Ruxolitinib

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Identification

Summary

Ruxolitinib is a kinase inhibitor used to treat various types of myelofibrosis, polycythemia vera in patients who have not responded to or cannot tolerate hydroxyurea, and to treat graft-versus-host disease in cases that are refractory to steroid treatment.

Brand Names

Jakafi, Jakavi, Opzelura

Generic Name

Ruxolitinib

DrugBank Accession Number

DB08877

Background

Ruxolitinib, formerly known as INCB018424 or INC424, is an anticancer drug and a Janus kinase (JAK) inhibitor. It is a potent and selective inhibitor of JAK1 and JAK2,³ which are tyrosine kinases involved in cytokine signalling and hematopoiesis.² Myeloproliferative neoplasms, such as myelofibrosis and polycythemia vera, are often characterized by aberrant activation of the JAK-STAT pathway, leading to abnormal blood cell counts and thrombotic complications. By inhibiting JAK1 and JAK2, ruxolitinib works to block the dysregulated cell signalling pathways and prevents abnormal blood cell proliferation.⁵ Due to a large number of patients with myeloproliferative neoplasms who have JAK2 mutations, ruxolitinib was the first ATP-competitive inhibitor of JAK1 and JAK2 ever developed.¹⁵

Ruxolitinib was first approved for the treatment of adult patients with myelofibrosis by the FDA in 2011, followed by EMA's approval in 2012.⁵ In 2014, it was approved for the treatment of polycythemia vera in adults who have an inadequate response to or are intolerant of hydroxyurea and in 2019, ruxolitinib was approved for use in steroid-refractory acute graft-versus-host disease in adults and children.¹⁹ The topical formulation of ruxolitinib is used to treat atopic dermatitis and vitiligo.²³ It is being investigated for other inflammatory skin conditions.¹²

Ruxolitinib has been investigated to treat patients with coronavirus disease 2019 (COVID-19) accompanied by severe systemic hyperinflammation. In phase II clinical trials, ruxolitinib improved chest computed tomography and improved recovery in patients with lymphopenia.^6,7 However, phase III clinical trials later determined that ruxolitinib was inadequate in meeting its primary endpoint of reducing the number of hospitalized COVID-19 patients who experienced severe complications ²⁰ thus the drug was not approved as a treatment for COVID-19.

Type

Small Molecule

Groups

Approved

Structure

Similar Structures

Weight: Average: 306.365
Monoisotopic: 306.159294606
Chemical Formula: C₁₇H₁₈N₆

Synonyms

Ruxolitinib

External IDs

INC-424
INC424
INCB 18424
INCB-018424
INCB-18424
INCB018424
INCB18424
INCB424

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Pharmacology

Indication

Ruxolitinib is indicated for the treatment of the following conditions:

intermediate or high-risk myelofibrosis (MF), including prima1y MF, post-polycythemia vera MF and post-essential thrombocythemia MF in adults.¹⁶ It is also used to treat disease-related splenomegaly or symptoms in adult patients with these conditions.²²
polycythemia vera (PV) in adults who have had an inadequate response to or are intolerant of hydroxyurea.¹⁶
steroid-refracto1y acute graft-versus-host disease (GVHD) in adult and pediatric patients 12 years and older.¹⁶
chronic GVHD in patients aged 12 years and older who have failed one or two lines of systemic therapy.¹⁶

Topical ruxolitinib is indicated for:

the short-term and non-continuous chronic treatment of mild to moderate atopic dermatitis in non-immunocompromised patients patients 12 years of age and older whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable.²³
the treatment of non-segmental vitiligo in adult and pediatric patients 12 years of age and older.^23,24

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Associated Conditions

Indication Type	Indication	Approval Level	Age Group	Patient Characteristics	Dose Form
Management of	Acute graft-versus-host disease	••••••••••••	•••••• •••••••••	••••••• ••••••••••	••••••
Management of	Chronic graft-versus-host disease	••••••••••••	•••••• •••••••••	••••••• •• •• ••••• ••• ••••• •••••••• •••••••	••••••
Management of	Nonsegmental vitiligo	••••••••••••	••••••••••• •••••		•••••
Management of	Post-essential thrombocythemia myelofibrosis	••••••••••••	•••••		••••••
Management of	Post-polycythemia vera myelofibrosis	••••••••••••	•••••		••••••

Contraindications & Blackbox Warnings

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Pharmacodynamics

Ruxolitinib is an antineoplastic agent that inhibits cell proliferation, induces apoptosis of malignant cells, and reduces pro-inflammatory cytokine plasma levels by inhibiting JAK-induced phosphorylation of signal transducer and activator of transcription (STAT).⁴ Inhibition of STAT3 phosphorylation, which is used as a marker of JAK activity, ² by ruxolitinib is achieved at two hours after dosing which returned to near baseline by 10 hours in patients with myelofibrosis and polycythemia vera.¹⁶ In clinical trials, ruxolitinib reduced splenomegaly and improved symptoms of myelofibrosis.⁴ In a mouse model of myeloproliferative neoplasms, administration of ruxolitinib was associated with prolonged survival.² Ruxolitinib inhibits both mutant and wild-type JAK2 ⁴; however, JAK2V617F mutation, which is often seen in approximately 50% of patients with myelofibrosis, was shown to reduce ruxolitinib sensitivity, which may also be associated with possible resistance to JAK inhibitor treatment.¹⁴

