Lorlatinib

Identification

Summary

Lorlatinib is an anaplastic lymphoma kinase inhibitor used to treat anaplastic lymphoma kinase positive metastatic non small cell lung cancer.

Brand Names

Lorbrena

Generic Name

Lorlatinib

DrugBank Accession Number

DB12130

Background

Lorlatinib is a third-generation ALK tyrosine kinase inhibitor (TKI) for patients with ALK-positive metastatic non-small cell lung cancer¹¹ which was first approved by the US FDA in November of 2018. It was subsequently approved by the EMA in 2019 for the treatment of select patients with previously treated advanced ALK-positive non-small cell lung cancer, followed by an expanded approval in 2022 to include lorlatinib as a first-line treatment option in advanced ALK-positive NSCLC. ¹²

Type

Small Molecule

Groups

Approved, Investigational

Structure

3D

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MOLSDF3D-SDFPDBSMILESInChI

Similar Structures

Structure for Lorlatinib (DB12130)

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Weight

Average: 406.421
Monoisotopic: 406.155352039

Chemical Formula

C₂₁H₁₉FN₆O₂

Synonyms

• Lorlatinib

External IDs

• PF 06463922
• PF-06463922

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Pharmacology

Indication

Lorlatinib is indicated for the treatment of adult patients with ALK-positive metastatic non-small cell lung cancer (NSCLC).¹¹ In the EU, it is indicated for the treatment of adult patients with ALK-positive advanced NSCLC not previously treated with an ALK inhibitor, or whose disease has progressed after using either alectinib or ceritinib, or crizotinib and at least one other ALK inhibitor.¹²

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Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics	Dose Form
Treatment of	Advanced non-small cell lung cancer (nsclc)		••••••••••••	•••••	••••••• ••••••••••• ••••• •••••••••• ••• •• ••• •••••••••	••••••• •••• ••••••
Treatment of	Advanced non-small cell lung cancer (nsclc)		••••••••••••	•••••	••••••• ••••••••••• ••••• ••••••••• •• •••••••••	••••••• •••• ••••••
Treatment of	Advanced non-small cell lung cancer (nsclc)		••••••••••••	•••••		••••••• •••• ••••••
Treatment of	Metastatic non-small cell lung cancer		••••••••••••	•••••		••••••

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Pharmacodynamics

Based on data from Study B7461001, exposure-response relationships for Grade 3 or 4 hypercholesterolemia and for any Grade 3 or 4 adverse reaction were observed at steady-state exposures achieved at the recommended dosage, with higher probability of the occurrence of adverse reactions with increasing lorlatinib exposure ^Label.

In 295 patients who received lorlatinib at the recommended dosage of 100 mg once daily and had an ECG measurement in the same Study B7461001, the maximum mean change from baseline for their PR interval was 16.4 ms (2-sided 90% upper confidence interval [CI] 19.4 ms) ^Label. Among the 284 patients with PR interval <200 ms at baseline, 14% had PR interval prolongation ≥200 ms after starting use with lorlatinib ^Label. The prolongation of PR interval occurred in a concentration-dependent manner and atrioventricular block occurred in 1% of patients ^Label.

Finally, in 275 patients who received lorlatinib at the recommended dosage in the activity-estimating portion of Study B7461001, no large mean increases from baseline in the QTcF interval (i.e., >20 ms) were detected ^Label.

Mechanism of action

Non-small cell lung cancer (NSCLC) accounts for up to 85% of lung cancer cases worldwide and remains a particularly difficult to treat condition ¹⁰. The gene rearrangement of anaplastic lymphoma kinase (ALK) is a genetic alteration that drives the development of NSCLC in a number of patients ^6,7. Ordinarily, ALK is a natural endogenous tyrosine kinase receptor that plays an important role in the development of the brain and elicits activity on various specific neurons in the nervous system ^2,5,6.

