Acalabrutinib 100mg tablets
Requires a prescription from a doctor or prescriber
To date, acalabrutinib has been used in trials studying the treatment of B-All, myelofibrosis, ovarian cancer, multiple myeloma, and Hodgkin lymphoma, among others.
Official documents, adverse reaction reporting, and safety monitoring
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Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Acalabrutinib
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Acalabrutinib
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
MHRA licensed products
View all licensed products for Acalabrutinib on the MHRA register
Calquence 100mg tablets
Therapeutically similar medicines
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Clinical guidelines and formulary information
British National Formulary
Acalabrutinib
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(4)
Acalabrutinib for treating chronic lymphocytic leukaemia (TA689)
Zanubrutinib for treating chronic lymphocytic leukaemia (TA931)
Ibrutinib with venetoclax for untreated chronic lymphocytic leukaemia (TA891)
Venetoclax for treating chronic lymphocytic leukaemia (TA796)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Supply & product information
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
6.9 hours
Mechanism
Mantle Cell Lymphoma (MCL) is a rare yet aggressive type of B-cell non-Hodgkin l…
Food interactions
5 warnings
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
25%
[L10241]
Half-life
100 mg
Protein binding
97.5%
Volume of distribution
34 L
[L10241]
Metabolism
50%
Elimination
100 mg
[L10241]…
Clearance
159 L/h
[L10241]…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
As of October 31, 2017 the FDA approved Astra Zeneca's orally administered Calquence (acalabrutinib, capsules). This Bruton tyrosine kinase (BTK) inhibitor indicated for the treatment of chronic lymphocytic leukemia, small lymphocytic lymphoma, and in adult patients with Mantle cell lymphoma (MCL) who have already received at least one prior therapy.[L10241] In August 2022, the FDA approved a new tablet formulation of Calquence, enabling the co-administration of this drug with proton pump inhibitors (PPIs).[L42795][L42800] Unlike Calquence capsules, the co-administration of Calquence tablets and PPIs does not have an effect in the pharmacokinetics of acalabrutinib.[L10241][L42795]
Also known as ACP-196, acalabrutinib is also considered a second generation BTK inhibitor because it was rationally designed to be more potent and selective than ibrutinib, theoretically expected to demonstrate fewer adverse effects owing to minimized bystander effects on targets other than BTK.
Nevertheless, acalabrutinib was approved under the FDA's accelerated approval pathway, which is based upon overall response rate and faciliates earlier approval of medicines that treat serious conditions or/and that fill an unmet medical need based on a surrogate endpoint. Continued approval for acalabrutinib's currently accepted indication may subsequently be contingent upon ongoing verification and description of clinical benefit in confimatory trials.
Furthermore, the FDA granted this medication Priority Review and Breakthrough Therapy designations. It also received Orphan Drug designation, which provides incentives to assist and encourage the development of drugs for rare diseases. At this time, more than 35 clinical trials across 40 countries with more than 2500 patients are underway or have been completed with regards to further research into better understanding and expanding the therapeutic uses of acalabrutinib [L1009].
- The treatment of adult patients with Mantle Cell Lymphoma (MCL) who have received at least one prior therapy.
[L10241]
- The treatment of adult patients with chronic lymphocytic leukemia and small lymphocytic lymphoma.
[L10241]
- In combination with [rituximab] and [bendamustine] for the treatment of adult patients with previously untreated mantle cell lymphoma (MCL) who are ineligible for autologous hematopoietic stem cell transplantation (HSCT).
[L42795]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 643 interactions
[L10241]
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) [L1008].
Bruton Tyrosine Kinase (BTK) is a signalling molecule of the B-cell antigen receptor and cytokine receptor pathways. Such BTK signaling causes the activation of pathways necessary for B-cell proliferation, trafficking, chemotaxis, and adhesion.[L10241]
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.[A31253][L1008] As a result, acalabrutinib inhibits BTK-mediated activation of downstream signaling proteins CD86 and CD69, which ultimately inhibits malignant B-cell proliferation and survival[L1008]
Whereas ibrutinib is typically recognized as the first-in-class BTK inhibitor,[A31253] 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.[A31253]
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.