Mechanism of action

The Janus kinase (JAK) family of protein tyrosine kinases comprises JAK1, JAK2, JAK3, and non-receptor tyrosine kinase 2 (TYK2).⁴ JAKs play a pivotal role in intracellular signalling pathways of various cytokines and growth factors essential to hematopoiesis, such as interleukin, erythropoietin, and thrombopoietin.² JAKs have diverse functions: JAK1 and JAK3 promote lymphocyte differentiation, survival, and function, while JAK2 promotes signal transduction of erythropoietin and thrombopoietin.^4,10 JAKs are in close proximity to the cytokine and growth factor receptor’s cytoplasmic region. Upon binding of cytokines and growth factors, JAKs are activated, undergoing cross-phosphorylation and tyrosine phosphorylation. This process also reveals selective binding sites for STATs, which are DNA-binding proteins that also bind to the cytoplasmic region of cytokine or growth factor receptors. Activated JAKs and STATs translocate to the nucleus as transcription factors to regulate gene expression of pro-inflammatory cytokines such as IL-6, IL-10, and nuclear factor κB (NF-κB).¹⁵ They also activate downstream pathways that promote erythroid, myeloid, and megakaryocytic development.⁴

The molecular pathogenesis of myeloproliferative neoplasms is not fully understood; however, JAK2 is constitutively activated and the JAK-STAT signalling pathway becomes deregulated and aberrant.^2,15 Ruxolitinib is a selective and potent inhibitor of JAK2 and JAK1, with some affinity against JAK3 and TYK2. Anticancer effects of ruxolitinib are attributed to its inhibition of JAKs and JAK-mediated phosphorylation of STAT3.¹⁶ By downregulating the JAK-STAT pathway, ruxolitinib inhibits myeloproliferation and suppresses the plasma levels of pro-inflammatory cytokines such as IL-6 and TNF-α.⁴

Activated JAKs are also implicated in graft-versus-host-disease (GVHD), which is a severe immune complication of allogeneic hematopoietic cell transplantation GVHD is associated with significant morbidity and mortality, especially for patients who do not respond well to corticosteroid therapy. Activated JAKS stimulate T-effector cell responses, leading to increased proliferation of effector T cells and heightened production of pro-inflammatory cytokines. By blocking JAK1 and JAk2, ruxolitinib inhibits donor T-cell expansion and suppresses pro-inflammatory responses.¹³

Target	Actions	Organism
AUrokinase plasminogen activator surface receptor	inhibitor	Humans
ATyrosine-protein kinase JAK2	inhibitor	Humans
ATyrosine-protein kinase JAK1	inhibitor	Humans
ATyrosine-protein kinase JAK3	inhibitor	Humans
ANon-receptor tyrosine-protein kinase TYK2	inhibitor	Humans

Absorption

Following oral administration, ruxolitinib undergoes rapid absorption ¹⁰ and the peak concentrations are reached within one hour after administration.⁴ Over a single-dose range of 5 mg to 200 mg, the mean maximal plasma concentration (C_max) increases proportionally. C_max ranged from 205 nM to 7100 nM and AUC ranged from 862 nM x hr to 30700 nM x hr. T_max ranges from one to two hours following oral administration. Oral bioavailability is at least 95%.¹⁶

Volume of distribution

The mean volume of distribution (%coefficient of variation) at steady-state is 72 L (29%) in patients with myelofibrosis and 75 L (23%) in patients with polycythemia vera.¹⁶ It is not known whether ruxolitinib crosses the blood-brain barrier.²¹

Protein binding

Ruxolitinib is approximately 97% bound to plasma proteins, mostly to albumin.¹⁶

Metabolism

More than 99% of orally-administered ruxolitinib undergoes metabolism⁴ mediated by CYP3A4 and, to a lesser extent, CYP2C9.¹⁶ The major circulating metabolites in human plasma were M18 formed by 2-hydroxylation, and M16 and M27 (stereoisomers) formed by 3-hydroxylation. Other identified metabolites include M9 and M49, which are formed by hydroxylation and ketone formation. Not all metabolite structures are fully characterized and it is speculated that many metabolites exist in stereoisomers.¹⁰ Metabolites of ruxolitinib retain inhibitory activity against JAK1 and JAk2 to a lesser degree than the parent drug.¹¹

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Ruxolitinib

Route of elimination

Following oral administration of a single radiolabeled dose of ruxolitinib, the drug was mainly eliminated through metabolism. About 74% of the total dose was excreted in urine and 22% was excreted in feces,¹⁶ mostly in the form of hydroxyl and oxo metabolites of ruxolitinib.¹⁰ The unchanged parent drug accounted for less than 1% of the excreted total radioactivity.¹⁶

Half-life

The mean elimination half-life of ruxolitinib is approximately 3 hours and the mean half-life of its metabolites is approximately 5.8 hours.¹⁶

Clearance

Ruxolitinib clearance (% coefficient of variation) is 17.7 L/h in women and 22.1 L/h in men with myelofibrosis. Drug clearance was 12.7 L/h (42%) in patients with polycythemia vera and 11.9 L/h (43%) in patients with acute graft-versus-host disease.¹⁶

Adverse Effects

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Toxicity

The oral LD₅₀ was 250 mg/kg.¹⁸

Single doses of ruxolitinib up to 200 mg were tolerated well. Higher doses than recommended repeat doses are associated with myelosuppression, including leukopenia, anemia, and thrombocytopenia. There is no known antidote for overdoses with ruxolitinib: it is recommended that patients are given appropriate supportive treatment. Hemodialysis is not expected to enhance the elimination of ruxolitinib.¹⁶

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.

Drug	Interaction
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Abacavir	Abacavir may decrease the excretion rate of Ruxolitinib which could result in a higher serum level.
Abametapir	The serum concentration of Ruxolitinib can be increased when it is combined with Abametapir.
Abatacept	The metabolism of Ruxolitinib can be increased when combined with Abatacept.
Abciximab	The risk or severity of bleeding can be increased when Abciximab is combined with Ruxolitinib.
Abrocitinib	The metabolism of Abrocitinib can be decreased when combined with Ruxolitinib.

Food Interactions

Avoid grapefruit products. Grapefruit inhibits CYP3A4 metabolism, which may increase the serum concentration of ruxolitinib.
Exercise caution with St. John's Wort. This herb induces CYP3A4 metabolism, which may reduce the serum levels of ruxolitinib.
Take with or without food. A high-fat, high-calorie meal had negligible effects on the pharmacokinetics of ruxolitinib.

