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<meta name="citation_inbook_title" content="LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]">
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yet</button><a id="jr-fip-next" class="wsprkl btn" title="Jump to next match">▶</a></nav></nav></div><div id="jr-epub-interstitial" class="hidden"></div><div id="jr-content"><article data-type="main"><div class="main-content lit-style" itemscope="itemscope" itemtype="http://schema.org/CreativeWork"><div class="meta-content fm-sec"><div class="fm-sec"><h1 id="_NBK548824_"><span class="title" itemprop="name">Duvelisib</span></h1><p class="fm-aai"><a href="#_NBK548824_pubdet_">Publication Details</a></p></div></div><div class="body-content whole_rhythm" itemprop="text"><div id="Duvelisib.OVERVIEW"><h2 id="_Duvelisib_OVERVIEW_">OVERVIEW</h2><div id="Duvelisib.Introduction"><h3>Introduction</h3><p>Duvelisib is an oral inhibitor of phosphatidylinositol 3-kinase (PI3K) that is approved for use in relapsed or refractory chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL). Duvelisib is associated with a high rate of serum enzyme elevations during therapy and with occasional concurrent rise in serum bilirubin and is a suspected but not proven cause of clinically apparent acute liver injury.</p></div><div id="Duvelisib.Background"><h3>Background</h3><p>Duvelisib (doo" ve lis' ib) is an orally available, small molecule inhibitor of the delta and gamma isoforms of phosphatidylinositol 3-kinase (PI3K δ/λ), which is an essential component in the B cell signaling pathways that drive migration of B cells to lymph nodes and bone marrow. Inhibition of this pathway inhibits B cell chemotaxis and adherence and reduces cell viability. This pathway is upregulated in many B cell malignancies and has been shown to be critical for proliferation and survival of leukemia and lymphomatous malignant B lymphocytes. Duvelisib was approved for use in the United States in 2018 as therapy for relapsed or refractory CLL and small lymphocytic lymphoma (SLL) as well as refractory forms of follicular lymphoma (an indication that was subsequently withdrawn). Duvelisib is available as capsules of 15 and 25 mg under the brand name Copiktra. The recommended dose is 25 orally mg twice daily until disease progression or unacceptable toxicity. Side effects are common but most often mild-to-moderate in severity, and include diarrhea, neutropenia, rash, fatigue, fever, cough, musculoskeletal pain and anemia. Common laboratory abnormalities can include cytopenias, liver enzyme elevations, hyper- or hypo-glycemia, and hyponatremia. Severe adverse events (for which it has a black box warning) can include severe diarrhea or colitis, pneumonitis, intestinal perforation, severe skin rash, anaphylaxis, neutropenia and embryo-fetal toxicity.</p></div><div id="Duvelisib.Hepatotoxicity"><h3>Hepatotoxicity</h3><p>In clinical trials of duvelisib in patients with CLL and lymphoma, the rates of serum enzyme elevations during therapy ranged from 39% to 57% and were above 5 times the ULN in 3% to 8%. Serum enzyme elevations typically arose within 4 to 12 weeks of starting therapy and usually resolved rapidly with dose reduction or temporary discontinuation. In many instances, the serum aminotransferase elevations resolved spontaneously and most (but not all) patients were able to restart duvelisib without recurrence. While there were no reported cases of clinically apparent liver injury with jaundice, up to 35% of patients discontinued duvelisib because of serum enzyme elevations and all patients were followed carefully during treatment. In one study, 2% of treated patients developed concurrent elevations in serum aminotransferase and bilirubin levels but there were no episodes considered to be clinically apparent liver injury and no deaths due to liver failure. Duvelisib has not been widely used since its approval, and its potential for causing acute clinically apparent liver injury with jaundice has not been well defined. Because duvelisib affects B cell function, it may also be capable of inducing reactivation of hepatitis B, although in published trials of the agent, reactivation was not reported.</p><p>Likelihood score: E* (unproved but suspected cause of clinically apparent liver injury).