma (MM). Pomalidomide is a distinct IMiD® immunomodulatory agent with a significant response rate in subjects with relapsed or refractory MM (RRMM), including those with prior lenalidomide treatment. We hypothesized that clarithromycin may similarly enhance the activity of pomalidomide + dexamethasone in patients with RRMM after prior lenalidomide therapy. We now report the initial results from a phase 2 tria

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16

Pegourie, Brigitte, Marie Odile Petillon, Lionel Karlin, et al. "Long-Term Exposure to Pomalidomide-Dexamethasone in Pts with Refractory Myeloma." Blood 124, no. 21 (2014): 3466. http://dx.doi.org/10.1182/blood.v124.21.3466.3466.

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Abstract Background. The IFM2009-02 study was launched in 2009, and randomized 84 patients (pts) with pomalidomide (oral 4 mg daily) and dexamethasone (oral 40 mg weekly) given either 21 days out of 28 or continuous. Whilst the overall median PFS was 4.6 months - this end stage very advanced RRMM population, we observed that 40% of the patients had a prolonged PFS and subsequently OS in the trial. We sought to analyze the characteristics of 58 pts that had more than 3 months of pomalidomide to study the effect of long exposure to Pomalidomide. Method. IFM 2009-02 was a multicentre phase 2 stud

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17

Cho, Hearn J., Craig Cole, Thomas G. Martin, et al. "A phase Ib study of atezolizumab (atezo) alone or in combination with lenalidomide or pomalidomide and/or daratumumab in patients (pts) with multiple myeloma (MM)." Journal of Clinical Oncology 35, no. 15_suppl (2017): TPS8053. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.tps8053.

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TPS8053 Background: The advent of proteasome inhibitors and immunomodulatory drugs (IMiDs) have significantly improved outcomes in MM, and the first monoclonal antibodies for MM have been recently approved (daratumumab, elotuzumab). Despite novel therapies and improved disease management, MM is still considered incurable and most pts relapse, confirming the need for additional treatment options. MM cells express PD-L1, with higher levels observed after relapse and with advanced disease. Additionally, PD-L1–expressing immune cells in the microenvironment promote MM cell survival and potential i

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18

Palumbo, Antonio, Alessandra Larocca, Angelo Michele Carella, et al. "A Phase I/II Study of Pomalidomide-Cyclophosphamide-Prednisone (PCP) in Patients with Multiple Myeloma Relapsed/Refractory to Lenalidomide." Blood 118, no. 21 (2011): 632. http://dx.doi.org/10.1182/blood.v118.21.632.632.

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Abstract Abstract 632 Background: Patients with multiple myeloma (MM) relapsed/refractory after immunomodulatory drugs and bortezomib have limited treatment options. Recently, the combination pomalidomide-dexamethasone has led to at least partial response (PR) of 25–42% in relapsed/refractory MM and 32% in patients refractory to lenalidomide. Aims: In this study we evaluate the safety and efficacy of the combination pomalidomide-cyclophosphamide-prednisone (PCP) in patients with MM who received 1–3 lines of treatment and were relapsed/refractory to lenalidomide therapy. Methods: Between August

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19

Berenson, James R., James D. Hilger, Leonard M. Klein, et al. "A Phase 1/2 Study of Pomalidomide, Dexamethasone and Pegylated Liposomal Doxorubicin for Patients with Relapsed/Refractory Multiple Myeloma." Blood 120, no. 21 (2012): 2979. http://dx.doi.org/10.1182/blood.v120.21.2979.2979.

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Abstract Abstract 2979 Background: Thalidomide and its immunomodulatory (IMiD) derivatives such as lenalidomide have shown great promise as a treatment option for multiple myeloma (MM) patients. Pomalidomide is a newer IMiD with high in vitro potency that has shown promise as an effective treatment option for relapsed/refractory (R/R) MM patients. Recent data has shown pomalidomide to be effective in combination with dexamethasone, even for patients who are refractory to bortezomib and lenalidomide. It has been demonstrated that the addition of pegylated liposomal doxorubicin (PLD) to lenalido

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Bondili, Suresh Kumar, Bhausaheb Bagal, Abhinav Zawar, et al. "Real-World Outcomes With Generic Pomalidomide in Relapsed Refractory Multiple Myeloma—Experience From a Tertiary Care Cancer Center." JCO Global Oncology, no. 7 (March 2021): 361–67. http://dx.doi.org/10.1200/go.20.00228.