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Product Ingredients

Ingredient	UNII	CAS	InChI Key
Ruxolitinib phosphate	436LRU32H5	1092939-17-7	JFMWPOCYMYGEDM-XFULWGLBSA-N
Ruxolitinib sulfate	Not Available	1092939-16-6	LGJWVXWQCTZSGC-UHFFFAOYSA-N

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End
Jakafi	Tablet	20.0 mg/1	Oral	Incyte Corporation	2011-11-16	Not applicable
Jakafi	Tablet	5.0 mg/1	Oral	Incyte Corporation	2011-11-16	Not applicable
Jakafi	Tablet	15.0 mg/1	Oral	Incyte Corporation	2011-11-16	Not applicable
Jakafi	Tablet	25.0 mg/1	Oral	Incyte Corporation	2011-11-16	Not applicable
Jakafi	Tablet	10.0 mg/1	Oral	Incyte Corporation	2011-11-16	Not applicable

Chemical Identifiers

UNII: 82S8X8XX8H
CAS number: 941678-49-5
InChI Key: HFNKQEVNSGCOJV-OAHLLOKOSA-N
InChI: InChI=1S/C17H18N6/c18-7-5-15(12-3-1-2-4-12)23-10-13(9-22-23)16-14-6-8-19-17(14)21-11-20-16/h6,8-12,15H,1-5H2,(H,19,20,21)/t15-/m1/s1
IUPAC Name: (3R)-3-cyclopentyl-3-(4-{7H-pyrrolo[2,3-d]pyrimidin-4-yl}-1H-pyrazol-1-yl)propanenitrile
SMILES: N#CC[C@H](C1CCCC1)N1C=C(C=N1)C1=C2C=CNC2=NC=N1

References

General References

Cervantes F, Martinez-Trillos A: Myelofibrosis: an update on current pharmacotherapy and future directions. Expert Opin Pharmacother. 2013 May;14(7):873-84. doi: 10.1517/14656566.2013.783019. Epub 2013 Mar 21. [Article]
Yang LP, Keating GM: Ruxolitinib: in the treatment of myelofibrosis. Drugs. 2012 Nov 12;72(16):2117-27. doi: 10.2165/11209340-000000000-00000. [Article]
Becker H, Engelhardt M, von Bubnoff N, Wasch R: Ruxolitinib. Recent Results Cancer Res. 2014;201:249-57. doi: 10.1007/978-3-642-54490-3_16. [Article]
Ostojic A, Vrhovac R, Verstovsek S: Ruxolitinib: a new JAK1/2 inhibitor that offers promising options for treatment of myelofibrosis. Future Oncol. 2011 Sep;7(9):1035-43. doi: 10.2217/fon.11.81. [Article]
Ajayi S, Becker H, Reinhardt H, Engelhardt M, Zeiser R, von Bubnoff N, Wasch R: Ruxolitinib. Recent Results Cancer Res. 2018;212:119-132. doi: 10.1007/978-3-319-91439-8_6. [Article]
Cao Y, Wei J, Zou L, Jiang T, Wang G, Chen L, Huang L, Meng F, Huang L, Wang N, Zhou X, Luo H, Mao Z, Chen X, Xie J, Liu J, Cheng H, Zhao J, Huang G, Wang W, Zhou J: Ruxolitinib in treatment of severe coronavirus disease 2019 (COVID-19): A multicenter, single-blind, randomized controlled trial. J Allergy Clin Immunol. 2020 Jul;146(1):137-146.e3. doi: 10.1016/j.jaci.2020.05.019. Epub 2020 May 26. [Article]
La Rosee F, Bremer HC, Gehrke I, Kehr A, Hochhaus A, Birndt S, Fellhauer M, Henkes M, Kumle B, Russo SG, La Rosee P: The Janus kinase 1/2 inhibitor ruxolitinib in COVID-19 with severe systemic hyperinflammation. Leukemia. 2020 Jul;34(7):1805-1815. doi: 10.1038/s41375-020-0891-0. Epub 2020 Jun 9. [Article]
Rosmarin D, Pandya AG, Lebwohl M, Grimes P, Hamzavi I, Gottlieb AB, Butler K, Kuo F, Sun K, Ji T, Howell MD, Harris JE: Ruxolitinib cream for treatment of vitiligo: a randomised, controlled, phase 2 trial. Lancet. 2020 Jul 11;396(10244):110-120. doi: 10.1016/S0140-6736(20)30609-7. [Article]
Kim BS, Howell MD, Sun K, Papp K, Nasir A, Kuligowski ME: Treatment of atopic dermatitis with ruxolitinib cream (JAK1/JAK2 inhibitor) or triamcinolone cream. J Allergy Clin Immunol. 2020 Feb;145(2):572-582. doi: 10.1016/j.jaci.2019.08.042. Epub 2019 Oct 17. [Article]
Shilling AD, Nedza FM, Emm T, Diamond S, McKeever E, Punwani N, Williams W, Arvanitis A, Galya LG, Li M, Shepard S, Rodgers J, Yue TY, Yeleswaram S: Metabolism, excretion, and pharmacokinetics of [14C]INCB018424, a selective Janus tyrosine kinase 1/2 inhibitor, in humans. Drug Metab Dispos. 2010 Nov;38(11):2023-31. doi: 10.1124/dmd.110.033787. Epub 2010 Aug 10. [Article]
Shi JG, Chen X, Emm T, Scherle PA, McGee RF, Lo Y, Landman RR, McKeever EG Jr, Punwani NG, Williams WV, Yeleswaram S: The effect of CYP3A4 inhibition or induction on the pharmacokinetics and pharmacodynamics of orally administered ruxolitinib (INCB018424 phosphate) in healthy volunteers. J Clin Pharmacol. 2012 Jun;52(6):809-18. doi: 10.1177/0091270011405663. Epub 2011 May 20. [Article]
Punwani N, Scherle P, Flores R, Shi J, Liang J, Yeleswaram S, Levy R, Williams W, Gottlieb A: Preliminary clinical activity of a topical JAK1/2 inhibitor in the treatment of psoriasis. J Am Acad Dermatol. 2012 Oct;67(4):658-64. doi: 10.1016/j.jaad.2011.12.018. Epub 2012 Jan 24. [Article]
Spoerl S, Mathew NR, Bscheider M, Schmitt-Graeff A, Chen S, Mueller T, Verbeek M, Fischer J, Otten V, Schmickl M, Maas-Bauer K, Finke J, Peschel C, Duyster J, Poeck H, Zeiser R, von Bubnoff N: Activity of therapeutic JAK 1/2 blockade in graft-versus-host disease. Blood. 2014 Jun 12;123(24):3832-42. doi: 10.1182/blood-2013-12-543736. Epub 2014 Apr 7. [Article]
Deshpande A, Reddy MM, Schade GO, Ray A, Chowdary TK, Griffin JD, Sattler M: Kinase domain mutations confer resistance to novel inhibitors targeting JAK2V617F in myeloproliferative neoplasms. Leukemia. 2012 Apr;26(4):708-15. doi: 10.1038/leu.2011.255. Epub 2011 Sep 16. [Article]
Mughal TI, Girnius S, Rosen ST, Kumar S, Wiestner A, Abdel-Wahab O, Kiladjian JJ, Wilson WH, Van Etten RA: Emerging therapeutic paradigms to target the dysregulated Janus kinase/signal transducer and activator of transcription pathway in hematological malignancies. Leuk Lymphoma. 2014 Sep;55(9):1968-79. doi: 10.3109/10428194.2013.863307. Epub 2014 Feb 17. [Article]
FDA Approved Drug Products: JAKAFI (ruxolitinib) tablets, for oral use [Link]
Santa Cruz Biotechnology, Inc.: Ruxolitinib Safety Data Sheet [Link]
LC Laboratories: Ruxolitinib Safety Data Sheet [Link]
Drugs.com: Jakafi FDA Approval History [Link]
Novartis: Novartis provides update on RUXCOVID study of ruxolitinib for hospitalized patients with COVID-19 [Link]
BC Cancer - Ruxolitinib monograph [Link]
EMA Approved Drug Products: Jakavi (ruxolitinib) oral tablets [Link]
FDA Approved Drug Products: OPZELURA (ruxolitinib) cream, for topical use [Link]
EMA Approved Drug Products: OPZELURA (ruxolitinib) Topical Cream [Link]

