Mavacamten

Identification

Summary

Mavacamten is a myosin inhibitor used to treat obstructive hypertrophic cardiomyopathy.

Brand Names

Camzyos

Generic Name

Mavacamten

DrugBank Accession Number

DB14921

Background

Mavacamten is a myosin inhibitor indicated for the treatment of adults with symptomatic New York Heart Association (NYHA) class II-III obstructive hypertrophic cardiomyopathy (HCM). It received initial US FDA approval in 2022, and it is one of the first myosin inhibitors to be used in humans.¹² Mavacamten was also approved by Health Canada in October 2022 and by EMA in July 2023 for the same indication.^14,16

Type

Small Molecule

Groups

Approved, Investigational

Structure

3D

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MOLSDF3D-SDFPDBSMILESInChI

Similar Structures

Structure for Mavacamten (DB14921)

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Weight

Average: 273.336
Monoisotopic: 273.147726864

Chemical Formula

C₁₅H₁₉N₃O₂

Synonyms

• 6-(((1S)-1-Phenylethyl)amino)-3-(propan-2-yl)-1,2,3,4 tetrahydropyrimidine-2,4-dione
• Mavacamten
• MYK-461

External IDs

• MYK-461

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Pharmacology

Indication

Mavacamten is indicated for the treatment of adults with symptomatic New York Heart Association (NYHA) class II-III obstructive hypertrophic cardiomyopathy (HCM) to improve functional capacity and symptoms by the FDA, Health Canada, and the EMA.^13,14,15

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Associated Conditions

Indication Type	Indication	Combined Product Details	Approval Level	Age Group	Patient Characteristics	Dose Form
Management of	Symptomatic obstructive hypertrophic cardiomyopathy		••••••••••••	•••••		•••••••
Management of	Symptomatic obstructive hypertrophic cardiomyopathy		••••••••••••	•••••		•••••••
Management of	Symptomatic obstructive hypertrophic cardiomyopathy		••••••••••••	•••••		•••••••

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Pharmacodynamics

Mavacamten is a myosin inhibitor to prevent muscle hypercontractility. It binds to myosin and inhibits myosin interaction with actin at various stages of the thermomechanical cycle. Mechanistic studies show that mavacamten can inhibit myosin in both its active and relaxed form, thus effectively alleviating excess sarcomere power, a hallmark of hypertrophic cardiomyopathy.^13,12

In the EXPLORER-HCM trial, patients achieved reductions in mean resting and provoked (Valsalva) LVOT gradient by Week 4 which were sustained throughout the 30-week trial. At Week 30, the mean (SD) changes from baseline in resting and Valsalva LVOT gradients were -39 (29) mmHg and -49 (34) mmHg, respectively, for the CAMZYOS group and -6 (28) mmHg and -12 (31) mmHg, respectively, for the placebo group. The reductions in the Valsalva LVOT gradient were accompanied by decreases in LVEF, generally within the normal range. Eight weeks after discontinuation of CAMZYOS, mean LVEF and Valsalva LVOT gradients were similar to baseline.¹³

Echocardiographic measurements of the cardiac structure showed a mean (SD) reduction from baseline at Week 30 in left ventricular mass index (LVMI) in the mavacamten group (-7.4 [17.8] g/m2) versus an increase in LVMI in the placebo group (8.9 [15.3] g/m2). There was also a mean (SD) reduction from baseline in left atrial volume index (LAVI) in the mavacamten group(-7.5 [7.8] mL/m2) versus no change in the placebo group (-0.1 [8.7] mL/m2). The clinical significance of these findings is unknown.¹³

A reduction in a biomarker of cardiac wall stress, NT-proBNP, was observed by Week 4 and sustained through the end of treatment. At Week 30 compared with baseline, the reduction in NT-proBNP after mavacamten treatment was 80% greater than for placebo (proportion of geometric mean ratio between the two groups, 0.20 [95% CI: 0.17, 0.24]). The clinical significance of these findings is unknown.¹³

In healthy volunteers receiving multiple doses of mavacamten, a concentration-dependent increase in the QTc interval was observed at doses up to 25 mg once daily. No acute QTc changes have been observed at similar exposures during single-dose studies. The mechanism of the QT prolongation effect is not known. A meta-analysis across clinical studies in HCM patients does not suggest clinically relevant increases in the QTc interval in the therapeutic exposure range. In HCM, the QT interval may be intrinsically prolonged due to the underlying disease, in association with ventricular pacing, or in association with drugs with the potential for QT prolongation commonly used in the HCM population. The effect of coadministration of mavacamten with QT-prolonging drugs or in patients with potassium channel variants resulting in a long QT interval has not been characterized.¹³