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PURPOSE The prognosis of relapsed and refractory multiple myeloma (RRMM) that is refractory to bortezomib and lenalidomide is very poor wherein the median survival is between 3 and 9 months. We did this retrospective analysis to study the pattern of utilization, tolerance, and outcomes with pomalidomide in these patients having RRMM. MATERIALS AND METHODS Retrospective analysis of all the patients who were treated with generic pomalidomide at Tata Memorial Centre, Mumbai, during the period of May 2017 to March 2019 was done. Patients with secretory disease and who had completed at least one cy

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Tagoug, Ines, Adriana Plesa, Julie Vendrell, and Charles Dumontet. "Effect of Imids on Gene Expression Profiles of Fresh Human Myeloma Cells." Blood 116, no. 21 (2010): 5013. http://dx.doi.org/10.1182/blood.v116.21.5013.5013.

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Abstract Abstract 5013 Immunomodulatory drugs represent a major therapeutic advance in the treatment of patients with multiple myeloma. While these agents appear to exert various effects on the microenvironment, including effect on immune cells and angiogenesis, a direct effect on the tumor cells themselves is also likely. To describe and compare the effect of the three clinically available agents (thalidomide, lenalidomide, pomalidomide) we analyzed the gene expression profiles of fresh human myeloma cells exposed to thalidomide, lenalidomide or pomalidomide, using high density DNA arrays. Fr

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Mo, Clifton C., and Paul G. Richardson. "Pomalidomide in lenalidomide‐refractory multiple myeloma: Far from futile." British Journal of Haematology 188, no. 4 (2019): 483–85. http://dx.doi.org/10.1111/bjh.16214.

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23

Milrod, Charles J., Frances Blevins, David Hughes, et al. "Incidence of skin hyperpigmentation in Black patients receiving treatment with immunomodulatory drugs." Blood 137, no. 21 (2021): 2987–89. http://dx.doi.org/10.1182/blood.2021010853.

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In a retrospective single-center review of patients with myeloma treated with the immunomodulatory drug thalidomide, lenalidomide, or pomalidomide, the authors report that marked hyperpigmentation occurred in 40% of Black patients, compared with 3.5% of White patients. Since only 2% of the participants in the original pivotal trial of lenalidomide were Black, this unexpectedly high rate was not previously recognized.

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Lacy, Martha Q., Jacob B. Allred, Morie A. Gertz, et al. "Pomalidomide plus low-dose dexamethasone in myeloma refractory to both bortezomib and lenalidomide: comparison of 2 dosing strategies in dual-refractory disease." Blood 118, no. 11 (2011): 2970–75. http://dx.doi.org/10.1182/blood-2011-04-348896.

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Abstract Pomalidomide at doses of 2 or 4 mg/d has demonstrated excellent activity in patients with multiple myeloma (MM). We opened 2 sequential phase 2 trials using the pomalidomide with weekly dexamethasone (Pom/dex) regimen at differing doses to study the efficacy of this regimen in patients who have failed both lenalidomide and bortezomib. Pomalidomide was given orally 2 or 4 mg daily with dexamethasone 40 mg weekly. Thirty-five patients were enrolled in each cohort. Confirmed responses in the 2-mg cohort consisted of very good partial response (VGPR) in 5 (14%), partial response (PR) in 4

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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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Zhu, Yuan Xiao, Esteban Braggio, Chang-Xin Shi, et al. "Cereblon Expression Is Required for the Anti-Myeloma Activity of Lenalidomide and Pomalidomide." Blood 118, no. 21 (2011): 127. http://dx.doi.org/10.1182/blood.v118.21.127.127.