External Links

KEGG Drug: D09959
PubChem Compound: 25126798
PubChem Substance: 175427129
ChemSpider: 25027389
BindingDB: 50355501
RxNav: 1193326
ChEBI: 66919
ChEMBL: CHEMBL1789941
ZINC: ZINC000043207851
PharmGKB: PA166123386
PDBe Ligand: RXT
RxList: RxList Drug Page
Drugs.com: Drugs.com Drug Page
Wikipedia: Ruxolitinib

PDB Entries

4u5j / 6vgl / 6vnk / 6wtn / 7f3g

FDA label

Download (399 KB)

MSDS

Download (210 KB)

Clinical Trials

Clinical Trials Clinical Trial & Rare Diseases Add-on Data Package Explore 4,000+ rare diseases, orphan drugs & condition pairs, clinical trial why stopped data, & more. Preview package

Phase	Status	Purpose	Conditions	Count	Start Date	Why Stopped	100+ additional columns
Unlock 175K+ rows when you subscribe.View sample data
Not Available	Approved for Marketing	Not Available	Graft-versus-host Disease (GVHD)	2	somestatus	stop reason	just information to hide
Not Available	Available	Not Available	Polycythemia Vera (PV)	1	somestatus	stop reason	just information to hide
Not Available	Available	Not Available	Polycythemia Vera (PV) / Post Polycythemia Vera Myelofibrosis / Post-essential Thrombocythemia Myelofibrosis (Post-ET MF) / Primary Myelofibrosis (PMF) / Severe/Very Severe COVID-19 Illness / Steroid Refractory Acute Graft Versus Host Disease (SR aGVHD) / Steroid Refractory Chronic Graft Versus Host Disease (SR cGVHD)	1	somestatus	stop reason	just information to hide
Not Available	Completed	Not Available	Myelofibrosis	1	somestatus	stop reason	just information to hide
Not Available	Completed	Not Available	Steroid Refractory GVHD	1	somestatus	stop reason	just information to hide

Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
Tablet	Oral	10.0 mg/1
Tablet	Oral	15.0 mg/1
Tablet	Oral	20.0 mg/1
Tablet	Oral	25.0 mg/1
Tablet	Oral	5.0 mg/1
Tablet	Oral	19.8 mg
Tablet	Oral	6.6 mg
Tablet	Oral	15 mg
Tablet	Oral	20 mg
Tablet	Oral	5 mg
Tablet	Oral
Tablet	Oral	10 mg
Tablet	Oral	1000000 mg
Tablet	Oral	2000000 mg
Cream	Cutaneous	15 mg/g
Cream	Topical	15 mg/1g

