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Last update 08 May 2025

Myotoxicity

Last update 08 May 2025

Basic Info

Synonyms

Drug Associated Myopathies, Drug Associated Myopathy, Drug Induced Myopathies

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Introduction

Damage to the muscle or its function secondary to toxic substances such as drugs used in CHEMOTHERAPY; IMMUNOTHERAPY; or RADIATION.

Clinical Trials associated with Myotoxicity

NCT06508177

/ RecruitingNot ApplicableIIT

Does Postoperative Analgesic Modalities Effect Blood Creatin Phosphokinase Levels After Laparoscopic Cholecystectomy Surgery?

Regional anesthesia and analgesia technics are widely and securely used during general surgery procedures. Interfascial plane blocks are the latest used ones for analgesia. There are studies in literature indicating that bupivacaine cause myotoxicity. The investigators aimed to examine plasma creatine phosphokinase (CPK) levels to see whether myotoxicity occurs or not after fascial plane blocks are applied to patients undergoing laparoscopic cholecystectomy.

Start Date05 Aug 2024

Sponsor / Collaborator-

NCT06707532

/ RecruitingNot ApplicableIIT

The Use of Muscle Relaxants During Electroporation Ablation (PFA) as a Potential Protective Factor Against Damage to Transverse Striated Muscle Tissue and the Heart

The study aims to improve the safety of the electroporation ablation (PFA) procedure by using muscle relaxants to reduce skeletal muscle damage during the procedure. It will also assess myocardial damage to improve the procedure's quality and speed up recovery after the procedure.

Start Date01 Aug 2024

Sponsor / Collaborator-

NCT05505890

/ CompletedNot ApplicableIIT

Effects of Postoperative Analgesic Modalities on Plasma Creatine Phosphokinase(CPK) Levels After Knee Artroplasty

Regional anesthesia and analgesia technics are widely and securely used during orthopedic surgery. Interfascial plane blocks are the latest used ones for analgesia. There are studies in literature indicating that bupivacaine cause myotoxicity. We aimed to examine plasma CPK(creatine phosphokinase) levels to see whether myotoxicity occurs or not after suprainguinal fascial plane block is applied to patients undergoing knee artroplasty surgery.

Start Date16 Dec 2022

Sponsor / Collaborator-

100 Clinical Results associated with Myotoxicity

100 Translational Medicine associated with Myotoxicity

0 Patents (Medical) associated with Myotoxicity

1,345

Literatures (Medical) associated with Myotoxicity

01 Jun 2025·Pharmacology Biochemistry and Behavior

Agomelatine with cognitive behavioral therapy reduces insomnia severity index and subjective units of distress scores than initial-dose clonazepam in moderate to severe insomnia patients: A quasi-experimental study

Article

Author: Ravikumar, Abinaya ; Sivaraman, Varadharajan ; Alqifari, Saleh F ; Jeyabalan, Anu Priya ; Ravikumar, Chandini ; Ravi, Bharath ; PannirukaiSelvan, Nithishadevi ; Shanmugasundaram, Natarajan ; Prabahar, Kousalya ; Sankar, Karthik

BACKGROUNDInsomnia can be caused by various factors including lack of sleep, stress, sadness, hormonal changes, excessive caffeine, anxiety, mental health disorders, and medications. Treatments include finding the cause, improving sleep patterns, using behavioral therapy, and taking sleeping pills in most cases. However, the drugs often cause worse side effects than insomnia. This study compared the efficacy of initial agomelatine and clonazepam doses with cognitive behavioral therapy for insomnia (CBT-i) in moderate to severe insomnia patients.METHODSThis quasi-experiment study involved 230 moderate to severe insomnia patients with group A as clonazepam 0.25 mg and B as agomelatine 25 mg. CBT-i was received by both of the groups and the Insomnia Severity Index (ISI), Subjective Units of Distress Scale (SUDS) score, medication adherence, and Adverse Drug Reactions (ADRs) were followed for up to 24 weeks.RESULTSIn the comparative analysis between and within groups, group B exhibited a significant reduction in ISI (p = 0.001) and SUDS (p = 0.001) scores at week 24 compared to group A. Overall, both groups demonstrated improved adherence. However, 12 patients in group A and 10 in group B experienced ADR, which included drowsiness, hypersalivation, diarrhea, maculopapular rash, and myotoxicity. The clonazepam-treated group showed reduced efficacy from week 12 onwards in the ISI and from week 16 in the SUDS median score, which was not observed in the agomelatine group.CONCLUSIONThe initial dose of agomelatine with CBT-i has a better impact on improving moderate to severe insomnia than the initial dose of clonazepam with CBT-i.

