Ivosidenib

Identification

Summary

Ivosidenib is an isocitrate dehydrogenase-1 inhibitor used to treat acute myeloid leukemia and cholangiocarcinoma in adults with a susceptible IDH1 mutation.

Brand Names

Tibsovo

Generic Name

Ivosidenib

DrugBank Accession Number

DB14568

Background

Ivosidenib is a first-in-class isocitrate dehydrogenase-1 (IDH1) inhibitor. IDH1 is an enzyme that is often mutated and overexpressed in some cancers, leading to aberrant cell growth and proliferation.⁶ Ivosidenib inhibits mutated IDH1, blocking the enzymatic activity and further differentiation of cancer cells.⁵

Ivosidenib was granted accelerated approval by the FDA in July 2018 for the treatment of relapsed of refractory acute myeloid leukemia in adults.⁵ It is currently approved to also treat newly diagnosed acute myeloid leukemia in older adults in combination azacitidine or as monotherapy, as well as locally advanced or metastatic cholangiocarcinoma and relapsed or refractory myelodysplastic syndromes in adults. The drug is only effective in patients with a susceptible IDH1 mutation.¹⁴

In February 2023, the EMA's Committee for Medicinal Products for Human Use (CHMP) adopted a positive opinion of ivosidenib and recommended it be granted marketing authorization for the treatment of acute myeloid leukemia and cholangiocarcinoma.¹⁰ It was fully approved by the EMA in May 2023.¹³

Type

Small Molecule

Groups

Approved, Investigational

Structure

3D

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MOLSDF3D-SDFPDBSMILESInChI

Similar Structures

Structure for Ivosidenib (DB14568)

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Weight

Average: 582.97
Monoisotopic: 582.1394008

Chemical Formula

C₂₈H₂₂ClF₃N₆O₃

Synonyms

• Ivosidenib

External IDs

• AG-120

Pharmacology

Indication

Ivosidenib is an isocitrate dehydrogenase-1 (IDH1) inhibitor approved for use in the US and Europe. It is indicated for the treatment of patients with a susceptible IDH1 mutation with:

• Newly Diagnosed Acute Myeloid Leukemia (AML) in combination azacitidine or as monotherapy for the treatment of newly diagnosed AML in adults who have comorbidities that preclude the use of intensive induction chemotherapy.^9,12 this indication is reserved for adults 75 years or older in the US.⁹

• Relapsed or refractory AML in adults in the US.⁹

• Locally Advanced or Metastatic Cholangiocarcinoma in adults who have been previously treated.^9,12

• Relapsed or Refractory Myelodysplastic Syndromes in adults.¹⁴

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Associated Conditions

• Acute Myeloid Leukemia
• Locally Advanced Cholangiocarcinoma
• Metastatic Cholangiocarcinoma
• Refractory Acute Myeloid Leukemia (AML)
• Refractory Myelodysplastic Syndromes
• Relapsed Acute Myelogenous Leukemia (AML)
• Relapsed Myelodysplastic Syndromes

Contraindications & Blackbox Warnings

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Pharmacodynamics

Ivosidenib is an antineoplastic agent that is effective in cancers with a susceptible IDH1 mutation, which indicates increased levels of oncometabolite D-2-hydroxyglutarate (D-2HG) in cancer cells.⁵ Ivosidenib decreases D-2HG levels in a dose-dependent manner by inhibiting the IDH1 enzyme. Ivosidenib inhibits both the mutant and wild-type IDH1 but does not inhibit IDH2.⁷