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Abstract Abstract 127 The precise molecular mechanism of action and targets through which thalidomide and related immunomodulatory drugs (IMiDs) exert their anti-tumor effects remains unclear. A landmark paper has recently identified cereblon (CRBN) as a primary target of thalidomide teratogenicity. We hypothesized that this protein would also be required for myeloma (MM) cytotoxicity. To examine this issue we first tested 12 MM cell lines: 4 of which (OCIMY5, OPM1, SKMM2 and KMS12 PE) were very resistant to treatment with both lenalidomide and pomalidomide. Of these, OCIMY5 and OPM1 showed CR

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Ma, Zi, Rui bo Zhang, Li He, et al. "Induction of CRBN(Cereblon) mRNA Expression by Baicalein." Blood 120, no. 21 (2012): 5025. http://dx.doi.org/10.1182/blood.v120.21.5025.5025.

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Abstract Abstract 5025 The CRBN gene that encodes the cereblon protein is found on the short arm at position p26. 3 of human chromosome 3. Cereblon is a primary target of thalidomide teratogenicity and required for the anti-myeloma activity of lenalidomide and pomalidomide. CRBN depletion myeloma cells become highly resistant to both lenalidomide and pomalidomide. Baicalein, a component of Scutellaria radix from HLJDT, not only suppressed proliferation and induced apoptosis of myeloma cells by down-regulating interleukin −6(IL-6) and XIAP gene expression, but also inhibited the signaling casca

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Richardson, P. G., C. C. Hofmeister, N. S. Raje, et al. "Pomalidomide, bortezomib and low-dose dexamethasone in lenalidomide-refractory and proteasome inhibitor-exposed myeloma." Leukemia 31, no. 12 (2017): 2695–701. http://dx.doi.org/10.1038/leu.2017.173.

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Abstract This phase 1 dose-escalation study evaluated pomalidomide, bortezomib (subcutaneous (SC) or intravenous (IV)) and low-dose dexamethasone (LoDEX) in lenalidomide-refractory and proteasome inhibitor-exposed relapsed or relapsed and refractory multiple myeloma (RRMM). In 21-day cycles, patients received pomalidomide (1–4 mg days 1–14), bortezomib (1–1.3 mg/m2 days 1, 4, 8 and 11 for cycles 1–8; days 1 and 8 for cycle ⩾9) and LoDEX. Primary endpoint was to determine the maximum tolerated dose (MTD). Thirty-four patients enrolled: 12 during escalation, 10 in the MTD IV bortezomib cohort an

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Grosicki, Sebastian, Martyna Bednarczyk, Agnieszka Barchnicka, and Olga Grosicka. "Elotuzumab in the treatment of relapsed and refractory multiple myeloma." Future Oncology 17, no. 13 (2021): 1581–91. http://dx.doi.org/10.2217/fon-2020-1088.

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Multiple myeloma (MM) is still considered an incurable disease. However, drugs with different mechanisms of action that can improve the efficiency of treatment offer hope. Still, there are concerns about an unacceptable increase in toxicity with such regimens. The results of recently published clinical studies of elotuzumab in combination with lenalidomide/dexamethasone or pomalidomide/dexamethasone confirm previous hopes to improve the effect of that treatment. Humanized monoclonal antibodies aimed at SLAMF7 stimulate natural killer cells to fight against MM cells. Elotuzumab used in combinat

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Lopez-Girona, Antonia, Courtney G. Havens, Gang Lu, et al. "CC-92480 Is a Novel Cereblon E3 Ligase Modulator with Enhanced Tumoricidal and Immunomodulatory Activity Against Sensitive and Resistant Multiple Myeloma Cells." Blood 134, Supplement_1 (2019): 1812. http://dx.doi.org/10.1182/blood-2019-124338.