Subsequnetly, lorlatinib is a kinase inhibitor with in vitro activity against ALK and number of other tyrosine kinase receptor related targets including ROS1, TYK1, FER, FPS, TRKA, TRKB, TRKC, FAK, FAK2, and ACK ^Label. Lorlatinib demonstrated in vitro activity against multiple mutant forms of the ALK enzyme, including some mutations detected in tumors at the time of disease progression on crizotinib and other ALK inhibitors ^Label. Moreover, lorlatinib possesses the capability to cross the blood-brain barrier, allowing it to reach and treat progressive or worsening brain metastases as well ^10,5. The overall antitumor activity of lorlatinib in in-vivo models appears to be dose-dependent and correlated with the inhibition of ALK phosphorylation ^Label.

Although many ALK-positive metastatic NSCLC patients respond to initial tyrosine kinase therapies, such patients also often experience tumor progression ⁸. Various clinical trials performed with lorlatinib, however, have demonstrated its utility to effect tumor regression in ALK-positive metastatic NSCLC patients who experience tumor progression despite current use or having already used various first and second-generation tyrosine kinase inhibitors like crizotinib, alectinib, or ceritinib ⁹.

Target	Actions	Organism
AALK tyrosine kinase receptor	inhibitor	Humans

Absorption

The median lorlatinib Tmax was 1.2 hours (0.5 to 4 hours) following a single oral 100 mg dose and 2 hours (0.5 to 23 hours) following 100 mg orally once daily at steady state ^Label.

The mean absolute bioavailability is 81% (90% CI 75.7%, 86.2%) after oral administration compared to intravenous administration ^Label.

Administration of lorlatinib with a high fat, high-calorie meal (approximately 1000 calories with 150 calories from protein, 250 calories from carbohydrate, and 500 to 600 calories from fat) had no clinically meaningful effect on lorlatinib pharmacokinetics ^Label.

Volume of distribution

The mean (CV%) steady-state volume of distribution (Vss) was 305 L (28%) following a single intravenous dose ^Label.

Protein binding

In vitro, lorlatinib was 66% bound to plasma proteins at a concentration of 2.4 µM ^Label. The blood-to-plasma ratio was 0.99 ^Label.

Metabolism

In vitro, lorlatinib is metabolized primarily by CYP3A4 and UGT1A4, with minor contribution from CYP2C8, CYP2C19, CYP3A5, and UGT1A3 ^Label. In plasma, a benzoic acid metabolite (M8) of lorlatinib resulting from the oxidative cleavage of the amide and aromatic ether bonds of lorlatinib accounted for 21% of the circulating radioactivity in a human [14C] mass balance study ^Label. The oxidative cleavage metabolite, M8, is pharmacologically inactive ^Label.

Route of elimination

Following a single oral 100 mg dose of radiolabeled lorlatinib, 48% of the radioactivity was recovered in urine (<1% as unchanged) and 41% in feces (about 9% as unchanged) ^Label.

Half-life

The mean plasma half-life (t½) of lorlatinib was 24 hours (40%) after a single oral 100 mg dose of lorlatinib ^Label.

Clearance

The mean oral clearance (CL/F) was 11 L/h (35%) following a single oral 100 mg dose and increased to 18 L/h (39%) at steady state, suggesting autoinduction ^Label.

Adverse Effects

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Toxicity

Although there is no formal data available on the use of lorlatinib in pregnant women, based on findings from animal studies and its mechanism of action, it is believed that lorlatinib can cause embryo-fetal harm when administered to a pregnant woman ^Label.

There are no data on the presence of lorlatinib or its metabolites in either human or animal milk or its effects on the breastfed infant or on milk production ^Label. Because of the potential for serious adverse reactions in breastfed infants, instruct women not to breastfeed during treatment with lorlatinib and for 7 days after the final dose ^Label.

Advise female patients of reproductive potential to use effective non-hormonal contraception during treatment with lorlatinib and for at least 6 months after the final dose ^Label. Advise females of reproductive potential to use a non-hormonal method of contraception, because lorlatinib can render hormonal contraceptives ineffective ^Label.

Based on genotoxicity findings, advise males with female partners of reproductive potential to use effective contraception during treatment with lorlatinib and for at least 3 months after the final dose ^Label.

Based on findings from animal studies, use of lorlatinib may transiently impair male fertility ^Label.

The safety and effectiveness of lorlatinib in pediatric patients have not been established ^Label.