Mechanism of action

Isocitrate dehydrogenase 1 (IDH1) is a metabolic enzyme in the cytoplasm and peroxisomes that plays a role in many cellular processes, including mitochondrial oxidative phosphorylation, glutamine metabolism, lipogenesis, glucose sensing, and regulation of cellular redox status.¹ IDH1 converts isocitrate to α-ketoglutarate (α-KG), a normal metabolite in the carboxylic acid cycle.¹ Multiple cancers are associated with missense mutations in IDH1, leading to the substitution of the amino acid arginine 132 in the enzyme active site, acquired gain-of-function activity, and increased enzyme activity.^5,7 IDH1 mutation results in the accumulation of D-2-hydroxyglutarate (D-2HG), an oncometabolite that is structurally similar to α-KG.^1,4 D-2HG inhibits α-KG-dependent dioxygenases, including histone and DNA demethylases, which play a role in histone and DNA demethylation along with other cellular processes.⁴ Inhibition of these enzymes leads to histone and DNA hypermethylation and a block in cell differentiation,¹ including hematopoietic differentiation.³ With histone hypermethylation, methylation-sensitive insulators cannot regulate the activation of oncogenes.² Excess D-2HG ultimately interferes with cellular metabolism and alters epigenetic regulation towards oncogenesis.^1,4

Ivosidenib inhibits the mutant IDH1 at much lower concentrations than the wild-type enzyme.⁹ It targets gene mutations at position R132, with R132H and R132C being the most common mutations.⁵ In mouse xenograft models of IDH1-mutated AML, ivosidenib caused a decrease in D-2HG levels in a dose-dependent manner and induced myeloid differentiation in vitro and in vivo.⁹ Ivosidenib works to inhibit histone demethylases and restore normal methylation conditions to promote cell differentiation and oncogene regulation.⁴

Target	Actions	Organism
AIsocitrate dehydrogenase [NADP] cytoplasmic	inhibitor	Humans

Absorption

Following oral administration, ivosidenib is rapidly absorbed.⁷ The C_max following a single oral dose is 4503 ng/mL in patients with relapsed or refractory AML, 4820 ng/mL in patients with newly diagnosed AML who were also treated with azacitidine, and 4060 ng/mL in patients with cholangiocarcinoma. The steady-state was reached within 14 days. The steady-state C_max is 6551 ng/mL in patients with relapsed or refractory AML, 6145 ng/mL in patients with newly diagnosed AML who were also treated with azacitidine, and 4799 ng/mL in patients with cholangiocarcinoma. The T_max ranges from two to three hours.⁹

A high-fat meal increases ivosidenib exposure.⁹

Volume of distribution

The apparent volume of distribution at steady state is 403 L in patients with relapsed or refractory AML, 504 L in patients with newly diagnosed AML who were also treated with azacitidine, and 706 L in patients with cholangiocarcinoma.⁹

Protein binding

In vitro, ivosidenib is 92-96% bound to plasma proteins.⁹

Metabolism

Ivosidenib is predominantly metabolized by CYP3A4 via oxidation. The exact chemical structures of the metabolites formed from CYP3A4-mediated oxidation have not been fully characterized. Ivosidenib can also undergo N-dealkylation and hydrolysis as minor metabolic pathways.^7,8,9

Hover over products below to view reaction partners

• Ivosidenib
  • Ivosidenib M30 metabolite
  • Ivosidenib M39 metabolite
    • Ivosidenib M37 metabolite

Route of elimination

Following oral administration of ivosidenib, about 77% of the dose was eliminated in feces, where 67% was in the form of unchanged parent drug. About 17% of the dose was excreted in urine, where 10% was in the form of unchanged ivosidenib.⁹

Half-life

The terminal half-life at steady state is 58 hours in patients with relapsed or refractory AML, 98 hours in patients with newly diagnosed AML who were also treated with azacitidine, and 129 hours in patients with cholangiocarcinoma.⁹

Clearance

The apparent clearance at steady state is 5.6 L/h in patients with relapsed or refractory AML, 4.6 L/h in patients with newly diagnosed AML who were also treated with azacitidine, and 6.1 L/h in patients with cholangiocarcinoma.⁹

Adverse Effects

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Toxicity

There is limited information regarding the LD₅₀ or overdose of ivosidenib.