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)
US7598257	Yes	2009-10-06	2028-06-24
US8822481	Yes	2014-09-02	2028-12-12
US8829013	Yes	2014-09-09	2028-12-12
US9079912	Yes	2015-07-14	2027-06-12
US8415362	Yes	2013-04-09	2028-06-24
US8722693	Yes	2014-05-13	2028-12-12
US9662335	No	2017-05-30	2026-12-12
US10016429	Yes	2018-07-10	2028-12-12
US9814722	Yes	2017-11-14	2027-06-12
US9974790	Yes	2018-05-22	2027-06-12
US10610530	Yes	2020-04-07	2028-12-12
US10639310	Yes	2020-05-05	2027-06-12
US10869870	Yes	2020-12-22	2031-11-20
US10758543	Yes	2020-09-01	2031-11-20
US11219624	Yes	2011-11-20	2031-11-20
US11510923	No	2020-09-04	2040-09-04
US11571425	No	2011-05-20	2031-05-20
US11590136	No	2011-05-20	2031-05-20
US11590137	No	2020-09-04	2040-09-04
US11590138	No	2020-06-10	2040-06-10
US11602536	No	2021-05-05	2041-05-05

Properties

State

Solid

Experimental Properties

Property	Value	Source
melting point (°C)	86	MSDS
boiling point (°C)	592.6	MSDS
water solubility	Soluble in aqueous buffers across a pH of 1-8	FDA label

Predicted Properties

Property	Value	Source
Water Solubility	0.116 mg/mL	ALOGPS
logP	2.94	ALOGPS
logP	2.48	Chemaxon
logS	-3.4	ALOGPS
pKa (Strongest Acidic)	13.89	Chemaxon
pKa (Strongest Basic)	3.91	Chemaxon
Physiological Charge	0	Chemaxon
Hydrogen Acceptor Count	4	Chemaxon
Hydrogen Donor Count	1	Chemaxon
Polar Surface Area	83.18 Å²	Chemaxon
Rotatable Bond Count	4	Chemaxon
Refractivity	98.01 m³·mol^-1	Chemaxon
Polarizability	33.07 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

Property	Value	Probability
Human Intestinal Absorption	+	1.0
Blood Brain Barrier	+	0.9673
Caco-2 permeable	-	0.5198
P-glycoprotein substrate	Non-substrate	0.7838
P-glycoprotein inhibitor I	Non-inhibitor	0.8228
P-glycoprotein inhibitor II	Inhibitor	0.7092
Renal organic cation transporter	Non-inhibitor	0.5098
CYP450 2C9 substrate	Non-substrate	0.8394
CYP450 2D6 substrate	Non-substrate	0.8075
CYP450 3A4 substrate	Non-substrate	0.6535
CYP450 1A2 substrate	Inhibitor	0.6426
CYP450 2C9 inhibitor	Non-inhibitor	0.7731
CYP450 2D6 inhibitor	Non-inhibitor	0.9208
CYP450 2C19 inhibitor	Non-inhibitor	0.6689
CYP450 3A4 inhibitor	Non-inhibitor	0.6655
CYP450 inhibitory promiscuity	High CYP Inhibitory Promiscuity	0.5753
Ames test	AMES toxic	0.5681
Carcinogenicity	Non-carcinogens	0.9308
Biodegradation	Not ready biodegradable	0.9917
Rat acute toxicity	2.5724 LD50, mol/kg	Not applicable
hERG inhibition (predictor I)	Weak inhibitor	0.633
hERG inhibition (predictor II)	Non-inhibitor	0.8772

ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)

Not Available

Spectra

Spectrum	Spectrum Type	Splash Key
Predicted MS/MS Spectrum - 10V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0a4i-0009000000-e061956fd8cac1731cd0
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0a4i-0039000000-f768be23bba650537a6b
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0arr-0193000000-d9dd0614d8244fa91643
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-03di-1292000000-03e9230574c42a376b26
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-05oa-0390000000-1cc47e9bbeec706a740b
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-02al-1940000000-aedb326c4b72231b1389
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]-	188.106314	predicted	DarkChem Lite v0.1.0
[M-H]-	167.28233	predicted	DeepCCS 1.0 (2019)
[M+H]+	189.312114	predicted	DarkChem Lite v0.1.0
[M+H]+	169.64034	predicted	DeepCCS 1.0 (2019)
[M+Na]+	188.699014	predicted	DarkChem Lite v0.1.0
[M+Na]+	175.74132	predicted	DeepCCS 1.0 (2019)

Targets

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Details1. Urokinase plasminogen activator surface receptor

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Inhibitor

General Function: Acts as a receptor for urokinase plasminogen activator (PubMed:15677461). Plays a role in localizing and promoting plasmin formation. Mediates the proteolysis-independent signal transduction activation effects of U-PA. It is subject to negative-feedback regulation by U-PA which cleaves it into an inactive form
Specific Function: Enzyme binding
Gene Name: PLAUR
Uniprot ID: Q03405
Uniprot Name: Urokinase plasminogen activator surface receptor
Molecular Weight: 36977.62 Da

References

Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]

Property	Measurement	pH	Temperature (°C)	References
EC 50 (nM)	12	N/A	N/A	A31020
IC 50 (nM)	3	N/A	N/A	A31016
IC 50 (nM)	2.8	N/A	N/A	A31019
IC 50 (nM)	6.85	N/A	N/A	A31146
Kd (nM)	0.036	N/A	N/A	A28058
Ki (nM)	0.1	N/A	N/A	A31020
Ki (nM)	0.24	N/A	N/A	A31146

Details2. Tyrosine-protein kinase JAK2

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Inhibitor
Curator comments: In vitro, ruxolitinib inhibited JAK2 with a mean half-maximal inhibitory concentration (IC50) of 2.8 nmol/L (Yang & Keating, 2012).

