Apalutamide

Identification

Summary

Apalutamide is an androgen receptor inhibitor used to treat non-metastatic castration-resistant and metastatic castration-sensitive prostate cancer.

Brand Names

Erleada

Generic Name

Apalutamide

DrugBank Accession Number

DB11901

Background

Apalutamide is a potent androgen receptor (AR) antagonist that selectively binds to the ligand-binding domain of AR and blocks AR nuclear translocation or binding to androgen response elements ¹. It has been used in trials studying the treatment of Prostate Cancer, Hepatic Impairment, Prostatic Neoplasms, Castration-Resistant Prostate Cancer, and Prostatic Neoplasms, Castration-Resistant, among others. Exerting an antitumor action, apalutamide blocking the effect of androgens that promote tumor growth. It targets the AR ligand-binding domain and prevents AR nuclear translocation, DNA binding, and transcription of AR gene targets in prostate tumors ¹. In mice bearing human CRPC xenograft models, apalutamide treatment produced tumor regressions in a dose-dependent manner that was more effective than that of Bicalutamide or Enzalutamide. Unlike bicalutamide, apalutamide antagonized AR-mediated signaling in AR overexpressing human CRPC cell lines ¹.

Androgen-deprivation therapy, or hormone therapy, can be used as part of maintenance therapy for patients with non-metastatic prostate cancer. Although most patients achieve therapeutic responses at the initial hormone therapy, many patients progress to non-metastatic castration-resistant (resistance to hormone therapy) prostate cancer which is the second-most common cause of cancer-related deaths in American males ². Castration-resistant prostate cancer is often incurable, which poses significant clinical challenges for patients. Approximately 10 to 20 % of prostate cancer cases are castration-resistant, and up to 16% of these patients show no evidence of cancer metastasis at the time of castration-resistant diagnosis ⁵. Higher prostate-specific antigen (PSA) and shorter PSA doubling time (PSA DT) are associated with a higher risk for metastases and death ¹. In a phase-2 multicenter open-label study, 89% of patients with non-metastatic, castration-resistant prostate cancer had ≥50% PSA decline at week 12 of apalutamide treatment ¹. In a randomized trial, the median metastasis-free survival for patients taking apalutamide was 40.5 months compared to 16.2 months for patients taking a placebo ⁵. Apalutamide displayed good tolerability and safety profile in clinical studies.

Apalutamide was approved in February 2018 by the FDA as Erleada for the treatment of patients with non-metastatic prostate cancer that is resistant to treatment with hormone therapy (castration-resistant). It is available as oral tablets. Apalutamide is the first FDA-approved treatment for non-metastatic, castration-resistant prostate cancer ⁵.

Type

Small Molecule

Groups

Approved, Investigational

Structure

3D

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MOLSDF3D-SDFPDBSMILESInChI

Similar Structures

Structure for Apalutamide (DB11901)

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Weight

Average: 477.44
Monoisotopic: 477.088258569

Chemical Formula

C₂₁H₁₅F₄N₅O₂S

Synonyms

• Apalutamide

External IDs

• JNJ-56021927

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Pharmacology

Indication

Apalutamide is indicated for the treatment of patients with metastatic castration-sensitive prostate cancer and non-metastatic castration-resistant prostate cancer.⁶

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Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics	Dose Form
Treatment of	Metastatic castration sensitive prostate cancer		••••••••••••			••••••
Used as adjunct in combination for therapy	Metastatic hormone-sensitive prostate cancer (mhspc)		••••••••••••	•••••		••••••
Treatment of	Non-metastatic castration-resistant prostate cancer		••••••••••••	•••••	•••• •••• •• •••••••••• •••••••••• •••••••	••••••
Treatment of	Non-metastatic castration-resistant prostate cancer		••••••••••••			••••••