Mechanism of action

Myosin is a family of enzymes that can produce mechanical output by an ATP-mediated cyclic interaction with actin. When ATP is bound to the myosin head, it is hydrolyzed into ADP and organophosphate by myosin ATPase activity, and the energy produced from the reaction is stored in the myosin head. As the organophosphate dissociates from myosin, it shifts myosin into a strong binding state to actin, thus creating a myosin-actin complex otherwise known as "cross-bridging".^2,3,5Dissociation of the organophosphate also causes a conformation change in myosin that creates strain in the actin-myosin bridge that can only be released once the actin and myosin filaments slide past each other, thus shortening the sarcomere and create a muscle contraction.^5,9 Once the sliding is completed, ADP is released to create further movement of the myosin head.⁹ Although this ADP release-induced movement is minor and unlikely to contribute to the sarcomere movement, researchers have hypothesized that this movement is likely essential in limiting the sliding velocity of actin.^6,7,8,9Finally, myosin then bind to a new ATP molecule to initiate the chemomechanical cycle again.

Mavacamten reduces sarcomere hypercontractility by acting as an allosteric and reversible modulator of the beta-cardiac isoform of myosin to reduce its ATPase activity, thus reducing actin-myosin cross bridging.⁴ Specifically, mavacamten inhibits the phosphate release, the cycle's rate-limiting step, without affecting the ADP release rate in actin-bound myosin.¹Also, mavacamten inhibits binding of ADP-bound myosin to actin as well as ADP release to prime the myosin head to initiate turnover.³Recently, it was also discovered when myosin is not in its active state to interact with actin, it exists in equilibrium between 2 energy sparing states: a disordered relaxed state, where interaction between actin and myosin by the thin filament regulatory proteins, and a super relaxed state, where significant myosin head-to-head interaction lengthen ATP turnover rate.^10,11. Mavacamten's binding to myosin can shift the equilibrium toward the super relaxed state, effectively exerting both a basal and actin-activated ATP inhibition.^10,13

Target	Actions	Organism
AMyosin-7	inhibitory allosteric modulator	Humans

Absorption

Mavacamten has an estimated oral bioavailability of at least 85% and T_max of 1 hour.¹³ Mavacamten exposures (AUC) increased up to 220% in patients with mild (Child-Pugh A) or moderate (Child-Pugh B) hepatic impairment. The effect of severe (Child-Pugh C) hepatic impairment is unknown.¹³

Volume of distribution

Through the use of a simple 4-species (mouse, rat, dog, and cynomolgus monkey) allometric scaling of unbound blood steady-state volume of distribution, the human volume of distribution of mavacamten is predicted to be 9.5 L/kg.¹

Protein binding

Plasma protein binding of mavacamten is between 97 and 98%.¹³

Metabolism

Mavacamten is extensively metabolized, primarily through CYP2C19 (74%), CYP3A4 (18%), and CYP2C9 (8%).¹³

Hover over products below to view reaction partners

• Mavacamten
  • MYK-2210
    • MYK-2210 glucuronide
  • MYK-1078

Route of elimination

Following a single 25 mg dose of radiolabeled mavacamten, 7% of the dose was recovered in feces (1% unchanged) and 85% in urine (3% unchanged).¹³

Half-life

Mavacamten has a variable terminal t1/2 that depends on CYP2C19 metabolic status. Mavacamten's terminal half-life is 6-9 days in CYP2C19 normal metabolizers (NMs), which is prolonged in CYP2C19 poor metabolizers (PMs) to 23 days.¹³

Clearance

Mavacamten demonstrates a long terminal half-life and thus low clearance, with an estimated plasma clearance using human hepatocytes of less than 4.9 mL/min/kg.¹ Assuming a one-compartment model, using simple allometric scaling of unbound blood clearance of mouse, rat, dog, and cynomolgus monkey, human plasma clearance of mavacamten is estimated to be 0.51 mL/min/kg.¹

Adverse Effects

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Toxicity

Human experience of overdose with CAMZYOS is limited. CAMZYOS has been given as a single dose of up to 144 mg in patients with HCM. One subject administered a single dose of 144 mg experienced serious adverse events including vasovagal reaction, hypotension, and asystole, but the subject recovered. In healthy subjects, doses of up to 25 mg have been administered for up to 25 days, with 3 of 8 participants treated at the 25-mg dose level experiencing 20% or greater reductions in LVEF. An infant's death was reported after accidental ingestion of three 15-mg capsules.¹³