General Function: Non-receptor tyrosine kinase involved in various processes such as cell growth, development, differentiation or histone modifications. Mediates essential signaling events in both innate and adaptive immunity. In the cytoplasm, plays a pivotal role in signal transduction via its association with type I receptors such as growth hormone (GHR), prolactin (PRLR), leptin (LEPR), erythropoietin (EPOR), thrombopoietin (THPO); or type II receptors including IFN-alpha, IFN-beta, IFN-gamma and multiple interleukins (PubMed:7615558, PubMed:9657743, PubMed:15690087). Following ligand-binding to cell surface receptors, phosphorylates specific tyrosine residues on the cytoplasmic tails of the receptor, creating docking sites for STATs proteins (PubMed:9618263, PubMed:15690087). Subsequently, phosphorylates the STATs proteins once they are recruited to the receptor. Phosphorylated STATs then form homodimer or heterodimers and translocate to the nucleus to activate gene transcription. For example, cell stimulation with erythropoietin (EPO) during erythropoiesis leads to JAK2 autophosphorylation, activation, and its association with erythropoietin receptor (EPOR) that becomes phosphorylated in its cytoplasmic domain (PubMed:9657743). Then, STAT5 (STAT5A or STAT5B) is recruited, phosphorylated and activated by JAK2. Once activated, dimerized STAT5 translocates into the nucleus and promotes the transcription of several essential genes involved in the modulation of erythropoiesis. Part of a signaling cascade that is activated by increased cellular retinol and that leads to the activation of STAT5 (STAT5A or STAT5B) (PubMed:21368206). In addition, JAK2 mediates angiotensin-2-induced ARHGEF1 phosphorylation (PubMed:20098430). Plays a role in cell cycle by phosphorylating CDKN1B (PubMed:21423214). Cooperates with TEC through reciprocal phosphorylation to mediate cytokine-driven activation of FOS transcription. In the nucleus, plays a key role in chromatin by specifically mediating phosphorylation of 'Tyr-41' of histone H3 (H3Y41ph), a specific tag that promotes exclusion of CBX5 (HP1 alpha) from chromatin (PubMed:19783980)
Specific Function: Acetylcholine receptor binding
Gene Name: JAK2
Uniprot ID: O60674
Uniprot Name: Tyrosine-protein kinase JAK2
Molecular Weight: 130672.475 Da

References

Cervantes F, Martinez-Trillos A: Myelofibrosis: an update on current pharmacotherapy and future directions. Expert Opin Pharmacother. 2013 May;14(7):873-84. doi: 10.1517/14656566.2013.783019. Epub 2013 Mar 21. [Article]
Yang LP, Keating GM: Ruxolitinib: in the treatment of myelofibrosis. Drugs. 2012 Nov 12;72(16):2117-27. doi: 10.2165/11209340-000000000-00000. [Article]
Ostojic A, Vrhovac R, Verstovsek S: Ruxolitinib: a new JAK1/2 inhibitor that offers promising options for treatment of myelofibrosis. Future Oncol. 2011 Sep;7(9):1035-43. doi: 10.2217/fon.11.81. [Article]

Details3. Tyrosine-protein kinase JAK1

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Inhibitor
Curator comments: In vitro, ruxolitinib inhibited JAK1 with a mean half-maximal inhibitory concentration (IC50) of 3.3 nmol/L (Yang & Keating, 2012).

General Function: Tyrosine kinase of the non-receptor type, involved in the IFN-alpha/beta/gamma signal pathway (PubMed:16239216, PubMed:28111307, PubMed:32750333, PubMed:7615558, PubMed:8232552). Kinase partner for the interleukin (IL)-2 receptor (PubMed:11909529) as well as interleukin (IL)-10 receptor (PubMed:12133952). Kinase partner for the type I interferon receptor IFNAR2 (PubMed:16239216, PubMed:28111307, PubMed:32750333, PubMed:7615558, PubMed:8232552). In response to interferon-binding to IFNAR1-IFNAR2 heterodimer, phosphorylates and activates its binding partner IFNAR2, creating docking sites for STAT proteins (PubMed:7759950). Directly phosphorylates STAT proteins but also activates STAT signaling through the transactivation of other JAK kinases associated with signaling receptors (PubMed:16239216, PubMed:32750333, PubMed:8232552)
Specific Function: Atp binding
Gene Name: JAK1
Uniprot ID: P23458
Uniprot Name: Tyrosine-protein kinase JAK1
Molecular Weight: 133275.995 Da

References

Cervantes F, Martinez-Trillos A: Myelofibrosis: an update on current pharmacotherapy and future directions. Expert Opin Pharmacother. 2013 May;14(7):873-84. doi: 10.1517/14656566.2013.783019. Epub 2013 Mar 21. [Article]
Yang LP, Keating GM: Ruxolitinib: in the treatment of myelofibrosis. Drugs. 2012 Nov 12;72(16):2117-27. doi: 10.2165/11209340-000000000-00000. [Article]
Ostojic A, Vrhovac R, Verstovsek S: Ruxolitinib: a new JAK1/2 inhibitor that offers promising options for treatment of myelofibrosis. Future Oncol. 2011 Sep;7(9):1035-43. doi: 10.2217/fon.11.81. [Article]

Details4. Tyrosine-protein kinase JAK3

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Inhibitor
Curator comments: In vitro, ruxolitinib inhibited JAK3 with a mean half-maximal inhibitory concentration (IC50) of 428 nmol/L (Yang & Keating, 2012).

General Function: Non-receptor tyrosine kinase involved in various processes such as cell growth, development, or differentiation. Mediates essential signaling events in both innate and adaptive immunity and plays a crucial role in hematopoiesis during T-cells development. In the cytoplasm, plays a pivotal role in signal transduction via its association with type I receptors sharing the common subunit gamma such as IL2R, IL4R, IL7R, IL9R, IL15R and IL21R. Following ligand binding to cell surface receptors, phosphorylates specific tyrosine residues on the cytoplasmic tails of the receptor, creating docking sites for STATs proteins. Subsequently, phosphorylates the STATs proteins once they are recruited to the receptor. Phosphorylated STATs then form homodimer or heterodimers and translocate to the nucleus to activate gene transcription. For example, upon IL2R activation by IL2, JAK1 and JAK3 molecules bind to IL2R beta (IL2RB) and gamma chain (IL2RG) subunits inducing the tyrosine phosphorylation of both receptor subunits on their cytoplasmic domain. Then, STAT5A and STAT5B are recruited, phosphorylated and activated by JAK1 and JAK3. Once activated, dimerized STAT5 translocates to the nucleus and promotes the transcription of specific target genes in a cytokine-specific fashion
Specific Function: Atp binding
Gene Name: JAK3
Uniprot ID: P52333
Uniprot Name: Tyrosine-protein kinase JAK3
Molecular Weight: 125097.565 Da