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Associated Therapies

• Androgen Deprivation Therapy

Contraindications & Blackbox Warnings

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Pharmacodynamics

In androgen receptors (AR)-overexpressing LNCaP cells, apaludatamide was reported to have a 7 to 10-fold greater affinity to the AR than bicalutamide.³ Additionally, apalutamide still possesses total antagonistic activity in AR-overexpressing cell lines with bicalutamide-resistance mutations such as T878A and W741C.⁴ In castrate mice with LNCaP/AR(cs) tumors, apalutamide produced tumor regression (defined by >50% regression in tumor volume) in 8 mice compared to only 1 for bicalutamide.² The apalutamide-treated tumors also have a 60% decrease in proliferative index and a 10-fold increase in apoptotic rate compared with vehicle.²

In an open-label, uncontrolled, multicenter, single-arm dedicated QT study in 45 patients with CRPC, an exposure-QT analysis suggested a concentration-dependent increase in QTcF for apalutamide and its active metabolite. Apalutamide demonstrated antitumor activity in the mouse xenograft models of prostate cancer, where it decreased tumor cell proliferation and reduced tumor volume.⁶

Mechanism of action

Persistent androgen receptor (AR) signaling is a common feature of castration-resistant prostate cancer (CRPC), attributed to AR gene amplification, AR gene mutation, increased AR expression, or increased androgen biosynthesis in prostate tumors.² Apalutamide is an antagonist of AR that binds directly to the ligand-binding domain of the AR with the IC50 of 16 nM. Upon binding, apalutamide disrupts AR signalling, inhibits DNA binding, and impedes AR-mediated gene transcription.⁶ Apalutamide impairs the translocation of AR from the cytoplasm to the nucleus thus reducing the concentrations of AR available to interact with the androgen response elements (AREs).² Upon treatment with apalutamide, AR was not recruited to the DNA promoter regions.²

Its main metabolite, N-desmethyl apalutamide, is a less potent inhibitor of AR, and exhibited one-third of the activity of apalutamide in an in vitro transcriptional reporter assay.⁶

Target	Actions	Organism
AAndrogen receptor	antagonist	Humans
NGABA(A) Receptor	antagonist	Humans

Absorption

Mean absolute oral bioavailability was approximately 100%. The median time to achieve peak plasma concentration (t_max) was 2 hours (range: 1 to 5 hours). The major active metabolite N-desmethyl apalutamide C_max was 5.9 mcg/mL (1.0) and AUC was 124 mcg·h/mL (23) at steady-state after the recommended dosage. Administration of apalutamide to healthy subjects under fasting conditions and with a high-fat meal (approximately 500 to 600 fat calories, 250 carbohydrate calories, and 150 protein calories) resulted in no clinically relevant changes in C_max and AUC. The median time to reach t_max was delayed approximately 2 hours with food.⁶

Following administration of the recommended dosage, apalutamide steady-state was achieved after 4 weeks and the mean accumulation ratio was approximately 5-fold. Apalutamide C_max was 6.0 mcg/mL (1.7) and AUC was 100 mcg·h/mL (32) at steady-state. Daily fluctuations in apalutamide plasma concentrations were low, with the mean peak-to-trough ratio of 1.63.⁶

Oral administration of four 60 mg apalutamide tablets dispersed in applesauce resulted in no clinically relevant changes in Cmax and AUC compared to the administration of four intact 60 mg tablets under fasting conditions.⁶

Volume of distribution

The mean apparent volume of distribution at steady state of apalutamide was approximately 276 L.⁶

Protein binding

Apalutamide was 96% and N-desmethyl apalutamide was 95% bound to plasma proteins with no concentration dependency.⁶

Metabolism

Metabolism is the main route of elimination of apalutamide. Apalutamide is primarily metabolized by CYP2C8 and CYP3A4 to form active metabolite, N-desmethyl apalutamide. The contribution of CYP2C8 and CYP3A4 in the metabolism of apalutamide is estimated to be 58% and 13% following single dose but changes to 40% and 37%, respectively at steady-state.⁶ The auto-induction of CYP3A4-mediated metabolism by apalutamide may explain the increase in CYP3A4 enzymatic activity at steady-state.⁶