</p></div><div id="Duvelisib.Mechanism_of_Injury"><h3>Mechanism of Injury</h3><p>The reason why duvelisib causes serum enzyme elevations is not known, but may be a direct toxicity to hepatocytes caused by inhibition of PI3K activity or the result of change in B cell activity and caused by induction of immune mediated liver injury as has been reported with other small molecule PI3K inhibitors such as idelalisib. Duvelisib is metabolized primarily in the liver by cytochrome P450 (CYP 3A4) and is susceptible to drug-drug interactions with strong inducers or inhibitors of CYP 3A4 and itself may inhibit CYP 3A4 activity and affect plasma levels of other drugs metabolized by this microsomal enzyme.</p></div><div id="Duvelisib.Outcome_and_Management"><h3>Outcome and Management</h3><p>Serum enzyme elevations are not uncommon during cancer chemotherapy with duvelisib and may occasionally be dose limiting. Duvelisib should not be used with other agents with hepatotoxic potential. Furthermore, regular monitoring of liver tests is recommended during duvelisib therapy, with more frequent monitoring if serum aminotransferase values rise. Duvelisib should be held if ALT or AST values rise above 5 times the ULN, and treatment resumed only if values fall below 3 times ULN and then with careful monitoring or at a reduced dose. Elevations of aminotransferase values of more than 20 times the ULN, or appearance of jaundice or symptoms should trigger permanent discontinuation. Corticosteroids are often used if the liver injury does not resolve rapidly with stopping duvelisib and continuing the corticosteroids may help prevent recurrence of injury with restarting therapy. There is no known cross sensitivity to hepatic injury among the different protein kinase inhibitors.</p><p>Drug Class: <a href="/books/n/livertox/AntineoplasticAgents/?report=reader">Antineoplastic Agents</a>, <a href="/books/n/livertox/ProteinKinaseInhibit/?report=reader">Protein Kinase Inhibitors</a></p></div></div><div id="Duvelisib.PRODUCT_INFORMATION"><h2 id="_Duvelisib_PRODUCT_INFORMATION_">PRODUCT INFORMATION</h2><p>
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<b>REPRESENTATIVE TRADE NAMES</b>
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</p><p>Duvelisib – Copiktra®</p><p>
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<b>DRUG CLASS</b>
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</p><p>Antineoplastic Agents</p><p>
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<a href="https://dailymed.nlm.nih.gov/dailymed/search.cfm?labeltype=all&query=Duvelisib" ref="pagearea=body&targetsite=external&targetcat=link&targettype=uri">COMPLETE LABELING</a>
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</p><p>Product labeling at DailyMed, National Library of Medicine, NIH</p></div><div id="Duvelisib.CHEMICAL_FORMULA_AND_STRUCTURE"><h2 id="_Duvelisib_CHEMICAL_FORMULA_AND_STRUCTURE_">CHEMICAL FORMULA AND STRUCTURE</h2><div class="iconblock whole_rhythm clearfix ten_col table-wrap" id="figDuvelisibTc"><a href="/books/NBK548824/table/Duvelisib.Tc/?report=objectonly" target="object" title="Table" class="img_link icnblk_img figpopup" rid-figpopup="figDuvelisibTc" rid-ob="figobDuvelisibTc"><img class="small-thumb" src="/books/NBK548824/table/Duvelisib.Tc/?report=thumb" src-large="/books/NBK548824/table/Duvelisib.Tc/?report=previmg" alt="Image " /></a><div class="icnblk_cntnt"><h4 id="Duvelisib.Tc"><a href="/books/NBK548824/table/Duvelisib.Tc/?report=objectonly" target="object" rid-ob="figobDuvelisibTc">Table</a></h4></div></div></div><div id="Duvelisib.ANNOTATED_BIBLIOGRAPHY"><h2 id="_Duvelisib_ANNOTATED_BIBLIOGRAPHY_">ANNOTATED BIBLIOGRAPHY</h2><p>References updated: 12 July 2022</p><p>Abbreviations: CLL, chronic lymphocytic leukemia; PI3K, phosphatidylinositol 3-kinase; SLL, small cell lymphocytic lymphoma.</p><ul class="first-line-outdent"><li><div class="bk_ref" id="Duvelisib.REF.zimmerman.1999">Zimmerman HJ. Hepatotoxicity: the adverse effects of drugs and other chemicals on the liver. 2nd ed. Philadelphia: Lippincott, 1999.<div><i>(Review of hepatotoxicity published in 1999 before the availability of tyrosine kinase receptor inhibitors).</i></div></div></li><li><div class="bk_ref" id="Duvelisib.REF.deleve.2013">DeLeve LD. Kinase inhibitors. Cancer chemotherapy. In, Kaplowitz N, DeLeve LD, eds. Drug-induced liver disease. 3rd ed. Amsterdam: Elsevier, 2013, p. 556.<div><i>(Review of hepatotoxicity of cancer chemotherapeutic agents; does not discuss duvelisib or other PI3K inhibitors).