References

Yang LP, Keating GM: Ruxolitinib: in the treatment of myelofibrosis. Drugs. 2012 Nov 12;72(16):2117-27. doi: 10.2165/11209340-000000000-00000. [Article]
Ostojic A, Vrhovac R, Verstovsek S: Ruxolitinib: a new JAK1/2 inhibitor that offers promising options for treatment of myelofibrosis. Future Oncol. 2011 Sep;7(9):1035-43. doi: 10.2217/fon.11.81. [Article]

Details5. Non-receptor tyrosine-protein kinase TYK2

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Inhibitor
Curator comments: In vitro, ruxolitinib inhibited TYK2 with a mean half-maximal inhibitory concentration (IC50) of 19 nmol/L (Yang & Keating, 2012).

General Function: Tyrosine kinase of the non-receptor type involved in numerous cytokines and interferons signaling, which regulates cell growth, development, cell migration, innate and adaptive immunity (PubMed:10542297, PubMed:10995743, PubMed:7657660, PubMed:7813427, PubMed:8232552). Plays both structural and catalytic roles in numerous interleukins and interferons (IFN-alpha/beta) signaling (PubMed:10542297). Associates with heterodimeric cytokine receptor complexes and activates STAT family members including STAT1, STAT3, STAT4 or STAT6 (PubMed:10542297, PubMed:7638186). The heterodimeric cytokine receptor complexes are composed of (1) a TYK2-associated receptor chain (IFNAR1, IL12RB1, IL10RB or IL13RA1), and (2) a second receptor chain associated either with JAK1 or JAK2 (PubMed:10542297, PubMed:25762719, PubMed:7526154, PubMed:7813427). In response to cytokine-binding to receptors, phosphorylates and activates receptors (IFNAR1, IL12RB1, IL10RB or IL13RA1), creating docking sites for STAT members (PubMed:7526154, PubMed:7657660). In turn, recruited STATs are phosphorylated by TYK2 (or JAK1/JAK2 on the second receptor chain), form homo- and heterodimers, translocate to the nucleus, and regulate cytokine/growth factor responsive genes (PubMed:10542297, PubMed:25762719, PubMed:7657660). Negatively regulates STAT3 activity by promototing phosphorylation at a specific tyrosine that differs from the site used for signaling (PubMed:29162862)
Specific Function: Atp binding
Gene Name: TYK2
Uniprot ID: P29597
Uniprot Name: Non-receptor tyrosine-protein kinase TYK2
Molecular Weight: 133648.77 Da

References

Ostojic A, Vrhovac R, Verstovsek S: Ruxolitinib: a new JAK1/2 inhibitor that offers promising options for treatment of myelofibrosis. Future Oncol. 2011 Sep;7(9):1035-43. doi: 10.2217/fon.11.81. [Article]
Yang LP, Keating GM: Ruxolitinib: in the treatment of myelofibrosis. Drugs. 2012 Nov 12;72(16):2117-27. doi: 10.2165/11209340-000000000-00000. [Article]

Enzymes

Details1. Cytochrome P450 3A4

Kind: Protein
Organism: Humans
Pharmacological action: Unknown
Actions: Substrate

General Function: A cytochrome P450 monooxygenase involved in the metabolism of sterols, steroid hormones, retinoids and fatty acids (PubMed:10681376, PubMed:11093772, PubMed:11555828, PubMed:12865317, PubMed:14559847, PubMed:15373842, PubMed:15764715, PubMed:19965576, PubMed:20702771, PubMed:21490593, PubMed:21576599). Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via cytochrome P450 reductase (NADPH--hemoprotein reductase). Catalyzes the hydroxylation of carbon-hydrogen bonds (PubMed:12865317, PubMed:14559847, PubMed:15373842, PubMed:15764715, PubMed:21490593, PubMed:21576599, PubMed:2732228). Exhibits high catalytic activity for the formation of hydroxyestrogens from estrone (E1) and 17beta-estradiol (E2), namely 2-hydroxy E1 and E2, as well as D-ring hydroxylated E1 and E2 at the C-16 position (PubMed:11555828, PubMed:12865317, PubMed:14559847). Plays a role in the metabolism of androgens, particularly in oxidative deactivation of testosterone (PubMed:15373842, PubMed:15764715, PubMed:22773874, PubMed:2732228). Metabolizes testosterone to less biologically active 2beta- and 6beta-hydroxytestosterones (PubMed:15373842, PubMed:15764715, PubMed:2732228). Contributes to the formation of hydroxycholesterols (oxysterols), particularly A-ring hydroxylated cholesterol at the C-4beta position, and side chain hydroxylated cholesterol at the C-25 position, likely contributing to cholesterol degradation and bile acid biosynthesis (PubMed:21576599). Catalyzes bisallylic hydroxylation of polyunsaturated fatty acids (PUFA) (PubMed:9435160). Catalyzes the epoxidation of double bonds of PUFA with a preference for the last double bond (PubMed:19965576). Metabolizes endocannabinoid arachidonoylethanolamide (anandamide) to 8,9-, 11,12-, and 14,15-epoxyeicosatrienoic acid ethanolamides (EpETrE-EAs), potentially modulating endocannabinoid system signaling (PubMed:20702771). Plays a role in the metabolism of retinoids. Displays high catalytic activity for oxidation of all-trans-retinol to all-trans-retinal, a rate-limiting step for the biosynthesis of all-trans-retinoic acid (atRA) (PubMed:10681376). Further metabolizes atRA toward 4-hydroxyretinoate and may play a role in hepatic atRA clearance (PubMed:11093772). Responsible for oxidative metabolism of xenobiotics. Acts as a 2-exo-monooxygenase for plant lipid 1,8-cineole (eucalyptol) (PubMed:11159812). Metabolizes the majority of the administered drugs. Catalyzes sulfoxidation of the anthelmintics albendazole and fenbendazole (PubMed:10759686). Hydroxylates antimalarial drug quinine (PubMed:8968357). Acts as a 1,4-cineole 2-exo-monooxygenase (PubMed:11695850). Also involved in vitamin D catabolism and calcium homeostasis. Catalyzes the inactivation of the active hormone calcitriol (1-alpha,25-dihydroxyvitamin D(3)) (PubMed:29461981)
Specific Function: 1,8-cineole 2-exo-monooxygenase activity
Gene Name: CYP3A4
Uniprot ID: P08684
Uniprot Name: Cytochrome P450 3A4
Molecular Weight: 57342.67 Da