Of the 295 patients in Study B7461001 who received 100 mg lorlatinib orally once daily, 18% of patients were aged 65 years or older ^Label. Although data are limited, no clinically important differences in safety or efficacy were observed between patients aged 65 years or older and younger patients ^Label.

No dose adjustment is recommended for patients with mild hepatic impairment (total bilirubin ≤ upper limit of normal [ULN] with AST > ULN or total bilirubin >1 to 1.5 × ULN with any AST) ^Label. The recommended dose of lorlatinib has not been established for patients with moderate or severe hepatic impairment ^Label.

No dose adjustment is recommended for patients with mild or moderate renal impairment (creatinine clearance [CLcr] 30 to 89 mL/min estimated by Cockcroft-Gault) ^Label. The recommended dose of lorlatinib has not been established for patients with severe renal impairment ^Label.

Carcinogenicity studies have not been conducted with lorlatinib ^Label. Lorlatinib was aneugenic in an in vitro assay in human lymphoblastoid TK6 cells and positive for micronuclei formation in vivo in the bone marrow of rats. Lorlatinib was not mutagenic in an in vitro bacterial reverse mutation (Ames) assay ^Label.

Dedicated fertility studies were not conducted with lorlatinib ^Label. Findings in male reproductive organs occurred in repeat-dose toxicity studies and included lower testicular, epididymal, and prostate weights; testicular tubular degeneration/atrophy; prostatic atrophy; and/or epididymal inflammation at 15 mg/kg/day and 7 mg/kg/day in rats and dogs, respectively (approximately 8 and 2 times, respectively, the human exposure at the recommended dose of 100 mg based on AUC) ^Label. The effects on male reproductive organs were reversible ^Label.

Distended abdomen, skin rash, and increased cholesterol and triglycerides occurred in animals ^Label. These findings were accompanied by hyperplasia and dilation of the bile ducts in the liver and acinar atrophy of the pancreas in rats at 15 mg/kg/day and in dogs at 2 mg/kg/day (approximately 8 and 0.5 times, respectively, the human exposure at the recommended dose of 100 mg based on AUC) ^Label. All effects were reversible within the recovery period ^Label.

Pathways

Not Available

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Interactions

Drug Interactions Learn More" title="About Drug Interactions" id="structured-interactions-info" class="drug-info-popup" href="javascript:void(0);">

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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Abametapir	The serum concentration of Lorlatinib can be increased when it is combined with Abametapir.
Abatacept	The metabolism of Lorlatinib can be increased when combined with Abatacept.
Abemaciclib	The serum concentration of Abemaciclib can be decreased when it is combined with Lorlatinib.
Acalabrutinib	The metabolism of Acalabrutinib can be increased when combined with Lorlatinib.
Acenocoumarol	The metabolism of Acenocoumarol can be increased when combined with Lorlatinib.

Food Interactions

• Avoid grapefruit products. Grapefruit inhibits CYP3A metabolism, which may increase the serum concentration of lorlatinib.
• Avoid St. John's Wort. This herb induces the CYP3A metabolism of lorlatinib and may reduce its serum concentration. Co-administration of lorlatinib with St. John's Wort is contraindicated.
• 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
Lorbrena	Tablet	100 mg	Oral	Pfizer Canada Ulc	2019-04-22	Not applicable
Lorbrena	Tablet, film coated	25 mg/1	Oral	Pfizer Laboratories Div Pfizer Inc	2018-11-19	Not applicable
Lorbrena	Tablet	25 mg	Oral	Pfizer Canada Ulc	2019-04-22	Not applicable
Lorbrena	Tablet, film coated	25 mg/1	Oral	U.S. Pharmaceuticals	2023-01-03	Not applicable
Lorbrena	Tablet, film coated	100 mg/1	Oral	Pfizer Laboratories Div Pfizer Inc	2018-11-19	Not applicable

Categories

ATC Codes

L01ED05 — Lorlatinib

• L01ED — Anaplastic lymphoma kinase (ALK) inhibitors
• L01E — PROTEIN KINASE INHIBITORS
• L01 — ANTINEOPLASTIC AGENTS
• L — ANTINEOPLASTIC AND IMMUNOMODULATING AGENTS