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L10241]
[L10241]
The half-life of the active metabolite, ACP-5862, is about 6.9 hours.
[L10241]
[L10241]
In vitro experiments at physiologic concentrations show that acalabrutinib can be 93.7% bound to human serum albumin and 41.1% bound to alpha-1-acid glycoprotein.
[A188027]
[L10241]
[L10241]
[L10241]
An irradiated dose of acalabrutinib was 34.7% recovered as the metabolite ACP-5862; 8.6% was recovered as unchanged acalabrutinub; 10.8 was recovered as a mixture of the M7, M8, M9, M10, and M11 metabolites; 5.9% was the M25 metabolite; 2.5% was recovered as the M3 metabolite.
[A188027]
[L10241]
Proteins and enzymes this drug interacts with in the body
PMID:19290921
Binding of antigen to the B-cell antigen receptor (BCR) triggers signaling that ultimately leads to B-cell activation .
PMID:19290921
After BCR engagement and activation at the plasma membrane, phosphorylates PLCG2 at several sites, igniting the downstream signaling pathway through calcium mobilization, followed by activation of the protein kinase C (PKC) family members .
PMID:11606584
PLCG2 phosphorylation is performed in close cooperation with the adapter protein B-cell linker protein BLNK .
PMID:11606584
BTK acts as a platform to bring together a diverse array of signaling proteins and is implicated in cytokine receptor signaling pathways .
PMID:16517732 PMID:17932028
Plays an important role in the function of immune cells of innate as well as adaptive immunity, as a component of the Toll-like receptors (TLR) pathway .
PMID:16517732
The TLR pathway acts as a primary surveillance system for the detection of pathogens and are crucial to the activation of host defense .
PMID:16517732
Especially, is a critical molecule in regulating TLR9 activation in splenic B-cells .
PMID:16517732 PMID:17932028
Within the TLR pathway, induces tyrosine phosphorylation of TIRAP which leads to TIRAP degradation .
PMID:16415872
BTK also plays a critical role in transcription regulation .
PMID:19290921
Induces the activity of NF-kappa-B, which is involved in regulating the expression of hundreds of genes .
PMID:19290921
BTK is involved on the signaling pathway linking TLR8 and TLR9 to NF-kappa-B .
PMID:19290921
Acts as an activator of NLRP3 inflammasome assembly by mediating phosphorylation of NLRP3 .
PMID:34554188
Transiently phosphorylates transcription factor GTF2I on tyrosine residues in response to BCR .
PMID:9012831
GTF2I then translocates to the nucleus to bind regulatory enhancer elements to modulate gene expression .
PMID:9012831
ARID3A and NFAT are other transcriptional target of BTK .
PMID:16738337
BTK is required for the formation of functional ARID3A DNA-binding complexes .
PMID:16738337
There is however no evidence that BTK itself binds directly to DNA .
PMID:16738337
BTK has a dual role in the regulation of apoptosis .
PMID:9751072
Plays a role in STING1-mediated induction of type I interferon (IFN) response by phosphorylating DDX41 PMID:25704810
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
Appears to function in modulating the activity of the immune system during the acute-phase reaction
ATC L01EL02
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Acalabrutinib
Additional database identifiers
Drugs Product Database (DPD)
23350
ChemSpider
36764951
BindingDB
50175583
PDB
XQQ
ZINC
ZINC000208774715
HUGO Gene Nomenclature Committee (HGNC)
HGNC:1133
GenAtlas
BTK
GeneCards
BTK
GenBank Gene Database
X58957
GenBank Protein Database
312467
Guide to Pharmacology
1948
UniProt Accession
BTK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:17450
GeneCards
CYP3A43
GenBank Gene Database
AF319634
GenBank Protein Database
12642642
UniProt Accession
CP343_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2640
GeneCards
CYP3A7
GenBank Gene Database
D00408
GenBank Protein Database
220149
UniProt Accession
CP3A7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8499
GeneCards
ORM2
GenBank Gene Database
BC015964
GenBank Protein Database
16359000
UniProt Accession
A1AG2_HUMAN
Patent information
9 active patents
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
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