References

Yang LP, Keating GM: Ruxolitinib: in the treatment of myelofibrosis. Drugs. 2012 Nov 12;72(16):2117-27. doi: 10.2165/11209340-000000000-00000. [Article]
Becker H, Engelhardt M, von Bubnoff N, Wasch R: Ruxolitinib. Recent Results Cancer Res. 2014;201:249-57. doi: 10.1007/978-3-642-54490-3_16. [Article]
Ajayi S, Becker H, Reinhardt H, Engelhardt M, Zeiser R, von Bubnoff N, Wasch R: Ruxolitinib. Recent Results Cancer Res. 2018;212:119-132. doi: 10.1007/978-3-319-91439-8_6. [Article]
FDA Approved Drug Products: JAKAFI (ruxolitinib) tablets, for oral use [Link]

Details2. Cytochrome P450 2C9

Kind: Protein
Organism: Humans
Pharmacological action: No
Actions: Substrate

General Function: A cytochrome P450 monooxygenase involved in the metabolism of various endogenous substrates, including fatty acids and steroids (PubMed:12865317, PubMed:15766564, PubMed:19965576, PubMed:21576599, PubMed:7574697, PubMed:9435160, PubMed:9866708). Mechanistically, uses molecular oxygen inserting one oxygen atom into a substrate, and reducing the second into a water molecule, with two electrons provided by NADPH via cytochrome P450 reductase (NADPH--hemoprotein reductase) (PubMed:12865317, PubMed:15766564, PubMed:19965576, PubMed:21576599, PubMed:7574697, PubMed:9435160, PubMed:9866708). Catalyzes the epoxidation of double bonds of polyunsaturated fatty acids (PUFA) (PubMed:15766564, PubMed:19965576, PubMed:7574697, PubMed:9866708). Catalyzes the hydroxylation of carbon-hydrogen bonds. Metabolizes cholesterol toward 25-hydroxycholesterol, a physiological regulator of cellular cholesterol homeostasis (PubMed:21576599). Exhibits low catalytic activity for the formation of catechol estrogens from 17beta-estradiol (E2) and estrone (E1), namely 2-hydroxy E1 and E2 (PubMed:12865317). Catalyzes bisallylic hydroxylation and hydroxylation with double-bond migration of polyunsaturated fatty acids (PUFA) (PubMed:9435160, PubMed:9866708). Also metabolizes plant monoterpenes such as limonene. Oxygenates (R)- and (S)-limonene to produce carveol and perillyl alcohol (PubMed:11950794). Contributes to the wide pharmacokinetics variability of the metabolism of drugs such as S-warfarin, diclofenac, phenytoin, tolbutamide and losartan (PubMed:25994031)
Specific Function: (r)-limonene 6-monooxygenase activity
Gene Name: CYP2C9
Uniprot ID: P11712
Uniprot Name: Cytochrome P450 2C9
Molecular Weight: 55627.365 Da

References

Umehara K, Huth F, Jin Y, Schiller H, Aslanis V, Heimbach T, He H: Drug-drug interaction (DDI) assessments of ruxolitinib, a dual substrate of CYP3A4 and CYP2C9, using a verified physiologically based pharmacokinetic (PBPK) model to support regulatory submissions. Drug Metab Pers Ther. 2019 May 30;34(2). pii: /j/dmdi.ahead-of-print/dmpt-2018-0042/dmpt-2018-0042.xml. doi: 10.1515/dmpt-2018-0042. [Article]
FDA Approved Drug Products: JAKAFI (ruxolitinib) tablets, for oral use [Link]

Carriers

Details1. Albumin

Kind: Protein
Organism: Humans
Pharmacological action: Unknown
Actions: Binder

General Function: Binds water, Ca(2+), Na(+), K(+), fatty acids, hormones, bilirubin and drugs (Probable). Its main function is the regulation of the colloidal osmotic pressure of blood (Probable). Major zinc transporter in plasma, typically binds about 80% of all plasma zinc (PubMed: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 (PubMed:6234017). Does not prevent iron uptake by the bacterial siderophore aerobactin (PubMed:6234017)
Specific Function: Antioxidant activity
Gene Name: ALB
Uniprot ID: P02768
Uniprot Name: Albumin
Molecular Weight: 69365.94 Da

References

FDA Approved Drug Products: JAKAFI (ruxolitinib) tablets, for oral use [Link]

Drug created at May 13, 2013 18:21 / Updated at September 15, 2024 21:55

Ruxolitinib

Identification

Structure for Ruxolitinib (DB08877)

Pharmacology

Interactions

Products

Categories

Chemical Identifiers

References

Clinical Trials

Clinical Trial & Rare Diseases Add-on Data Package

Pharmacoeconomics

Properties

Spectra

Collision Cross Sections (CCS)

Targets

References

References

References

References

References

Enzymes

References

References

Carriers

References