Hover over products below to view reaction partners

• Apalutamide
  • N-desmethyl apalutamide
    • M4 apalutamide

Route of elimination

Apalutamide and its main active metabolite are subject to both renal and focal elimination. Up to 70 days following a single oral administration of radiolabeled apalutamide, 65% of the dose was recovered in urine (1.2% of dose as unchanged apalutamide and 2.7% as N-desmethyl apalutamide) and 24% was recovered in feces (1.5% of dose as unchanged apalutamide and 2% as N-desmethyl apalutamide).⁶

Half-life

The mean effective half-life for apalutamide in patients with NM-CRPC was approximately 3 days at steady-state.⁶

Clearance

The CL/F of apalutamide was 1.3 L/h after single dosing and increased to 2.0 L/h at steady-state after once-daily dosing likely due to CYP3A4 auto-induction.⁶ The auto-induction effect likely reached its maximum at the recommended dosage because exposure to apalutamide across the dose range of 30 to 480 mg is dose-proportional.⁶

Adverse Effects

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Toxicity

There is no known specific antidote for apalutamide overdose. In the event of an overdose, stop apalutamide, undertake general supportive measures until clinical toxicity has been diminished or resolved.⁶

The safety and efficacy of apalutamide have not been established in females. Based on findings from animals and its mechanism of action, apalutamide can cause fetal harm and loss of pregnancy when administered to a pregnant female. There are no available data on apalutamide use in pregnant women to inform a drug-associated risk. In an animal reproduction study, oral administration of apalutamide to pregnant rats during and after organogenesis resulted in fetal abnormalities and embryo-fetal lethality at maternal exposures ≥ 2 times the human clinical exposure (AUC) at the recommended dose.⁶

In a 2-year carcinogenicity study in male rats, apalutamide was administered by oral gavage at doses of 5, 15 and 50 mg/kg/day. Apalutamide increased the incidence of Leydig interstitial cell adenoma in the testes at doses ≥ 5 mg/kg/day (0.2 times the human exposure based on AUC). The findings in the testes are considered to be related to the pharmacological activity of apalutamide. Rats are regarded as more sensitive than humans to developing interstitial cell tumors in the testes. Oral administration of apalutamide to male rasH2 transgenic mice for 6 months did not result in increased incidence of neoplasms at doses up to 30 mg/kg/day.⁶

Apalutamide did not induce mutations in the bacterial reverse mutation (Ames) assay and was not genotoxic in either in vitro chromosome aberration assay or the in vivo rat bone marrow micronucleus assay or the in vivo rat Comet assay. In repeat-dose toxicity studies in male rats (up to 26 weeks) and dogs (up to 39 weeks), atrophy of the prostate gland and seminal vesicles, aspermia/hypospermia, tubular degeneration and/or hyperplasia or hypertrophy of the interstitial cells in the reproductive system were observed at ≥ 25 mg/kg/day in rats (1.4 times the human exposure based on AUC) and ≥ 2.5 mg/kg/day in dogs (0.9 times the human exposure based on AUC).⁶

In a fertility study in male rats, a decrease in sperm concentration and motility, increased abnormal sperm morphology, lower copulation and fertility rates (upon pairing with untreated females) along with reduced weights of the secondary sex glands and epididymis were observed following 4 weeks of dosing at ≥ 25 mg/kg/day (0.8 times the human exposure based on AUC). A reduced number of live fetuses due to increased pre- and/or post-implantation loss was observed following 4 weeks of 150 mg/kg/day administration (5.7 times the human exposure based on AUC). Effects on male rats were reversible after 8 weeks from the last apalutamide administration.⁶

Pathways

Not Available

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Not Available

Interactions

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This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

• Approved
• Vet approved
• Nutraceutical
• Illicit
• Withdrawn
• Investigational
• Experimental
• All Drugs

Drug	Interaction
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1,2-Benzodiazepine	The serum concentration of 1,2-Benzodiazepine can be decreased when it is combined with Apalutamide.
Abacavir	Abacavir may decrease the excretion rate of Apalutamide which could result in a higher serum level.
Abametapir	The serum concentration of Apalutamide can be increased when it is combined with Abametapir.
Abatacept	The metabolism of Apalutamide can be increased when combined with Abatacept.
Abemaciclib	The serum concentration of Abemaciclib can be decreased when it is combined with Apalutamide.