Systolic dysfunction is the most likely result of overdosage of CAMZYOS. Treatment of overdose with CAMZYOS consists of discontinuation of CAMZYOS treatment as well as medically supportive measures to maintain hemodynamic stability, including close monitoring of vital signs and LVEF and management of the clinical status of the patient. Overdose in humans can be life-threatening and result in asystole refractory to any medical intervention.¹³

Mavacamten was not genotoxic in a bacterial reverse mutation test (Ames test), a human in vitro lymphocyte clastogenicity assay, or a rat in vivo micronucleus assay. There was no evidence of carcinogenicity seen in a 6-month rasH2 transgenic mouse study at mavacamten doses of up to 2.0 mg/kg/day in males and 3.0 mg/kg/day in females, which resulted in exposures (AUC) that were 1.8- and 3-fold in males and females, respectively, compared to AUC exposures in humans at the MRHD.¹³

In reproductive toxicity studies, there was no evidence of the effects of mavacamten on mating and fertility in male or female rats at doses up to 1.2 mg/kg/day, or on the viability and fertility of offspring of dams dosed up to 1.5 mg/kg/day. Plasma exposure (AUC) of mavacamten at the highest dose tested was the same as in humans at the MRHD.¹³

The safety of mavacamten has been evaluated in rats and dogs at multiple dose levels (0.06 to 10 mg/kg/day) orally. Noted toxicities, including echocardiographic findings, reduction in systolic function, cardiac dilation, and death, as well as increased heart weights in rats, were consistent with mavacamten’s mechanism of action and primary pharmacological activity. Other findings included cardiac osseous metaplasia in rats and QTc prolongation in dogs. Plasma exposures (AUC) at the NOAEL in rats and dogs were 0.1 and 0.3 times, respectively, human exposure (AUC) at the MRHD.¹³

Pathways

Not Available

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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 Mavacamten.
Abametapir	The serum concentration of Mavacamten can be increased when it is combined with Abametapir.
Abatacept	The metabolism of Mavacamten can be increased when combined with Abatacept.
Abemaciclib	The serum concentration of Abemaciclib can be decreased when it is combined with Mavacamten.
Abiraterone	The serum concentration of Abiraterone can be decreased when it is combined with Mavacamten.

Food Interactions

No interactions found.

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Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End	Region	Image
Camzyos	Capsule	10 mg	Oral	Bristol Myers Squibb Pharma Eeig	2023-07-26	Not applicable
Camzyos	Capsule	2.5 mg	Oral	Bristol Myers Squibb Pharma Eeig	2023-07-26	Not applicable
Camzyos	Capsule	10 mg	Oral	Bristol Myers Squibb	2023-06-13	Not applicable
Camzyos	Capsule	5 mg	Oral	Bristol Myers Squibb Pharma Eeig	2023-08-16	Not applicable
Camzyos	Capsule, gelatin coated	15 mg/1	Oral	Myokardia, Inc.	2022-04-28	Not applicable

Categories

ATC Codes

C01EB24 — Mavacamten

• C01EB — Other cardiac preparations
• C01E — OTHER CARDIAC PREPARATIONS
• C01 — CARDIAC THERAPY
• C — CARDIOVASCULAR SYSTEM

Drug Categories

• Amines
• Benzene Derivatives
• Benzyl Compounds
• Cardiac Myosin Inhibitor
• Cardiac Therapy
• Cytochrome P-450 CYP2B6 Inducers
• Cytochrome P-450 CYP2B6 Inducers (strength unknown)
• Cytochrome P-450 CYP2C19 Inducers
• Cytochrome P-450 CYP2C19 Inducers (strength unknown)
• Cytochrome P-450 CYP2C19 Substrates
• Cytochrome P-450 CYP2C8 Substrates
• Cytochrome P-450 CYP2C9 Inducers
• Cytochrome P-450 CYP2C9 Inducers (strength unknown)
• Cytochrome P-450 CYP2C9 Substrates
• 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 CYP3A5 Substrates
• Cytochrome P-450 Enzyme Inducers
• Cytochrome P-450 Substrates
• Pyrimidines
• Pyrimidinones