Ivosidenib is associated with a risk of differentiation syndrome, Guillain-Barre syndrome, and embryo-fetal toxicity.^6,9

Pathways

Not Available

Pharmacogenomic Effects/ADRs

Not Available

Interactions

Drug Interactions

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 metabolism of 1,2-Benzodiazepine can be increased when combined with Ivosidenib.
Abametapir	The serum concentration of Ivosidenib can be increased when it is combined with Abametapir.
Abatacept	The metabolism of Ivosidenib can be increased when combined with Abatacept.
Abemaciclib	The metabolism of Abemaciclib can be increased when combined with Ivosidenib.
Abiraterone	The metabolism of Abiraterone can be increased when combined with Ivosidenib.
Abrocitinib	The metabolism of Abrocitinib can be increased when combined with Ivosidenib.
Acalabrutinib	The metabolism of Acalabrutinib can be increased when combined with Ivosidenib.
Acenocoumarol	The metabolism of Acenocoumarol can be increased when combined with Ivosidenib.
Acetaminophen	The metabolism of Acetaminophen can be increased when combined with Ivosidenib.
Acetazolamide	The serum concentration of Ivosidenib can be increased when it is combined with Acetazolamide.

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Food Interactions

• Do not take with or immediately after a high-fat meal. Administration of ivosidenib with a high-fat meal increases the Cmax and AUC of ivosidenib by 98 and 25%, respectively.
• Exercise caution with grapefruit products. Grapefruit inhibits CYP3A metabolism, which may increase the serum concentration of ivosidenib. Dose adjustment may be necessary if co-administered.
• Exercise caution with St. John's Wort. This herb induces CYP3A metabolism and may reduce serum levels of ivosidenib.
• 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
Tibsovo	Tablet, film coated	250 mg/1	Oral	Agios Pharmaceuticals, Inc.	2018-07-20	2024-11-30
Tibsovo	Tablet, film coated	250 mg	Oral	Les Laboratoires Servier	2023-05-16	Not applicable
Tibsovo	Tablet, film coated	250 mg/1	Oral	Servier Pharmaceutical LLC	2021-10-19	Not applicable

Categories

ATC Codes

L01XX62 — Ivosidenib

• L01XX — Other antineoplastic agents
• L01X — OTHER ANTINEOPLASTIC AGENTS
• L01 — ANTINEOPLASTIC AGENTS
• L — ANTINEOPLASTIC AND IMMUNOMODULATING AGENTS

Drug Categories

• Amino Acids
• Amino Acids, Peptides, and Proteins
• Antineoplastic Agents
• Antineoplastic and Immunomodulating Agents
• Cytochrome P-450 CYP2B6 Inducers
• Cytochrome P-450 CYP2B6 Inducers (strength unknown)
• Cytochrome P-450 CYP2C8 Inducers
• Cytochrome P-450 CYP2C8 Inducers (strength unknown)
• Cytochrome P-450 CYP2C9 Inducers
• Cytochrome P-450 CYP2C9 Inducers (strength unknown)
• Cytochrome P-450 CYP3A Inducers
• Cytochrome P-450 CYP3A Substrates
• Cytochrome P-450 CYP3A4 Inducers
• Cytochrome P-450 CYP3A4 Inducers (strength unknown)
• Cytochrome P-450 CYP3A4 Substrates
• Cytochrome P-450 CYP3A4 Substrates with a Narrow Therapeutic Index
• Cytochrome P-450 Enzyme Inducers
• Cytochrome P-450 Substrates
• Enzyme Inhibitors
• Isocitrate Dehydrogenase 1 Inhibitor
• Isocitrate dehydrogenase-1 (IDH1) inhibitors
• Isocitrate Dehydrogenase-1 Inhibitors
• Moderate Risk QTc-Prolonging Agents
• Narrow Therapeutic Index Drugs
• OAT3/SLC22A8 Inhibitors
• P-glycoprotein inhibitors
• P-glycoprotein substrates
• P-glycoprotein substrates with a Narrow Therapeutic Index
• QTc Prolonging Agents

Chemical TaxonomyProvided by Classyfire

Description

This compound belongs to the class of organic compounds known as proline and derivatives. These are compounds containing proline or a derivative thereof resulting from reaction of proline at the amino group or the carboxy group, or from the replacement of any hydrogen of glycine by a heteroatom.