Food Interactions

• Take at the same time every day.
• Take with or without food.

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Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Erleada	Tablet	60 mg	Oral	Janssen Pharmaceuticals	2018-07-27	Not applicable
Erleada	Tablet, film coated	240 mg	Oral	Janssen Cilag International Nv	2023-11-28	Not applicable
Erleada	Tablet, film coated	60 mg	Oral	Janssen Cilag International Nv	2020-12-16	Not applicable
Erleada	Tablet	240 mg	Oral	Janssen Pharmaceuticals	2023-11-01	Not applicable
Erleada	Tablet, film coated	60 mg/1	Oral	Janssen Products, LP	2018-02-14	Not applicable

Categories

ATC Codes

L02BB05 — Apalutamide

• L02BB — Anti-androgens
• L02B — HORMONE ANTAGONISTS AND RELATED AGENTS
• L02 — ENDOCRINE THERAPY
• L — ANTINEOPLASTIC AND IMMUNOMODULATING AGENTS

Drug Categories

• Androgen Receptor Inhibitors
• Antiandrogens
• Antineoplastic Agents
• Antineoplastic and Immunomodulating Agents
• BCRP/ABCG2 Inducers
• Cytochrome P-450 CYP2C19 Inducers
• Cytochrome P-450 CYP2C19 Inducers (strong)
• Cytochrome P-450 CYP2C8 Substrates
• Cytochrome P-450 CYP2C9 Inducers
• Cytochrome P-450 CYP2C9 Inducers (weak)
• Cytochrome P-450 CYP3A Inducers
• Cytochrome P-450 CYP3A Inducers (strong)
• Cytochrome P-450 CYP3A Substrates
• Cytochrome P-450 CYP3A4 Inducers
• Cytochrome P-450 CYP3A4 Inducers (strong)
• Cytochrome P-450 CYP3A4 Substrates
• Cytochrome P-450 Enzyme Inducers
• Cytochrome P-450 Substrates
• Drugs that are Mainly Renally Excreted
• Endocrine Therapy
• Hormone Antagonists and Related Agents
• Imidazoles
• Imidazolidines
• MATE 1 Inhibitors
• MATE 2 Inhibitors
• MATE inhibitors
• OAT3/SLC22A8 Inhibitors
• OATP1B1/SLCO1B1 Inducers
• OCT2 Inhibitors
• P-glycoprotein inducers
• Prostatic Neoplasms, drug therapy

Chemical TaxonomyProvided by Classyfire

Description

This compound belongs to the class of organic compounds known as phenylimidazolidines. These are polycyclic compounds containing an imidazoline substituted by a phenyl group.

Kingdom

Organic compounds

Super Class

Organoheterocyclic compounds

Class

Azolidines

Sub Class

Imidazolidines

Direct Parent

Phenylimidazolidines

Alternative Parents

2-halobenzoic acids and derivatives / Alpha amino acids and derivatives / N-phenylthioureas / Benzamides / Benzoyl derivatives / Fluorobenzenes / Pyridines and derivatives / Imidazolidinones / Aryl fluorides / Vinylogous halides / Heteroaromatic compounds / Thioureas / Secondary carboxylic acid amides / Nitriles / Azacyclic compounds / Carbonyl compounds / Hydrocarbon derivatives / Organic oxides / Alkyl fluorides / Organofluorides