Drug Categories

• Amides
• Amines
• Anaplastic lymphoma kinase (ALK) inhibitors
• Antineoplastic Agents
• Antineoplastic and Immunomodulating Agents
• BCRP/ABCG2 Inhibitors
• Cytochrome P-450 CYP2B6 Inducers
• Cytochrome P-450 CYP2B6 Inducers (strength unknown)
• Cytochrome P-450 CYP2C19 Substrates
• Cytochrome P-450 CYP2C8 Substrates
• Cytochrome P-450 CYP3A Inducers
• Cytochrome P-450 CYP3A Inhibitors
• Cytochrome P-450 CYP3A Substrates
• Cytochrome P-450 CYP3A4 Inducers
• Cytochrome P-450 CYP3A4 Inducers (strength unknown)
• Cytochrome P-450 CYP3A4 Inhibitors
• Cytochrome P-450 CYP3A4 Inhibitors (strength unknown)
• Cytochrome P-450 CYP3A4 Substrates
• Cytochrome P-450 CYP3A5 Substrates
• Cytochrome P-450 Enzyme Inducers
• Cytochrome P-450 Enzyme Inhibitors
• Cytochrome P-450 Substrates
• Kinase Inhibitor
• Lactams
• MATE 1 Inhibitors
• MATE inhibitors
• OAT3/SLC22A8 Inhibitors
• Organic Cation Transporter 1 Inhibitors
• P-glycoprotein inducers
• Protein Kinase Inhibitors
• Pyridines
• UGT1A3 substrates

Chemical TaxonomyProvided by Classyfire

Description

This compound belongs to the class of organic compounds known as macrolactams. These are cyclic amides of amino carboxylic acids, having a 1-azacycloalkan-2-one structure, or analogues having unsaturation or heteroatoms replacing one or more carbon atoms of the ring. They are nitrogen analogues (the a nitrogen atom replacing the o atom of the cyclic carboxylic acid group ) of the naturally occurring macrolides.

Kingdom

Organic compounds

Super Class

Phenylpropanoids and polyketides

Class

Macrolactams

Sub Class

Not Available

Direct Parent

Macrolactams

Alternative Parents

Pyrazolylpyridines / Alkyl aryl ethers / Aminopyridines and derivatives / Aryl fluorides / Benzenoids / Imidolactams / Tertiary carboxylic acid amides / Pyrazoles / Heteroaromatic compounds / Amino acids and derivatives / Lactams / Oxacyclic compounds / Azacyclic compounds / Nitriles / Organic oxides / Primary amines / Organofluorides / Hydrocarbon derivatives

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Substituents

3-pyrazolylpyridine / Alkyl aryl ether / Amine / Amino acid or derivatives / Aminopyridine / Aromatic heteropolycyclic compound / Aryl fluoride / Aryl halide / Azacycle / Azole / Benzenoid / Carbonitrile / Carboxamide group / Carboxylic acid derivative / Cyanide / Ether / Heteroaromatic compound / Hydrocarbon derivative / Imidolactam / Lactam / Macrolactam / Nitrile / Organic nitrogen compound / Organic oxide / Organic oxygen compound / Organofluoride / Organohalogen compound / Organoheterocyclic compound / Organonitrogen compound / Organooxygen compound / Oxacycle / Primary amine / Pyrazole / Pyridine / Tertiary carboxylic acid amide

show 25 more

Molecular Framework

Aromatic heteropolycyclic compounds

External Descriptors

Not Available

Affected organisms

• Humans and other mammals

Chemical Identifiers

UNII

OSP71S83EU

CAS number

1454846-35-5

InChI Key

IIXWYSCJSQVBQM-LLVKDONJSA-N

InChI

InChI=1S/C21H19FN6O2/c1-11-15-7-13(22)4-5-14(15)21(29)27(2)10-16-19(17(8-23)28(3)26-16)12-6-18(30-11)20(24)25-9-12/h4-7,9,11H,10H2,1-3H3,(H2,24,25)/t11-/m1/s1

