## 1.2 1.1 Introduction  
A type of cancer called leukemia appears in the tissues that produce blood (e.g., bone marrow). Chronic lymphocytic leukemia (CLL), a hematologic malignancy, produces an excessive number of B-lymphocytes (immature lymphoid stem cells) [1]. Small lymphocytic lymphoma (SLL) and chronic lymphocytic leukemia (CLL) are two cancers that are similar enough to one another that their names are occasionally interchanged [1; 2]. Chemotherapy with a variety of drugs (given as single or in combination) and immunotherapy are the standard treatments for CLL and SLL. These therapies include monoclonal antibodies, immunomodulatory-antiangiogenic drugs, nucleoside analogs, and alkylating agents. Although some of these regimens have median survival times of more than 10 years and overall response rates of less than 90%, eventually relapse happens with shorter survival times and response rates [3; 4]. This demands the development of contemporary, secure, and safe medications with novel mechanisms of action. One of the important targets is the phosphoinositide 3-kinase (PI3K) enzyme which is a lipid kinase involved in intracellular signal transmission. There are four isoforms of the catalytic subunit of PI3K: \(\alpha\), \(\beta\), \(\delta\), and \(\gamma\)[5; 6]. Malignant cell proliferation and migration are blocked by the tumor microenvironment when both PI3K-\(\delta\) and PI3K-\(\gamma\) are inhibited [7; 8; 9]. Moreover, both PI3K-\(\delta\) and PI3K-\(\gamma\) suppression contribute to the death of tumor cells [10; 11]. As a result, concurrent inhibition of PI3K-\(\delta\) and PI3K-\(\gamma\) may enhance therapeutic results in patients with lymphoid malignancies [12]. The recognized involvement of PI3K-\(\delta\) and PI3K-\(\gamma\) in hematologic malignancies has led to the present development of class-specific PI3K inhibitors for use as anticancer drugs [11]. Idelalisib is the first PI3K inhibitor that has been approved for the treatment of CLL (in combination with rituximab) and as a monotherapy for relapsed SLL and relapsed follicular lymphoma. Moreover, it was recommended by the FDA as first-line therapy for patients who were ineligible for chemimmunotherapy and had CLL with a dismal prognosis and 17p deletions or TP53 mutations [12]. Duvelisib (DUV, also known as IPI-145) is a novel drug with a small molecular weight and possesses a dual PI3K-\(\delta\) and PI3K-\(\gamma\) inhibitory action. Its chemical structure is depicted in Figure 1. DUV exhibits leukemia cell-specific antiproliferative action [13]. DUV was created by Verastem, Inc., Needham, MA, USA) and has recently (on 24 September 2018) received FDA approval for the treatment of adults with relapsed or refractory CLL or SLL [14] as well as accelerated approval for relapsed or refractory follicular lymphoma management [15]. This may be attributed to its high success response rate. DUV may also potentially diminish T-cell lymphoma [14; 15]. DUV is sold under the brand name of Copiktra\({}^{\text{\textregistered}}\) (Verastem, Inc., Needham, MA, USA) and its dosage is 25 mg twice daily as oral capsules throughout a 28-day therapy cycle [14]. The quality of the copiktra capsules and the assessment of plasma concentrations in patients during therapy dictates the efficacy and safety of DUV therapy. To ensure copiktra capsules with good quality and assess the plasma concentrations of DUV in the patients, a proper analytical method is required. The existing methods for the determination of DUV in its capsules and plasma samples are very limited [16; 17; 18; 19; 20; 21]. [PERSON] et al. [16] provided a descrip  
Figure 1: Panel (**A**): the chemical structure of duvelisib (DUV) and its absorption spectrum. The concentration of DUV was 20 \(\upmu\)g/mL in methanol. Panel (**B**): the fluorescence spectra (excitation and emission) of DUV. The concentration of DUV solution used for recording the spectra was 200 ng/mL in methanol.