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Lenalidomide- and pomalidomide-based therapies are effective drugs in the treatment of patients with multiple myeloma (MM), however most patients with MM eventually relapse or become resistant. CC-92480, a novel cereblon (CRBN) E3 ligase modulator (CELMoD) with multiple activities including potent immunomodulation and single-agent antiproliferative effects, is being investigated in a phase 1 clinical trial (CC-92480-MM-001; NCT03374085) for patients with relapsed/refractory MM (RRMM). The present study investigates the preclinical data and mechanism of action of CC-92480 in MM models. CELMoD a

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Xu, Yibing, Jianwu Li, Gregory D. Ferguson, et al. "Immunomodulatory drugs reorganize cytoskeleton by modulating Rho GTPases." Blood 114, no. 2 (2009): 338–45. http://dx.doi.org/10.1182/blood-2009-02-200543.

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Abstract IMiDs immunomodulatory drugs, including lenalidomide and pomalidomide represent a novel class of small molecule anticancer and anti-inflammatory drugs with broad biologic activities. However, the molecular mechanism through which these drugs exert their effects is largely undefined. Using pomalidomide and primary human monocytes, we report that pomalidomide rapidly and selectively activated RhoA and Rac1, but not Cdc42 or Ras, in the absence of any costimulation. Consistent with the activation of Rho GTPases, we found that pomalidomide enhanced F-actin formation, stabilized microtubul

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Mark, Tomer M., Angelique Boyer, Adriana C. Rossi, et al. "ClaPD (Clarithromycin, Pomalidomide, Dexamethasone) Therapy in Relapsed or Refractory Multiple Myeloma." Blood 120, no. 21 (2012): 77. http://dx.doi.org/10.1182/blood.v120.21.77.77.

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Abstract Abstract 77 Background: The addition of clarithromycin has been reported to enhance anti-myeloma activity of lenalidomide+dexamethasone in the upfront treatment of multiple myeloma (MM). Pomalidomide is a distinct IMiD® immunomodulatory agent with a significant response rate in subjects with relapsed or refractory MM (RRMM), including those with prior lenalidomide treatment. We have shown initial results that clarithromycin may similarly enhance the activity of pomalidomide + dexamethasone in patients with RRMM after prior lenalidomide therapy (Rossi et al, ASCO 2012). We now report u

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Ruchelman, Alexander L., Hon-Wah Man, Weihong Zhang, et al. "Isosteric analogs of lenalidomide and pomalidomide: Synthesis and biological activity." Bioorganic & Medicinal Chemistry Letters 23, no. 1 (2013): 360–65. http://dx.doi.org/10.1016/j.bmcl.2012.10.071.

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Rossi, Adriana C., Tomer Martin Mark, Melissa Rodriguez, et al. "Clarithromycin, pomalidomide, and dexamethasone (ClaPD) in relapsed or refractory multiple myeloma." Journal of Clinical Oncology 30, no. 15_suppl (2012): 8036. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.8036.

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8036 Background: Clarithromycin has been shown to enhance anti-myeloma activity of lenalidomide+dexamethasone in the upfront treatment of multiple myeloma (MM). Pomalidomide is an immunomodulatory agent effective in relapsed/refractory MM (RRMM). We hypothesized that clarithromycin may similarly enhance pomalidomide + dexamethasone in RRMM. We now report updated results from a phase 2 trial of ClaPD in RRMM. Methods: 73 patients with RRMM were enrolled in a single-institution phase 2 study of ClaPD. All subjects had ≥ 3 prior lines of therapy, one of which must have included lenalidomide. ClaP

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Anderson, Sarah M., Bradley Beck, Susan Sterud, Robin Lockhorst, and Surachat Ngorsuraches. "Evaluating the use of appropriate anticoagulation with lenalidomide and pomalidomide in patients with multiple myeloma." Journal of Oncology Pharmacy Practice 25, no. 4 (2018): 806–12. http://dx.doi.org/10.1177/1078155218758500.

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Background Lenalidomide and pomalidomide are two immunomodulatory medications with the potential to improve outcomes for patients with multiple myeloma; however, a black box warning for venous thromboembolism exists. Purpose The purpose of this study was to assess overall adherence to guideline recommendations for anticoagulation therapy with lenalidomide and pomalidomide in multiple myeloma patients. Methods This retrospective study at an ambulatory oncology clinic utilized chart reviews from the calendar years 2013–2016. The primary endpoint was prescription of appropriate anticoagulation up

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Jimenez Zepeda, Victor H., Peter Duggan, Paola E. Neri, and Nizar J. Bahlis. "Pomalidomide and Dexamethasone Is an Effective Regimen for Advanced-Stage Relapsed/Refractory Multiple Myeloma: Experience of a Single Center." Blood 124, no. 21 (2014): 5747. http://dx.doi.org/10.1182/blood.v124.21.5747.5747.