</i></div></div></li><li><div class="bk_ref" id="Duvelisib.REF.wellstein.2018">Wellstein A, Giaccone G, Atkins MB, Sausville EA. Pathway-targeted therapies: monoclonal antibodies, protein kinase inhibitors, and various small molecules. In, Brunton LL, Hilal-Dandan R, Knollman BC, eds. Goodman & Gilman's the pharmacological basis of therapeutics. 13th ed. New York: McGraw-Hill, 2018, pp. 1203-36.<div><i>(Textbook of pharmacology and therapeutics).</i></div></div></li><li><div class="bk_ref" id="Duvelisib.REF.fda">FDA. <a href="https://www.accessdata.fda.gov/drugsatfda_docs/nda/2018/211155Orig1Orig2s000MultidisciplineR.pdf" ref="pagearea=cite-ref&targetsite=external&targetcat=link&targettype=uri">https://www<wbr style="display:inline-block"></wbr>​.accessdata<wbr style="display:inline-block"></wbr>​.fda.gov/drugsatfda_docs<wbr style="display:inline-block"></wbr>​/nda/2018/211155Orig1Orig2s000MultidisciplineR.pdf</a>.<div><i>(FDA Drug Approvals website that has product labels [package inserts], letters of approval and full FDA scientific review of the new drug application for safety and efficacy; mentions that duvelisib has serious hepatotoxicity and that review of laboratory test results found 8 cases of concomitant elevations in ALT or AST with bilirubin that was twice normal; ALT elevations arose in 43% of treated patients and to above 5 times ULN in 8% although there were no deaths from hepatic failure).</i></div></div></li><li><div class="bk_ref" id="Duvelisib.REF.furman.2014.997">Furman RR, Sharman JP, Coutre SE, Cheson BD, Pagel JM, Hillmen P, Barrientos JC, et al. Idelalisib and rituximab in relapsed chronic lymphocytic leukemia. <span><span class="ref-journal">N Engl J Med. </span>2014;<span class="ref-vol">370</span>:997–1007.</span> [<a href="/pmc/articles/PMC4161365/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC4161365</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/24450857" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 24450857</span></a>]<div>
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<i>(Among 220 patients with relapsed CLL treated in a placebo controlled trial, progression free survival improved with idelalisib and rituximab compared to rituximab alone, but side effects were more common with the combination including ALT or AST elevations [35% vs 19%] which were above 5 times ULN in 5% vs 1% and led to drug discontinuations in some patients, but there were no clinically apparent cases of liver injury).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.lampson.2016.195">Lampson BL, Kasar SN, Matos TR, Morgan EA, Rassenti L, Davids MS, Fisher DC, et al. Idelalisib given front-line for treatment of chronic lymphocytic leukemia causes frequent immune-mediated hepatotoxicity. <span><span class="ref-journal">Blood. </span>2016;<span class="ref-vol">128</span>:195–203.</span> [<a href="/pmc/articles/PMC4946200/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC4946200</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/27247136" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 27247136</span></a>]<div>
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<i>(Among 24 patients with relapsed or refractory CLL treated with idelalisib, 19 [79%] developed ALT elevations which were above 5 times ULN in 13 [54%], usually within 28 days of starting therapy and sometimes worsening despite drug discontinuation leading to corticosteroid therapy in 16 subjects; rechallenge with idelalisib led to recurrence within a few days, but abnormalities were mild and tolerable in those on corticosteroids).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.brown.2016.260">Brown JR. The PI3K pathway: clinical inhibition in chronic lymphocytic leukemia. <span><span class="ref-journal">Semin Oncol. </span>2016;<span class="ref-vol">43</span>:260–4.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/27040704" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 27040704</span></a>]<div>