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Substituents

2-halobenzoic acid or derivatives / Alkyl fluoride / Alkyl halide / Alpha-amino acid or derivatives / Aromatic heteropolycyclic compound / Aryl fluoride / Aryl halide / Azacycle / Benzamide / Benzenoid / Benzoic acid or derivatives / Benzoyl / Carbonitrile / Carbonyl group / Carboxamide group / Carboxylic acid derivative / Cyanide / Fluorobenzene / Halobenzene / Halobenzoic acid or derivatives / Heteroaromatic compound / Hydrocarbon derivative / Imidazolidinone / Monocyclic benzene moiety / N-phenylthiourea / Nitrile / Organic nitrogen compound / Organic oxide / Organic oxygen compound / Organofluoride / Organohalogen compound / Organonitrogen compound / Organooxygen compound / Organosulfur compound / Phenylimidazolidine / Pyridine / Secondary carboxylic acid amide / Thiourea / Vinylogous halide

show 29 more

Molecular Framework

Aromatic heteropolycyclic compounds

External Descriptors

Not Available

Affected organisms

• Humans and other mammals

Chemical Identifiers

UNII

4T36H88UA7

CAS number

956104-40-8

InChI Key

HJBWBFZLDZWPHF-UHFFFAOYSA-N

InChI

InChI=1S/C21H15F4N5O2S/c1-27-17(31)13-4-3-11(8-15(13)22)30-19(33)29(18(32)20(30)5-2-6-20)12-7-14(21(23,24)25)16(9-26)28-10-12/h3-4,7-8,10H,2,5-6H2,1H3,(H,27,31)

IUPAC Name

4-{7-[6-cyano-5-(trifluoromethyl)pyridin-3-yl]-8-oxo-6-sulfanylidene-5,7-diazaspiro[3.4]octan-5-yl}-2-fluoro-N-methylbenzamide

SMILES

CNC(=O)C1=CC=C(C=C1F)N1C(=S)N(C(=O)C11CCC1)C1=CC(=C(N=C1)C#N)C(F)(F)F

References

General References

1. Smith MR, Antonarakis ES, Ryan CJ, Berry WR, Shore ND, Liu G, Alumkal JJ, Higano CS, Chow Maneval E, Bandekar R, de Boer CJ, Yu MK, Rathkopf DE: Phase 2 Study of the Safety and Antitumor Activity of Apalutamide (ARN-509), a Potent Androgen Receptor Antagonist, in the High-risk Nonmetastatic Castration-resistant Prostate Cancer Cohort. Eur Urol. 2016 Dec;70(6):963-970. doi: 10.1016/j.eururo.2016.04.023. Epub 2016 May 6. [Article]
2. Clegg NJ, Wongvipat J, Joseph JD, Tran C, Ouk S, Dilhas A, Chen Y, Grillot K, Bischoff ED, Cai L, Aparicio A, Dorow S, Arora V, Shao G, Qian J, Zhao H, Yang G, Cao C, Sensintaffar J, Wasielewska T, Herbert MR, Bonnefous C, Darimont B, Scher HI, Smith-Jones P, Klang M, Smith ND, De Stanchina E, Wu N, Ouerfelli O, Rix PJ, Heyman RA, Jung ME, Sawyers CL, Hager JH: ARN-509: a novel antiandrogen for prostate cancer treatment. Cancer Res. 2012 Mar 15;72(6):1494-503. doi: 10.1158/0008-5472.CAN-11-3948. Epub 2012 Jan 20. [Article]
3. Rathkopf DE, Scher HI: Apalutamide for the treatment of prostate cancer. Expert Rev Anticancer Ther. 2018 Sep;18(9):823-836. doi: 10.1080/14737140.2018.1503954. [Article]
4. Joseph JD, Lu N, Qian J, Sensintaffar J, Shao G, Brigham D, Moon M, Maneval EC, Chen I, Darimont B, Hager JH: A clinically relevant androgen receptor mutation confers resistance to second-generation antiandrogens enzalutamide and ARN-509. Cancer Discov. 2013 Sep;3(9):1020-9. doi: 10.1158/2159-8290.CD-13-0226. Epub 2013 Jun 18. [Article]
5. FDA Press Announcements: FDA approves new treatment for a certain type of prostate cancer using novel clinical trial endpoint [Link]
6. FDA Approved Drug Products: ERLEADA® (apalutamide) tablets, for oral use [Link]
7. EMA Approved Drug Products: ERLEADA® (apalutamide) tablets, for oral use [Link]