Classification

Not classified

Affected organisms

Not Available

Chemical Identifiers

UNII

QX45B99R3J

CAS number

1642288-47-8

InChI Key

RLCLASQCAPXVLM-NSHDSACASA-N

InChI

InChI=1S/C15H19N3O2/c1-10(2)18-14(19)9-13(17-15(18)20)16-11(3)12-7-5-4-6-8-12/h4-11,16H,1-3H3,(H,17,20)/t11-/m0/s1

IUPAC Name

6-{[(1S)-1-phenylethyl]amino}-3-(propan-2-yl)-1,2,3,4-tetrahydropyrimidine-2,4-dione

SMILES

CC(C)N1C(=O)NC(N[C@@H](C)C2=CC=CC=C2)=CC1=O

References

General References

1. Grillo MP, Erve JCL, Dick R, Driscoll JP, Haste N, Markova S, Brun P, Carlson TJ, Evanchik M: In vitro and in vivo pharmacokinetic characterization of mavacamten, a first-in-class small molecule allosteric modulator of beta cardiac myosin. Xenobiotica. 2019 Jun;49(6):718-733. doi: 10.1080/00498254.2018.1495856. Epub 2018 Oct 1. [Article]
2. Pham S, Puckett Y: Physiology, Skeletal Muscle Contraction . [Article]
3. Kawas RF, Anderson RL, Ingle SRB, Song Y, Sran AS, Rodriguez HM: A small-molecule modulator of cardiac myosin acts on multiple stages of the myosin chemomechanical cycle. J Biol Chem. 2017 Oct 6;292(40):16571-16577. doi: 10.1074/jbc.M117.776815. Epub 2017 Aug 14. [Article]
4. Green EM, Wakimoto H, Anderson RL, Evanchik MJ, Gorham JM, Harrison BC, Henze M, Kawas R, Oslob JD, Rodriguez HM, Song Y, Wan W, Leinwand LA, Spudich JA, McDowell RS, Seidman JG, Seidman CE: A small-molecule inhibitor of sarcomere contractility suppresses hypertrophic cardiomyopathy in mice. Science. 2016 Feb 5;351(6273):617-21. doi: 10.1126/science.aad3456. [Article]
5. Brenner B, Eisenberg E: The mechanism of muscle contraction. Biochemical, mechanical, and structural approaches to elucidate cross-bridge action in muscle. Basic Res Cardiol. 1987;82 Suppl 2:3-16. doi: 10.1007/978-3-662-11289-2_1. [Article]
6. Jackson DR Jr, Baker JE: The energetics of allosteric regulation of ADP release from myosin heads. Phys Chem Chem Phys. 2009 Jun 28;11(24):4808-14. doi: 10.1039/b900998a. Epub 2009 May 8. [Article]
7. Siemankowski RF, Wiseman MO, White HD: ADP dissociation from actomyosin subfragment 1 is sufficiently slow to limit the unloaded shortening velocity in vertebrate muscle. Proc Natl Acad Sci U S A. 1985 Feb;82(3):658-62. doi: 10.1073/pnas.82.3.658. [Article]
8. Veigel C, Wang F, Bartoo ML, Sellers JR, Molloy JE: The gated gait of the processive molecular motor, myosin V. Nat Cell Biol. 2002 Jan;4(1):59-65. doi: 10.1038/ncb732. [Article]
9. Houdusse A, Sweeney HL: How Myosin Generates Force on Actin Filaments. Trends Biochem Sci. 2016 Dec;41(12):989-997. doi: 10.1016/j.tibs.2016.09.006. Epub 2016 Oct 4. [Article]
10. Gollapudi SK, Ma W, Chakravarthy S, Combs AC, Sa N, Langer S, Irving TC, Nag S: Two Classes of Myosin Inhibitors, Para-nitroblebbistatin and Mavacamten, Stabilize beta-Cardiac Myosin in Different Structural and Functional States. J Mol Biol. 2021 Nov 19;433(23):167295. doi: 10.1016/j.jmb.2021.167295. Epub 2021 Oct 8. [Article]
11. McNamara JW, Li A, Dos Remedios CG, Cooke R: The role of super-relaxed myosin in skeletal and cardiac muscle. Biophys Rev. 2015 Mar;7(1):5-14. doi: 10.1007/s12551-014-0151-5. Epub 2014 Dec 20. [Article]
12. Pysz P, Rajtar-Salwa R, Smolka G, Olivotto I, Wojakowski W, Petkow-Dimitrow P: Mavacamten - a new disease-specific option for pharmacological treatment of symptomatic patients with hypertrophic cardiomyopathy. Kardiol Pol. 2021;79(9):949-954. doi: 10.33963/KP.a2021.0064. Epub 2021 Jul 16. [Article]
13. FDA Approved Drug Proucts: CAMZYOS (mavacamten) capsules for oral use [Link]
14. Health Canada Approved Drug Products: CAMZYOS (mavacamten) Oral Capsules [Link]
15. EMA Approved Drug Products: CAMZYOS (Mavacamten) capsules, for oral use [Link]
16. EC approves BMS’ Camzyos for hypertrophic cardiomyopathy [Link]