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<i>(Review of the role of aberrant PI3K signaling in cancer with delta and lambda isoenzymes predominantly expressed in hematopoietic cells making them candidates for targeted therapy in B cell related leukemias and lymphomas).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.flinn.2018.1311">Flinn IW, Patel M, Oki Y, Horwitz S, Foss FF, Allen K, Douglas M, et al. Duvelisib, an oral dual PI3K-δ,γ inhibitor, shows clinical activity in indolent non-Hodgkin lymphoma in a phase 1 study. <span><span class="ref-journal">Am J Hematol. </span>2018;<span class="ref-vol">93</span>:1311–7.</span> [<a href="/pmc/articles/PMC6220789/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC6220789</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30033575" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30033575</span></a>]<div>
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<i>(Among 31 patients with refractory, indolent non-Hodgkin lymphoma treated with 8 different doses of duvelisib, the overall response rate was 58% and dose limiting toxicities were rash and ALT or AST elevations, which arose in 57% of patients, and to above 5 times ULN in 43% with 11 dose modifications and 4 discontinuations but no instance of enzyme elevations with jaundice).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.flinn.2018.2446">Flinn IW, Hillmen P, Montillo M, Nagy Z, Illés Á, Etienne G, Delgado J, et al. The phase 3 DUO trial: duvelisib vs ofatumumab in relapsed and refractory CLL/SLL. <span><span class="ref-journal">Blood. </span>2018;<span class="ref-vol">132</span>:2446–55.</span> [<a href="/pmc/articles/PMC6284216/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC6284216</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30287523" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30287523</span></a>]<div>
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<i>(Among 159 patients with relapsed or refractory CLL or SLL treated with duvelisib [25 mg twice daily] or ofatumumab [iv every 3 weeks], progression-free survival was greater with duvelisib [13.3 vs 9.9 months] and adverse reactions included diarrhea [51%], neutropenia [33%], fever [29%], nausea [23%], cough [21%], fatigue [13%], rash [10%] and ALT elevations above 5 times ULN [3%]).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.obrien.2018.1318">O'Brien S, Patel M, Kahl BS, Horwitz SM, Foss FM, Porcu P, Jones J, et al. Duvelisib, an oral dual PI3K-δ,γ inhibitor, shows clinical and pharmacodynamic activity in chronic lymphocytic leukemia and small lymphocytic lymphoma in a phase 1 study. <span><span class="ref-journal">Am J Hematol. </span>2018;<span class="ref-vol">93</span>:1318–26.</span> [<a href="/pmc/articles/PMC8260004/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC8260004</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/30094870" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30094870</span></a>]<div>
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<i>(Among 79 patients with CLL treated with duvelisib in multiple dose levels [8 to 75 mg twice daily] given in 28-day cycles, the overall response rate was 56% [in relapsed or refractory patients] and 83% [in treatment-naïve], and adverse events were common including ALT elevations in 31% which were above 5 times ULN in 11%).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.blair.2018.1847">Blair HA. Duvelisib: first global approval. <span><span class="ref-journal">Drugs. </span>2018;<span class="ref-vol">78</span>:1847–53.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/30430368" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30430368</span></a>]<div>
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<i>(Review of the mechanism of action, history of development, pharmacology, clinical efficacy and safety of duvelisib shortly after its approval as monotherapy for CLL and SLL; mentions that it has “manageable tolerability” and increased ALT and AST levels occur in 3% of patients).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.flinn.2019.1325">Flinn IW, Cherry MA, Maris MB, Matous JV, Berdeja JG, Patel M. Combination trial of duvelisib (IPI-145) with rituximab or bendamustine/rituximab in patients with non-Hodgkin lymphoma or chronic lymphocytic leukemia. <span><span class="ref-journal">Am J Hematol. </span>2019;<span class="ref-vol">94</span>:1325–1334.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/31490009" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 31490009</span></a>]<div>