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Abstract Introduction Almost all patients with MM eventually relapse, and the remission duration in relapsed MM decreases with each regimen. Pomalidomide is an IMiD with antiproliferative, anti-inflammatory and anti-angiogenic effects that was recently approved for the use of relapsed MM failing lenalidomide and bortezomib. Based on these findings, we aimed to evaluate the efficacy of pomalidomide and dexamethasone (PD) for heavily-pretreated relapsed or refractory MM (RRMM) at our Institution. Methods We retrospectively reviewed the records of all patients with RRMM treated with PD at Tom Bak

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Bjorklund, Chad C., Jian Kang, Ling Lu, et al. "CC-220 Is a Potent Cereblon Modulating Agent That Displays Anti-Proliferative, Pro-Apoptotic and Immunomodulatory Activity on Sensitive and Resistant Multiple Myeloma Cell Lines." Blood 128, no. 22 (2016): 1591. http://dx.doi.org/10.1182/blood.v128.22.1591.1591.

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Abstract Background: CC-220 is a Cereblon (CRBN) binding compound currently under clinical investigation for systemic lupus erythematosus. Comparable to other Cereblon-binding agents, ex vivo treatment of CC-220 on B-cells, T-cells and monocytes leads to the degradation of the hematopoietic transcription factors Ikaros (IKZF1) and Aiolos (IKZF3).(1) Currently, CC-220 is being investigated in a phase Ib/IIa study CC-220-MM-001 (clintrial.gov trial #NCT02773030) as a single agent, or in combination with dexamethasone in relapsed/refractory multiple myeloma (RRMM) in patients who may have previou

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Schafer, Peter H., Emily Rychak, Derek Mendy, et al. "Targeting Cereblon with the High Affinity Immunomodulatory Compound CC-220: A Novel Therapeutic Agent for B Cell Dyscrasias." Blood 120, no. 21 (2012): 1055. http://dx.doi.org/10.1182/blood.v120.21.1055.1055.

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Abstract Abstract 1055 Background: Cereblon (CRBN) is a component of the E3 ubiquitin ligase complex including CUL4A, DDB1, and ROC-1, and was found to be the molecular binding target of thalidomide (Thalomid®), lenalidomide (Revlimid®), and pomalidomide. CC-220 is a novel immunomodulatory compound developed with increased potency and is currently in development for the treatment of immune conditions. The effect of CC-220 on CRBN binding, ubiquitination, and cell proliferation was profiled. Methods: Binding studies to CRBN were conducted using thalidomide analog-conjugated beads in a competiti

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Tsang, Mazie, Joseph Cleveland, Miguel Carlos Cerejo, Huimin Geng, and James L. Rubenstein. "Survival and Patient-Reported Outcomes of Older Adults with Primary Central Nervous System Lymphoma on Low-Dose Lenalidomide." Blood 136, Supplement 1 (2020): 21–22. http://dx.doi.org/10.1182/blood-2020-143070.

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Introduction: Management of primary CNS lymphoma (PCNSL) in patients age &gt;70 represents a significant challenge. In most clinical series, median OS for PCNSL patients age &gt;70 is &lt;1 year (Mendez et al., Neuro-Oncology 2018). Since late 2011, our group has used low-dose lenalidomide as maintenance therapy in older patients with newly-diagnosed PCNSL who had &gt;partial response (PR) to induction chemotherapy or salvage chemotherapy for relapsed disease. A preliminary report by our group supported the feasibility and efficacy of low-dose lenalidomide maintenance for 13 ol

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Lacy, Martha Q., Suzanne R. Hayman, Morie A. Gertz, et al. "Pomalidomide (CC4047) Plus Low-Dose Dexamethasone As Therapy for Relapsed Multiple Myeloma." Journal of Clinical Oncology 27, no. 30 (2009): 5008–14. http://dx.doi.org/10.1200/jco.2009.23.6802.