External Links

Human Metabolome Database

HMDB0248608

PubChem Compound

24872560

PubChem Substance

347828234

ChemSpider

28424131

BindingDB

50094975

RxNav

1999574

ChEMBL

CHEMBL3183409

ZINC

ZINC000043174901

Wikipedia

Apalutamide

FDA label

Download (233 KB)

Clinical Trials

Clinical Trials Learn More" title="About Clinical Trials" id="clinical-trials-info" class="drug-info-popup" href="javascript:void(0);">

Phase	Status	Purpose	Conditions	Count
4	Active Not Recruiting	Treatment	Neoplasms of the Prostate	1
4	Recruiting	Screening	Metastatic Castration Sensitive Prostate Cancer (mCSPC)	1
3	Active Not Recruiting	Treatment	Neoplasms of the Prostate	4
3	Active Not Recruiting	Treatment	Prostate Cancer	3
3	Recruiting	Treatment	Adenocarcinoma of Prostate / Biochemically Recurrent Prostate Carcinoma / Metastatic Carcinoma of the Prostate / Stage IVB Prostate Cancer AJCC v8	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
Tablet	Oral	240 mg
Tablet	Oral	60 mg
Tablet	Oral	60.000 mg
Tablet, coated	Oral	60 mg
Tablet, film coated	Oral
Tablet, film coated	Oral	240 mg/1
Tablet, film coated	Oral	240 mg
Tablet, film coated	Oral	60 mg/1
Tablet, film coated	Oral	60 mg

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
US9481663	No	2016-11-01	2033-06-04
US8802689	No	2014-08-12	2027-03-27
US8445507	No	2013-05-21	2030-09-15
US9884054	No	2018-02-06	2033-09-23
US9388159	No	2016-07-12	2027-03-27
US10052314	No	2018-08-21	2033-09-23
US9987261	No	2018-06-05	2027-03-27
US10849888	No	2020-12-01	2033-09-23
US10702508	No	2020-07-07	2038-04-30
USRE49353	No	2013-09-23	2033-09-23

Properties

State

Solid

Experimental Properties

Property	Value	Source
water solubility	practically insoluble in aqueous media	L45538

Predicted Properties

Property	Value	Source
Water Solubility	0.00178 mg/mL	ALOGPS
logP	3.05	ALOGPS
logP	3.46	Chemaxon
logS	-5.4	ALOGPS
pKa (Strongest Acidic)	13.05	Chemaxon
pKa (Strongest Basic)	-0.75	Chemaxon
Physiological Charge	0	Chemaxon
Hydrogen Acceptor Count	4	Chemaxon
Hydrogen Donor Count	1	Chemaxon
Polar Surface Area	89.33 Å2	Chemaxon
Rotatable Bond Count	4	Chemaxon
Refractivity	113.6 m3·mol-1	Chemaxon
Polarizability	43.44 Å3	Chemaxon
Number of Rings	4	Chemaxon
Bioavailability	1	Chemaxon
Rule of Five	Yes	Chemaxon
Ghose Filter	Yes	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	No	Chemaxon

Predicted ADMET Features

Not Available

Spectra

Mass Spec (NIST)

Not Available

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-004i-0000900000-b6c2978b61a4c909c43d
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-004i-0001900000-62189e26573bdc232663
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0a4j-0002900000-edde52e50f19648bc71b
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0002-0001900000-b9e037c5d63941ef3d0d
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0umr-0324900000-b47e8767435c3fb7f549
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-08i0-0193200000-cb5e11874b3f9fd8cf31
Predicted 1H NMR Spectrum	1D NMR	Not Applicable
Predicted 13C NMR Spectrum	1D NMR	Not Applicable

Chromatographic Properties

Collision Cross Sections (CCS)

Adduct	CCS Value (Å2)	Source type	Source
[M-H]-	195.70319	predicted	DeepCCS 1.0 (2019)
[M+H]+	198.09874	predicted	DeepCCS 1.0 (2019)
[M+Na]+	204.01128	predicted	DeepCCS 1.0 (2019)

Targets

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Details1. Androgen receptor

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Antagonist

Curator comments

IC50=16 nM

General Function

Zinc ion binding

Specific Function

Steroid hormone receptors are ligand-activated transcription factors that regulate eukaryotic gene expression and affect cellular proliferation and differentiation in target tissues. Transcription ...