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<i>(Among 46 patients with relapsed or refractory non-Hodgkin lymphoma or CLL treated with duvelisib and rituximab alone or with bendamustine, the overall response rate was 72% and common adverse events were neutropenia, fatigue and rash; ALT elevations arose in 22% which were above 5 times ULN in 6.5% but there were no cases of clinically apparent liver injury with jaundice or deaths from liver disease).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.flinn.2019.912">Flinn IW, Miller CB, Ardeshna KM, Tetreault S, Assouline SE, Mayer J, Merli M, et al. DYNAMO: a phase II study of duvelisib (IPI-145) in patients with refractory indolent non-Hodgkin lymphoma. <span><span class="ref-journal">J Clin Oncol. </span>2019;<span class="ref-vol">37</span>:912–922.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/30742566" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 30742566</span></a>]<div>
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<i>(Among 129 patients with refractory or relapsing non-Hodgkin lymphoma treated with duvelisib [25 mg twice daily in 28 day cycles], the overall response rate was 47% and adverse events included diarrhea [49%], nausea [30%], neutropenia [29%], fatigue [28%], cough [27%] and ALT elevations above 5 times ULN [5.4%] but without clinically apparent liver injury).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.davids.2020.2096">Davids MS, Kuss BJ, Hillmen P, Montillo M, Moreno C, Essell J, Lamanna N, et al. Efficacy and safety of duvelisib following disease progression on ofatumumab in patients with relapsed/refractory CLL or SLL in the DUO crossover extension study. <span><span class="ref-journal">Clin Cancer Res. </span>2020;<span class="ref-vol">26</span>:2096–2103.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/31964785" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 31964785</span></a>]<div>
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<i>(Among 90 patients who received ofatumumab in the phase III DUO trial [Flinn 2018] who were switched to duvelisib [25 mg twice daily], 69 [77%] had an objective response while common adverse events were diarrhea [47%], neutropenia [26%], fever [24%], rash [23%] and thrombocytopenia [10%]; ALT elevations above 5 times ULN occurred in 2-3% and resulted in drug discontinuation in 1% of patients).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.ghia.2020.2849">Ghia P, Pluta A, Wach M, Lysak D, Kozak T, Simkovic M, Kaplan P, et al. ASCEND: phase III, randomized trial of acalabrutinib versus idelalisib plus rituximab or bendamustine plus rituximab in relapsed or refractory chronic lymphocytic leukemia. <span><span class="ref-journal">J Clin Oncol. </span>2020;<span class="ref-vol">38</span>:2849–2861.</span> [<a href="https://pubmed.ncbi.nlm.nih.gov/32459600" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 32459600</span></a>]<div>
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<i>(Among 310 patients with relapsed or refractory CLL treated with acalabrutinib vs idelalisib and rituximab with or without bendamustine, the 12 month predicted progression-free survival was 88% vs 68% and serious adverse event rates were 29% vs 56% and ALT elevations above 5 times ULN arose in 1% vs 6%).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.lampson.2021.807">Lampson BL, Brown JR. The evolving use of phosphatidylinositol 3-kinase inhibitors for the treatment of chronic lymphocytic leukemia. <span><span class="ref-journal">Hematol Oncol Clin North Am. </span>2021;<span class="ref-vol">35</span>:807–826.</span> [<a href="/pmc/articles/PMC8239250/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC8239250</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/34174987" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 34174987</span></a>]<div>
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<i>(Review of the mechanisms of action, clinical efficacy and safety of three PI3K inhibitors [idelalisib, duvelisib and umbralisib] as therapy of CLL, all of which were promising in early studies among refractory patients, but when used as front line therapy they had higher rates of adverse events including infections and immune mediated colitis, pneumonitis and hepatitis that were often corticosteroid responsive).</i>