IUPAC Name

(16R)-19-amino-13-fluoro-4,8,16-trimethyl-9-oxo-17-oxa-4,5,8,20-tetraazatetracyclo[16.3.1.0^{2,6}.0^{10,15}]docosa-1(22),2,5,10(15),11,13,18,20-octaene-3-carbonitrile

SMILES

C[C@H]1OC2=C(N)N=CC(=C2)C2=C(C#N)N(C)N=C2CN(C)C(=O)C2=C1C=C(F)C=C2

References

Synthesis Reference

Johnson TW, Richardson PF, Bailey S, et al. Discovery of (10R)-7-amino-12-fluoro-2,10,16-trimethyl-15-oxo-10,15,16,17-tetrahydro-2H-8,4-(metheno)pyrazolo[4,3-h][2,5,11]-benzoxadiazacyclotetradecine-3-carbonitrile (PF-06463922), a macrocyclic inhibitor of anaplastic lymphoma kinase (ALK) and c-ros oncogene 1 (ROS1) with preclinical brain exposure and broad-spectrum potency against ALK-resistant mutations. J Med Chem. 2014;57(11):4720-44.

General References

1. Shaw AT, Felip E, Bauer TM, Besse B, Navarro A, Postel-Vinay S, Gainor JF, Johnson M, Dietrich J, James LP, Clancy JS, Chen J, Martini JF, Abbattista A, Solomon BJ: Lorlatinib in non-small-cell lung cancer with ALK or ROS1 rearrangement: an international, multicentre, open-label, single-arm first-in-man phase 1 trial. Lancet Oncol. 2017 Dec;18(12):1590-1599. doi: 10.1016/S1470-2045(17)30680-0. Epub 2017 Oct 23. [Article]
2. Authors unspecified: Lorlatinib in NSCLC: Robust Efficacy Seen. Cancer Discov. 2017 Dec;7(12):1360-1361. doi: 10.1158/2159-8290.CD-NB2017-153. Epub 2017 Nov 3. [Article]
3. Shaw AT, Friboulet L, Leshchiner I, Gainor JF, Bergqvist S, Brooun A, Burke BJ, Deng YL, Liu W, Dardaei L, Frias RL, Schultz KR, Logan J, James LP, Smeal T, Timofeevski S, Katayama R, Iafrate AJ, Le L, McTigue M, Getz G, Johnson TW, Engelman JA: Resensitization to Crizotinib by the Lorlatinib ALK Resistance Mutation L1198F. N Engl J Med. 2016 Jan 7;374(1):54-61. doi: 10.1056/NEJMoa1508887. Epub 2015 Dec 23. [Article]
4. Authors unspecified: Lorlatinib Is Active in Drug-Resistant NSCLC. Cancer Discov. 2016 Aug;6(8):OF1. doi: 10.1158/2159-8290.CD-NB2016-087. Epub 2016 Jul 8. [Article]
5. Collier TL, Maresca KP, Normandin MD, Richardson P, McCarthy TJ, Liang SH, Waterhouse RN, Vasdev N: Brain Penetration of the ROS1/ALK Inhibitor Lorlatinib Confirmed by PET. Mol Imaging. 2017 Jan-Dec;16:1536012117736669. doi: 10.1177/1536012117736669. [Article]
6. Chiarle R, Voena C, Ambrogio C, Piva R, Inghirami G: The anaplastic lymphoma kinase in the pathogenesis of cancer. Nat Rev Cancer. 2008 Jan;8(1):11-23. doi: 10.1038/nrc2291. [Article]
7. Guerin A, Sasane M, Zhang J, Macalalad AR, Galebach P, Jarvis J, Kageleiry A, Culver K, Wu EQ, Wakelee H: ALK rearrangement testing and treatment patterns for patients with ALK-positive non-small cell lung cancer. Cancer Epidemiol. 2015 Jun;39(3):307-12. doi: 10.1016/j.canep.2015.04.005. Epub 2015 Apr 23. [Article]
8. Lin JJ, Riely GJ, Shaw AT: Targeting ALK: Precision Medicine Takes on Drug Resistance. Cancer Discov. 2017 Feb;7(2):137-155. doi: 10.1158/2159-8290.CD-16-1123. Epub 2017 Jan 25. [Article]
9. Waqar SN, Morgensztern D: Lorlatinib: a new-generation drug for ALK-positive NSCLC. Lancet Oncol. 2018 Dec;19(12):1555-1557. doi: 10.1016/S1470-2045(18)30789-7. Epub 2018 Nov 6. [Article]
10. Drugs.com: FDA Approves Lorbrena [Link]
11. FDA Approved Drug Products: Lorbrena (lorlatinib) tablets for oral use [Link]
12. EMA Summary of Product Characteristics: Lorviqua (lorlatinib) film-coated tablets for oral use [Link]

