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Acalabrutinib 100mg

Each hard gelatine capsule contains:
Acalabrutinib…… 100mg
Approved colours used in empty capsule shell.

Acalabrutinib is a Burton tyrosine kinase inhibitor used to treat mantle Lymphoma chronic lymphocytic leukaemia and small lymphocytic lymphoma

Acalabrutinib is currently indicated for the treatment of adult patients with Mantle Cell Lymphoma (MCL) who have received at least one prior therapy.6 It has also been recently approved for chronic lymphocytic leukaemia and small lymphocytic lymphoma.

Mechanism of action
Mantle Cell Lymphoma (MCL) is a rare yet aggressive type of B-cell non-Hodgkin lymphoma (NHL) with poor prognosis 2,4. Subsequently, relapse is common in MCL patients and ultimately represents disease progression 4.

Lymphoma occurs when immune system lymphocytes grow and multiply uncontrollably. Such cancerous lymphocytes may travel to many parts of the body, including the lymph nodes, spleen, bone marrow, blood, and other organs where they can multiply and form a mass(es) called a tumor. One of the main kinds of lymphocytes that can develop into cancerous lymphomas are the body’s own B-lymphocytes (B-cells) 4.

Bruton Tyrosine Kinase (BTK) is a signalling molecule of the B-cell antigen receptor and cytokine receptor pathways. Such BTK signalling causes the activation of pathways necessary for B-cell proliferation, trafficking, chemotaxis, and adhesion.6

Acalabrutinib is a small molecule inhibitor of BTK. Both acalabrutinib and its active metabolite, ACP-5862, act to form a covalent bond with a cysteine residue (Cys481) in the BTK active site, leading to inhibition of BTK enzymatic activity.2,4 As a result, acalabrutinib inhibits BTK-mediated activation of downstream signalling proteins CD86 and CD69, which ultimately inhibits malignant B-cell proliferation and survival4

Whereas ibrutinib is typically recognized as the first-in-class BTK inhibitor,2 acalabrutinib is considered a second generation BTK inhibitor primarily because it demonstrates highter selectivity and inhibition of the targeted activity of BTK while having a much greater IC50 or otherwise virtually no inhibition on the kinase activities of ITK, EGFR, ERBB2, ERBB4, JAK3, BLK, FGR, FYN, HCK, LCK, LYN, SRC, and YES1.2

In effect, acalabrutinib was rationally designed to be more potent and selective than ibrutinib, all the while demonstrating fewer adverse effects – in theory – because of the drug’s minimized off target effects.

Acalabrutinib is mainly metabolized by CYP3A enzymes. ACP-5862 is identified to be the major active metabolite in plasma with a geometric mean exposure (AUC) that is about 2-3 times greater than the exposure of acalabrutinib. ACP-5862 is about 50% less potent than acalabrutinib in regards to the inhibition of BTK.6

Acalabrutinib M27 Metabolite (ACP-5862)
Acalabrutinib M2 Metabolite
Acalabrutinib M3 Metabolite
Acalabrutinib M16 Metabolite
Acalabrutinib M2 Metabolite
Acalabrutinib M23 Metabolite (ACP-5134)
Acalabrutinib M24 Metabolite
Acalabrutinib M45 Metabolite
Acalabrutinib M5 Metabolite (ACP-5530)
Acalabrutinib M7 Metabolite (ACP-5531)
Acalabrutinib M10 Metabolite (ACP-5461)
Acalabrutinib M25 Metabolite
Acalabrutinib M37 Metabolite
Acalabrutinib M14 Metabolite (ACP-5825)

Recommended dose is 100 mg orally approximately every twelve hours Swallow whole with water and with or without food. Advice patients not to break, open, or chew capsules. Manage toxicities using treatment interruption, dose reduction,

Store at 20°C-25°C (68°F-77°F); excursions permitted to 15°C-30°C (59°F-86°F) [see USP Controlled
Room Temperature]


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