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</div></div></li><li><div class="bk_ref" id="Duvelisib.REF.davids.2021.1064">Davids MS, Fisher DC, Tyekucheva S, McDonough M, Hanna J, Lee B, Francoeur K, et al. A phase 1b/2 study of duvelisib in combination with FCR (DFCR) for frontline therapy for younger CLL patients. <span><span class="ref-journal">Leukemia. </span>2021;<span class="ref-vol">35</span>:1064–1072.</span> [<a href="/pmc/articles/PMC7895867/" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pmc">PMC free article<span class="bk_prnt">: PMC7895867</span></a>] [<a href="https://pubmed.ncbi.nlm.nih.gov/32820271" ref="pagearea=cite-ref&targetsite=entrez&targetcat=link&targettype=pubmed">PubMed<span class="bk_prnt">: 32820271</span></a>]<div>
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<i>(Among 32 patients treated with duvelisib [25 mg once or twice daily] for 1 week and then with standard chemotherapy for 6 cycles, followed by duvelisib alone for up to 2 years, adverse events were frequent [94%], including thrombocytopenia [81%], neutropenia [78%], lymphopenia [77%], nausea, fatigue, fever and ALT or AST elevations above 5 times ULN in 28).</i>
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</div></div></li></ul></div><div id="bk_toc_contnr"></div></div></div><div class="fm-sec"><h2 id="_NBK548824_pubdet_">Publication Details</h2><h3>Publication History</h3><p class="small">Last Update: <span itemprop="dateModified">July 12, 2022</span>.</p><h3>Copyright</h3><div><div class="half_rhythm"><a href="/books/about/copyright/">Copyright Notice</a></div></div><h3>Publisher</h3><p><a href="https://www.niddk.nih.gov/" ref="pagearea=page-banner&targetsite=external&targetcat=link&targettype=publisher">National Institute of Diabetes and Digestive and Kidney Diseases</a>, Bethesda (MD)</p><h3>NLM Citation</h3><p>LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-. Duvelisib. [Updated 2022 Jul 12].<span class="bk_cite_avail"></span></p></div><div class="small-screen-prev"><a href="/books/n/livertox/Dutasteride/?report=reader"><svg xmlns="http://www.w3.org/2000/svg" viewBox="0 0 100 100" preserveAspectRatio="none"><path d="M75,30 c-80,60 -80,0 0,60 c-30,-60 -30,0 0,-60"></path><text x="20" y="28" textLength="60" style="font-size:25px">Prev</text></svg></a></div><div class="small-screen-next"><a href="/books/n/livertox/Echinacea/?report=reader"><svg xmlns="http://www.w3.org/2000/svg" viewBox="0 0 100 100" preserveAspectRatio="none"><path d="M25,30c80,60 80,0 0,60 c30,-60 30,0 0,-60"></path><text x="20" y="28" textLength="60" style="font-size:25px">Next</text></svg></a></div></article><article data-type="table-wrap" id="figobDuvelisibTc"><div id="Duvelisib.Tc" class="table"><p class="large-table-link" style="display:none"><span class="right"><a href="/books/NBK548824/table/Duvelisib.Tc/?report=objectonly" target="object">View in own window</a></span></p><div class="large_tbl" id="__Duvelisib.Tc_lrgtbl__"><table><thead><tr><th id="hd_h_Duvelisib.Tc_1_1_1_1" scope="col" rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">DRUG</th><th id="hd_h_Duvelisib.Tc_1_1_1_2" scope="col" rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">CAS REGISTRY NO.</th><th id="hd_h_Duvelisib.Tc_1_1_1_3" scope="col" rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">MOLECULAR FORMULA</th><th id="hd_h_Duvelisib.Tc_1_1_1_4" scope="col" rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">STRUCTURE</th></tr></thead><tbody><tr><td headers="hd_h_Duvelisib.Tc_1_1_1_1" scope="row" rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">Duvelisib</td><td headers="hd_h_Duvelisib.Tc_1_1_1_2" rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">
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<a href="https://pubchem.ncbi.nlm.nih.gov/substance/164117634" ref="pagearea=body&targetsite=entrez&targetcat=link&targettype=pubchem">1201438-56-3</a>
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</td><td headers="hd_h_Duvelisib.Tc_1_1_1_3" rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">C22-H17-Cl-N6-O</td><td headers="hd_h_Duvelisib.Tc_1_1_1_4" rowspan="1" colspan="1" style="text-align:left;vertical-align:top;">
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<a href="https://pubchem.ncbi.nlm.nih.gov/substance/164117634" title="View this structure in PubChem" class="img_link" ref="pagearea=body&targetsite=entrez&targetcat=link&targettype=pubchem"><img src="https://pubchem.ncbi.nlm.nih.gov/image/imgsrv.fcgi?t=l&sid=164117634" alt="image 164117634 in the ncbi pubchem database" /></a>
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