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Purpose Thalidomide and lenalidomide are immunomodulatory drugs (IMiDs) that produce high remission rates in the treatment of multiple myeloma. Pomalidomide is a new IMiD with high in vitro potency. We report, to our knowledge, the first phase II trial of pomalidomide administered in combination with low-dose dexamethasone for the treatment of relapsed or refractory multiple myeloma. Patients and Methods Pomalidomide was administered orally at a dose of 2 mg daily on days 1 through 28 of a 28-day cycle. Dexamethasone 40 mg daily was administered orally on days 1, 8, 15, and 22 of each cycle. R

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Lacy, Martha Q., Betsy R. LaPlant, Kristina Laumann, et al. "Pomalidomide and Dexamethasone in Relapsed Myeloma: Results of 225 Patients Treated in Five Cohorts Over Three Years,." Blood 118, no. 21 (2011): 3963. http://dx.doi.org/10.1182/blood.v118.21.3963.3963.

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Abstract Abstract 3963 Background: Pomalidomide at doses of 2 or 4 mg/d has demonstrated excellent activity in patients with relapsed multiple myeloma (MM). Between November 2007 and November 2010, we opened 5 sequential phase 2 trials using the pomalidomide at differing doses with weekly dexamethasone (Pom/dex) regimen to study the efficacy of this regimen. Methods: The five cohorts consisted of: Cohort 1 (N=60): relapsed MM with 1–3 prior regimens, 2 mg dose; Cohort 2 (N=34): lenalidomide refractory, 2 mg dose; Cohort 3 (N=35): bortezomib/lenalidomide refractory, 2 mg dose; Cohort 4 (N=35):

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Paludo, Jonas, Joseph R. Mikhael, Betsy R. LaPlant, et al. "Pomalidomide, bortezomib, and dexamethasone for patients with relapsed lenalidomide-refractory multiple myeloma." Blood 130, no. 10 (2017): 1198–204. http://dx.doi.org/10.1182/blood-2017-05-782961.

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Sonneveld, Pieter, Hervé Avet-Loiseau, Sagar Lonial, et al. "Treatment of multiple myeloma with high-risk cytogenetics: a consensus of the International Myeloma Working Group." Blood 127, no. 24 (2016): 2955–62. http://dx.doi.org/10.1182/blood-2016-01-631200.

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AbstractThe International Myeloma Working Group consensus updates the definition for high-risk (HR) multiple myeloma based on cytogenetics Several cytogenetic abnormalities such as t(4;14), del(17/17p), t(14;16), t(14;20), nonhyperdiploidy, and gain(1q) were identified that confer poor prognosis. The prognosis of patients showing these abnormalities may vary with the choice of therapy. Treatment strategies have shown promise for HR cytogenetic diseases, such as proteasome inhibition in combination with lenalidomide/pomalidomide, double autologous stem cell transplant plus bortezomib, or combin

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Harousseau, Jean Luc, and Michel Attal. "How I treat first relapse of myeloma." Blood 130, no. 8 (2017): 963–73. http://dx.doi.org/10.1182/blood-2017-03-726703.

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Abstract The standard treatment of relapsed multiple myeloma has been either lenalidomide-dexamethasone (RD) or bortezomib-dexamethasone (VD) but it is changing rapidly for 2 reasons. First, lenalidomide and bortezomib are currently used in frontline treatment and many patients become resistant to these agents early in the course of their disease. Second, 6 second-line new agents have been recently developed and offer new possibilities (pomalidomide, carfilzomib and ixazomib, panobinostat, elotuzumab, and daratumumab). Recent randomized studies have shown that triple combinations adding 1 of t

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Rundgren, Ida Marie, Anita Ryningen, Tor Henrik Anderson Tvedt, Øystein Bruserud, and Elisabeth Ersvær. "Immunomodulatory Drugs Alter the Metabolism and the Extracellular Release of Soluble Mediators by Normal Monocytes." Molecules 25, no. 2 (2020): 367. http://dx.doi.org/10.3390/molecules25020367.