Kingdom

Organic compounds

Super Class

Organic acids and derivatives

Class

Carboxylic acids and derivatives

Sub Class

Amino acids, peptides, and analogues

Direct Parent

Proline and derivatives

Alternative Parents

Alpha amino acid amides / Phenylacetamides / Pyrrolidinecarboxamides / Chlorobenzenes / Pyrrolidine-2-ones / Pyridines and derivatives / Aryl chlorides / Aryl fluorides / Imidolactams / Tertiary carboxylic acid amides / Heteroaromatic compounds / Secondary carboxylic acid amides / Lactams / Nitriles / Azacyclic compounds / Organic oxides / Carbonyl compounds / Organochlorides / Organofluorides / Hydrocarbon derivatives / Alkyl fluorides

show 11 more

Substituents

2-pyrrolidone / Alkyl fluoride / Alkyl halide / Alpha-amino acid amide / Aromatic heteromonocyclic compound / Aryl chloride / Aryl fluoride / Aryl halide / Azacycle / Benzenoid / Carbonitrile / Carbonyl group / Carboxamide group / Chlorobenzene / Cyanide / Halobenzene / Heteroaromatic compound / Hydrocarbon derivative / Imidolactam / Lactam / Monocyclic benzene moiety / Nitrile / Organic nitrogen compound / Organic oxide / Organic oxygen compound / Organochloride / Organofluoride / Organohalogen compound / Organoheterocyclic compound / Organonitrogen compound / Organooxygen compound / Phenylacetamide / Proline or derivatives / Pyridine / Pyrrolidine / Pyrrolidine carboxylic acid or derivatives / Pyrrolidine-2-carboxamide / Pyrrolidone / Secondary carboxylic acid amide / Tertiary carboxylic acid amide

show 30 more

Molecular Framework

Aromatic heteromonocyclic compounds

External Descriptors

Not Available

Affected organisms

Not Available

Chemical Identifiers

UNII

Q2PCN8MAM6

CAS number

1448347-49-6

InChI Key

WIJZXSAJMHAVGX-DHLKQENFSA-N

InChI

InChI=1S/C28H22ClF3N6O3/c29-21-4-2-1-3-20(21)25(26(40)36-18-11-28(31,32)12-18)37(19-10-17(30)14-34-15-19)27(41)22-5-6-24(39)38(22)23-9-16(13-33)7-8-35-23/h1-4,7-10,14-15,18,22,25H,5-6,11-12H2,(H,36,40)/t22-,25-/m0/s1

IUPAC Name

(2S)-2-(2-chlorophenyl)-2-{1-[(2S)-1-(4-cyanopyridin-2-yl)-5-oxopyrrolidin-2-yl]-N-(5-fluoropyridin-3-yl)formamido}-N-(3,3-difluorocyclobutyl)acetamide