Gene Name

AR

Uniprot ID

P10275

Uniprot Name

Androgen receptor

Molecular Weight

98987.9 Da

References

1. Clegg NJ, Wongvipat J, Joseph JD, Tran C, Ouk S, Dilhas A, Chen Y, Grillot K, Bischoff ED, Cai L, Aparicio A, Dorow S, Arora V, Shao G, Qian J, Zhao H, Yang G, Cao C, Sensintaffar J, Wasielewska T, Herbert MR, Bonnefous C, Darimont B, Scher HI, Smith-Jones P, Klang M, Smith ND, De Stanchina E, Wu N, Ouerfelli O, Rix PJ, Heyman RA, Jung ME, Sawyers CL, Hager JH: ARN-509: a novel antiandrogen for prostate cancer treatment. Cancer Res. 2012 Mar 15;72(6):1494-503. doi: 10.1158/0008-5472.CAN-11-3948. Epub 2012 Jan 20. [Article]

Details2. GABA(A) Receptor (Protein Group)

Kind

Protein group

Organism

Humans

Pharmacological action

No

Actions

Antagonist

Curator comments

Apalutamide exhibits low micromolar affinity (IC50=3.0uM) for the GABAA receptor in radioligand binding-assays.

General Function

Inhibitory extracellular ligand-gated ion channel activity

Specific Function

Component of the heteropentameric receptor for GABA, the major inhibitory neurotransmitter in the vertebrate brain. Functions also as histamine receptor and mediates cellular responses to histamine...

---

Components:

Name	UniProt ID
Gamma-aminobutyric acid receptor subunit alpha-1	P14867
Gamma-aminobutyric acid receptor subunit alpha-2	P47869
Gamma-aminobutyric acid receptor subunit alpha-3	P34903
Gamma-aminobutyric acid receptor subunit alpha-4	P48169
Gamma-aminobutyric acid receptor subunit alpha-5	P31644
Gamma-aminobutyric acid receptor subunit alpha-6	Q16445
Gamma-aminobutyric acid receptor subunit beta-1	P18505
Gamma-aminobutyric acid receptor subunit beta-2	P47870
Gamma-aminobutyric acid receptor subunit beta-3	P28472
Gamma-aminobutyric acid receptor subunit delta	O14764
Gamma-aminobutyric acid receptor subunit epsilon	P78334
Gamma-aminobutyric acid receptor subunit gamma-1	Q8N1C3
Gamma-aminobutyric acid receptor subunit gamma-2	P18507
Gamma-aminobutyric acid receptor subunit gamma-3	Q99928
Gamma-aminobutyric acid receptor subunit pi	O00591
Gamma-aminobutyric acid receptor subunit theta	Q9UN88

References

1. Clegg NJ, Wongvipat J, Joseph JD, Tran C, Ouk S, Dilhas A, Chen Y, Grillot K, Bischoff ED, Cai L, Aparicio A, Dorow S, Arora V, Shao G, Qian J, Zhao H, Yang G, Cao C, Sensintaffar J, Wasielewska T, Herbert MR, Bonnefous C, Darimont B, Scher HI, Smith-Jones P, Klang M, Smith ND, De Stanchina E, Wu N, Ouerfelli O, Rix PJ, Heyman RA, Jung ME, Sawyers CL, Hager JH: ARN-509: a novel antiandrogen for prostate cancer treatment. Cancer Res. 2012 Mar 15;72(6):1494-503. doi: 10.1158/0008-5472.CAN-11-3948. Epub 2012 Jan 20. [Article]

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Drug created at October 20, 2016 20:58 / Updated at December 05, 2023 12:31