External Links

ChemSpider

57876199

RxNav

2600867

ChEMBL

CHEMBL4297517

PharmGKB

PA166272922

PDBe Ligand

XB2

Wikipedia

Mavacamten

PDB Entries

8qyq / 8qyr

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	Recruiting	Treatment	Hypertrophic Cardiomyopathy (HCM)	1
3	Active Not Recruiting	Treatment	Obstructive Hypertrophic Cardiomyopathy	3
3	Completed	Treatment	Obstructive Hypertrophic Cardiomyopathy	1
3	Not Yet Recruiting	Treatment	Hypertrophic Cardiomyopathy (HCM)	1
3	Recruiting	Treatment	Hypertrophic Cardiomyopathy (HCM)	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
Capsule	Oral	10 mg
Capsule	Oral	15 mg
Capsule	Oral	2.5 mg
Capsule	Oral	5 mg
Capsule, gelatin coated	Oral	10 mg/1
Capsule, gelatin coated	Oral	15 mg/1
Capsule, gelatin coated	Oral	2.5 mg/1
Capsule, gelatin coated	Oral	5 mg/1

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
US9585883	No	2017-03-07	2034-06-19
US9181200	No	2015-11-10	2034-06-19

Properties

State

Solid

Experimental Properties

Not Available

Predicted Properties

Property	Value	Source
Water Solubility	0.226 mg/mL	ALOGPS
logP	2.1	ALOGPS
logP	2.21	Chemaxon
logS	-3.1	ALOGPS
pKa (Strongest Acidic)	10.7	Chemaxon
pKa (Strongest Basic)	-3.3	Chemaxon
Physiological Charge	0	Chemaxon
Hydrogen Acceptor Count	3	Chemaxon
Hydrogen Donor Count	2	Chemaxon
Polar Surface Area	61.44 Å2	Chemaxon
Rotatable Bond Count	4	Chemaxon
Refractivity	86.78 m3·mol-1	Chemaxon
Polarizability	29.92 Å3	Chemaxon
Number of Rings	2	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	splash10-00di-0190000000-3753a985bf52a671ecda
Predicted MS/MS Spectrum - 10V, Negative (Annotated)	Predicted LC-MS/MS	splash10-00di-0290000000-f4d5d73dc1aa9d657dc1
Predicted MS/MS Spectrum - 20V, Positive (Annotated)	Predicted LC-MS/MS	splash10-0ab9-0940000000-2a49b3fd07639fd837c4
Predicted MS/MS Spectrum - 20V, Negative (Annotated)	Predicted LC-MS/MS	splash10-05fr-0890000000-60d443b30daa6dff46d0
Predicted MS/MS Spectrum - 40V, Positive (Annotated)	Predicted LC-MS/MS	splash10-052f-4910000000-45d21a6ce7cc8ca5d8f5
Predicted MS/MS Spectrum - 40V, Negative (Annotated)	Predicted LC-MS/MS	splash10-0f6x-3910000000-c5f273f4e15a1910ac52
Predicted 1H NMR Spectrum	1D NMR	Not Applicable
Predicted 13C NMR Spectrum	1D NMR	Not Applicable

Chromatographic Properties

Collision Cross Sections (CCS)

Not Available

Targets

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Details1. Myosin-7

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitory allosteric modulator

General Function

Microfilament motor activity

Specific Function

Muscle contraction.

Gene Name

MYH7

Uniprot ID

P12883

Uniprot Name

Myosin-7

Molecular Weight

223095.5 Da

References

1. Kawas RF, Anderson RL, Ingle SRB, Song Y, Sran AS, Rodriguez HM: A small-molecule modulator of cardiac myosin acts on multiple stages of the myosin chemomechanical cycle. J Biol Chem. 2017 Oct 6;292(40):16571-16577. doi: 10.1074/jbc.M117.776815. Epub 2017 Aug 14. [Article]

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Drug created at May 20, 2019 14:35 / Updated at December 02, 2023 06:46