SMILES

[H][C@@](N(C(=O)[C@]1([H])CCC(=O)N1C1=NC=CC(=C1)C#N)C1=CC(F)=CN=C1)(C(=O)NC1CC(F)(F)C1)C1=C(Cl)C=CC=C1

References

General References

1. Mondesir J, Willekens C, Touat M, de Botton S: IDH1 and IDH2 mutations as novel therapeutic targets: current perspectives. J Blood Med. 2016 Sep 2;7:171-80. doi: 10.2147/JBM.S70716. eCollection 2016. [Article]
2. Flavahan WA, Drier Y, Liau BB, Gillespie SM, Venteicher AS, Stemmer-Rachamimov AO, Suva ML, Bernstein BE: Insulator dysfunction and oncogene activation in IDH mutant gliomas. Nature. 2016 Jan 7;529(7584):110-4. doi: 10.1038/nature16490. Epub 2015 Dec 23. [Article]
3. Figueroa ME, Abdel-Wahab O, Lu C, Ward PS, Patel J, Shih A, Li Y, Bhagwat N, Vasanthakumar A, Fernandez HF, Tallman MS, Sun Z, Wolniak K, Peeters JK, Liu W, Choe SE, Fantin VR, Paietta E, Lowenberg B, Licht JD, Godley LA, Delwel R, Valk PJ, Thompson CB, Levine RL, Melnick A: Leukemic IDH1 and IDH2 mutations result in a hypermethylation phenotype, disrupt TET2 function, and impair hematopoietic differentiation. Cancer Cell. 2010 Dec 14;18(6):553-67. doi: 10.1016/j.ccr.2010.11.015. Epub 2010 Dec 9. [Article]
4. Popovici-Muller J, Lemieux RM, Artin E, Saunders JO, Salituro FG, Travins J, Cianchetta G, Cai Z, Zhou D, Cui D, Chen P, Straley K, Tobin E, Wang F, David MD, Penard-Lacronique V, Quivoron C, Saada V, de Botton S, Gross S, Dang L, Yang H, Utley L, Chen Y, Kim H, Jin S, Gu Z, Yao G, Luo Z, Lv X, Fang C, Yan L, Olaharski A, Silverman L, Biller S, Su SM, Yen K: Discovery of AG-120 (Ivosidenib): A First-in-Class Mutant IDH1 Inhibitor for the Treatment of IDH1 Mutant Cancers. ACS Med Chem Lett. 2018 Jan 19;9(4):300-305. doi: 10.1021/acsmedchemlett.7b00421. eCollection 2018 Apr 12. [Article]
5. Merchant SL, Culos K, Wyatt H: Ivosidenib: IDH1 Inhibitor for the Treatment of Acute Myeloid Leukemia. J Adv Pract Oncol. 2019 Jul;10(5):494-500. doi: 10.6004/jadpro.2019.10.5.7. Epub 2019 Jul 1. [Article]
6. Authors unspecified: Ivosidenib . [Article]
7. Dhillon S: Ivosidenib: First Global Approval. Drugs. 2018 Sep;78(14):1509-1516. doi: 10.1007/s40265-018-0978-3. [Article]
8. Prakash C, Fan B, Altaf S, Agresta S, Liu H, Yang H: Pharmacokinetics, absorption, metabolism, and excretion of [(14)C]ivosidenib (AG-120) in healthy male subjects. Cancer Chemother Pharmacol. 2019 May;83(5):837-848. doi: 10.1007/s00280-019-03793-7. Epub 2019 Feb 13. [Article]
9. FDA Approved Drug Products: TIBSOVO (ivosidenib) tablets, for oral use [Link]
10. CHMP Summary of Positive Opinion: Tibsovo (ivosidenib) [Link]
11. CHMP Summary of Positive Opinion: Tidhesco (ivosidenib) [Link]
12. EMA Approved Drug Products: Tibsovo (ivosidenib) Oral Tablets [Link]
13. PR Newswire: Servier receives European Commission approval of Tibsovo® (ivosidenib tablets) in IDH1-mutated Acute Myeloid Leukemia and IDH1-mutated Cholangiocarcinoma [Link]
14. FDA Approved Drug Products: TIBSOVO® (ivosidenib tablets), for oral use (October 2023) [Link]