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Immunomodulatory drugs (IMiDs) are used in the treatment of hematological malignancies, especially multiple myeloma. IMiDs have direct anticancer effects but also indirect effects via cancer-supporting stromal cells. Monocytes are a stromal cell subset whose metabolism is modulated by the microenvironment, and they communicate with neighboring cells through extracellular release of soluble mediators. Toll-like receptor 4 (TLR4) is then a common regulator of monocyte metabolism and mediator release. Our aim was to investigate IMiD effects on these two monocyte functions. We compared effects of

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Palumbo, Antonio, Alessandra Larocca, Vittorio Montefusco, et al. "Pomalidomide Cyclophosphamide and Prednisone (PCP) Treatment for Relapsed/Refractory Multiple Myeloma." Blood 120, no. 21 (2012): 446. http://dx.doi.org/10.1182/blood.v120.21.446.446.

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Abstract Abstract 446 Background: The outcome of myeloma (MM) patients who are no longer responding to thalidomide, lenalidomide or bortezomib is poor, with a median event-free survival of 5 months and median overall survival (OS) of 9 months (Kumar SK et al, Leukemia 2012). The newer immunomodulatory drug pomalidomide, has shown significant activity in these clinical conditions. Aims: We assessed dosing, efficacy and safety of pomalidomide-cyclophosphamide-prednisone (PCP) in MM patients relapsed/refractory to lenalidomide. Methods: Pomalidomide was administered in doses ranging from 1 to 2.5

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Montefusco, Vittorio, and Marco Capecchi. "Diarrhea Incidence in Multiple Myeloma Patients Treated With Lenalidomide and Pomalidomide." Clinical Lymphoma Myeloma and Leukemia 17, no. 1 (2017): e46. http://dx.doi.org/10.1016/j.clml.2017.03.082.

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Garderet, Laurent, Frederique Kuhnowski, Benoit Berge, et al. "Pomalidomide, cyclophosphamide, and dexamethasone for relapsed multiple myeloma." Blood 132, no. 24 (2018): 2555–63. http://dx.doi.org/10.1182/blood-2018-07-863829.

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Abstract It is important to have an effective therapy for patients with multiple myeloma (MM) at first relapse, particularly if an autologous stem cell transplant (ASCT) is considered at this stage. This multicenter, phase 2 trial evaluated the efficacy and safety of weekly oral pomalidomide-cyclophosphamide-dexamethasone (PCD) in patients with MM in first relapse after treatment with lenalidomide-bortezomib-dexamethasone (RVD). All patients had received RVD as induction and consolidation therapy, plus lenalidomide maintenance for 1 year (arm A). Half had also received an ASCT after induction

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Oka, Satoko, Kazuo Ono, and Masaharu Nohgawa. "Successful retreatment with lenalidomide for relapsed and refractory multiple myeloma previously treated with bortezomib, lenalidomide and pomalidomide." Journal of Clinical Pharmacy and Therapeutics 43, no. 6 (2018): 914–17. http://dx.doi.org/10.1111/jcpt.12740.

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Sivaraj, Dharshan, Michael M. Green, Yubin Kang, et al. "Phase I/II dose expansion of a trial investigating bendamustine and pomalidomide with dexamethasone (BPd) in patients with relapsed/refractory multiple myeloma." Journal of Clinical Oncology 35, no. 15_suppl (2017): 8008. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.8008.

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8008 Background: The combination of bendamustine, pomalidomide, and dexamethasone (BPd) displays promising activity in heavily pretreated RRMM. In the Phase I portion, MTD was 120 mg/m2bendamustine/3mg pomalidomide/40mg dexamethasone. We report our combined findings from the additional phase II expansion cohort for the first phase I/II trial of BPd in patients with RRMM (NCT01754402). Methods: All patients had to be refractory to prior lenalidomide as well as be pomalidomide naïve, and must have relapsed or have been refractory to their most recent therapy. Treatment consisted of oral pomalido

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