External Links

PubChem Compound

71731823

PubChem Substance

347828429

ChemSpider

32813339

BindingDB

50018830

RxNav

2103164

ChEBI

143117

ChEMBL

CHEMBL3286830

ZINC

ZINC000098208524

PDBe Ligand

5P8

Wikipedia

Lorlatinib

PDB Entries

4cli / 4clj / 4uxl / 5a9u / 5aa8 / 5aa9

MSDS

Download (22.3 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	Carcinoma / Non Small Cell Lung	1
4	Completed	Treatment	Advanced Non-Small Cell Lung Cancer (NSCLC)	1
4	Recruiting	Treatment	Non-Small Cell Lung Cancer (NSCLC)	1
3	Active Not Recruiting	Treatment	Ganglioneuroblastoma / Neuroblastoma (NB)	1
3	Active Not Recruiting	Treatment	Non-Small Cell Lung Carcinoma	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
Tablet	Oral	100 mg
Tablet	Oral	25 mg
Tablet, film coated	Oral	100 mg/1
Tablet, film coated	Oral	25 mg/1
Tablet, coated	Oral	100 mg
Tablet, film coated	Oral	100 mg
Tablet, coated	Oral	25 mg
Tablet, film coated	Oral	25 mg

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
US8680111	No	2014-03-25	2033-03-05
US10420749	No	2019-09-24	2036-07-27
US11020376	No	2021-06-01	2036-07-27
US11299500	No	2018-10-04	2038-10-04

Properties

State

Solid

Experimental Properties

Not Available

Predicted Properties

Property	Value	Source
Water Solubility	0.108 mg/mL	ALOGPS
logP	2.01	ALOGPS
logP	1.63	Chemaxon
logS	-3.6	ALOGPS
pKa (Strongest Acidic)	19.7	Chemaxon
pKa (Strongest Basic)	5.71	Chemaxon
Physiological Charge	0	Chemaxon
Hydrogen Acceptor Count	6	Chemaxon
Hydrogen Donor Count	1	Chemaxon
Polar Surface Area	110.06 Å2	Chemaxon
Rotatable Bond Count	0	Chemaxon
Refractivity	121.17 m3·mol-1	Chemaxon
Polarizability	40.42 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 GC-MS Spectrum - GC-MS	Predicted GC-MS	splash10-002f-0009000000-e537208c5bf520bb96f4
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0a4i-0001900000-4cb45473dad0835a5c79
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0a4i-0003900000-f3686dca913cf2ebc591
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0a4i-0009800000-268de9b6ea6bd3de4382
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-05n0-6009500000-dc6a18773308ed1d281c
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-03k9-0009000000-ea2b848c1a128e2c06b2
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0229-0009000000-504bac2c8ae66a8bb759
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]-	194.90593	predicted	DeepCCS 1.0 (2019)
[M+H]+	197.3015	predicted	DeepCCS 1.0 (2019)
[M+Na]+	203.25719	predicted	DeepCCS 1.0 (2019)

Targets

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Details1. ALK tyrosine kinase receptor

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitor

General Function

Transmembrane receptor protein tyrosine kinase activity

Specific Function

Neuronal orphan receptor tyrosine kinase that is essentially and transiently expressed in specific regions of the central and peripheral nervous systems and plays an important role in the genesis a...

Gene Name

ALK

Uniprot ID

Q9UM73

Uniprot Name

ALK tyrosine kinase receptor

Molecular Weight

176440.535 Da

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Drug created at October 20, 2016 21:24 / Updated at February 20, 2024 23:54