External Links

ChemSpider

38772333

BindingDB

363689

RxNav

2049873

ChEBI

145430

ChEMBL

CHEMBL3989958

ZINC

ZINC000205136523

Wikipedia

Ivosidenib

Clinical Trials

Clinical Trials

Phase	Status	Purpose	Conditions	Count
3	Active Not Recruiting	Treatment	Acute Myeloid Leukemia / Acute Myeloid Leukemia Arising From Previous Myelodysplastic Syndrome / Newly Diagnosed Acute Myeloid Leukemia (AML) / Treatment Naive AML	1
3	Completed	Treatment	Cholangiocarcinoma Advanced / Metastatic Cholangiocarcinoma	1
3	Not Yet Recruiting	Treatment	Biliary Tract Neoplasms	1
3	Not Yet Recruiting	Treatment	Locally Advanced or Metastatic Conventional Chondrosarcoma With an IDH1 Mutation, Untreated or Previously Treated With 1 Systemic Treatment Regimen	1
3	Recruiting	Treatment	Acute Myeloid Leukemia	1
3	Recruiting	Treatment	Acute Myeloid Leukemia / Myelodysplastic Syndrome With Excess Blasts-2 (MDS-EB-2)	1
3	Recruiting	Treatment	Cholangiocarcinoma	1
2	Active Not Recruiting	Treatment	Cancer of Unknown Primary Site	1
2	Not Yet Recruiting	Treatment	Metastatic Cholangiocarcinoma / Non-Resectable Cholangiocarcinoma	1
2	Recruiting	Treatment	Acute Myeloid Leukemia	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
Tablet, film coated	Oral	250 mg
Tablet, film coated	Oral	250 mg/1

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
US9474779	No	2016-10-25	2033-08-19
US9850277	No	2017-12-26	2033-01-18
US9968595	No	2018-05-15	2035-03-13
US10449184	No	2019-10-22	2035-03-13
US10610125	No	2020-04-07	2030-06-21
US10799490	No	2020-10-13	2035-03-13
US10980788	No	2021-04-20	2039-06-07
US10717764	No	2020-07-21	2033-01-18
US10653710	No	2020-05-19	2036-10-18

Properties

State

Solid

Experimental Properties

Property	Value	Source
water solubility	<1 mg/mL	https://www.selleck.cn/msds/MSDS_S8206.pdf

Predicted Properties

Property	Value	Source
Water Solubility	0.0208 mg/mL	ALOGPS
logP	2.52	ALOGPS
logP	3.01	Chemaxon
logS	-4.4	ALOGPS
pKa (Strongest Acidic)	12.14	Chemaxon
pKa (Strongest Basic)	1.81	Chemaxon
Physiological Charge	0	Chemaxon
Hydrogen Acceptor Count	6	Chemaxon
Hydrogen Donor Count	1	Chemaxon
Polar Surface Area	119.29 Å2	Chemaxon
Rotatable Bond Count	7	Chemaxon
Refractivity	139.33 m3·mol-1	Chemaxon
Polarizability	53.42 Å3	Chemaxon
Number of Rings	5	Chemaxon
Bioavailability	1	Chemaxon
Rule of Five	No	Chemaxon
Ghose Filter	No	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	Yes	Chemaxon

Predicted ADMET Features

Not Available

Spectra

Mass Spec (NIST)

Not Available

Spectra

Not Available

Targets

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Details1. Isocitrate dehydrogenase [NADP] cytoplasmic

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitor

Curator comments

Ivosidenib inhibits both the wild-type and mutant forms of IDH1 with varying affinities.

General Function

Receptor binding

Specific Function

Not Available

Gene Name

IDH1

Uniprot ID

O75874

Uniprot Name

Isocitrate dehydrogenase [NADP] cytoplasmic

Molecular Weight

46659.005 Da

References

1. Megias-Vericat JE, Ballesta-Lopez O, Barragan E, Montesinos P: IDH1-mutated relapsed or refractory AML: current challenges and future prospects. Blood Lymphat Cancer. 2019 Jun 27;9:19-32. doi: 10.2147/BLCTT.S177913. eCollection 2019. [Article]
2. Merchant SL, Culos K, Wyatt H: Ivosidenib: IDH1 Inhibitor for the Treatment of Acute Myeloid Leukemia. J Adv Pract Oncol. 2019 Jul;10(5):494-500. doi: 10.6004/jadpro.2019.10.5.7. Epub 2019 Jul 1. [Article]
3. FDA Approved Drug Products: TIBSOVO (ivosidenib) tablets, for oral use [Link]

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Drug created at July 20, 2018 16:42 / Updated at November 24, 2023 04:34