28 May 2025·Nutrition and Cancer

Creatine Supplementation Mitigates Doxorubicin-Induced Skeletal Muscle Dysfunction but Not Cardiotoxicity

Article

Author: Marinello, Poliana Camila ; Chimin, Patrícia ; Nunes, J.H.C. ; de Matos, Ricardo Luís Nascimento ; Bracarense, Ana Paula Frederico Rodrigues Loureiro ; Guimarães, T.A.S. ; Cella, Paola Sanches ; Moura, Felipe Arruda ; Deminice, Rafael

Creatine has demosntrated protective effects against muscle dysfunction, but its potential protection against doxorubicin-induced cardio and skeletal muscle toxicity remains poorly understood. We aimed to investigate the protective effects of creatine supplementation against doxorubicin-induced cardio and skeletal muscle myotoxicity. This study analyzed twenty male C57BL/6J mice, divided into three groups: Control (C; n = 6), Dox (n = 7) which received weekly doxorubicin injections (16 mg/kg i.p. in 20 days) and DoxCr (n = 7) with both doxorubicin and creatine supplementation (4%). Doxorubicin administration induced skeletal muscle atrophy in extensor digitorum longus (EDL) (-28%) and soleus muscles (-17%), accompanied by a decline in muscle strength. This atrophic response was concomitant with increased oxidative stress and elevated levels of IL-6. Cardiotoxic effects of doxorubicin were marked by a 15% reduction in cardiac mass and a significant 21% decrease in cardiomyocyte diameter, alongside a substantial 58% rise in IL-6 levels. On the opposite creatine supplementation mitigated doxorubicin-induced oxidative stress (elevated MDA and IL-6, and reduced GSH/GSSG ratio) and prevented skeletal muscle atrophy in both the EDL and soleus muscles, while also enhancing muscle strength. However, protective effects were not observed in cardiac muscle. Creatine protects skeletal, but not cardiac muscle against doxorubicin-induced toxicity, atrophy and strength loss.

01 May 2025·British Journal of Pharmacology

Silencing drug transporters in human primary muscle cells modulates atorvastatin pharmacokinetics: A pilot study

Article

Author: Elens, Laure ; Terrasi, Romano ; Muccioli, Giulio G. ; Deldicque, Louise ; Hoste, Emilia ; Haufroid, Vincent ; Lingurski, Maxime ; Pyr dit Ruys, Sébastien ; Paquot, Adrien ; Panin, Nadtha

Background and PurposeNon‐adherence to atorvastatin treatment is relatively common and partly due to statin‐related myotoxicities (SRMs). The risk of developing SRM is dose‐ and concentration‐dependent, highlighting the importance of atorvastatin pharmacokinetics. This study explored the inter‐individual variabilities in expression of the atorvastatin transporter gene contributing to modulation of atorvastatin within the muscle cell.Experimental ApproachmRNA levels of efflux and influx transporters were measured and modulated with siRNAs to evaluate effects on intracellular accumulation of atorvastatin in primary cultures of differentiated myotubes from 12 human volunteers.Key ResultsAll genes assessed were expressed with a high inter‐individual variability. In differentiated myotubes, efflux transporters were expressed at higher levels than the influx carriers. When considering efflux and influx transporters separately, ABCC1 and SLCO2B1 are the most highly expressed efflux and influx transporters. Suppression of ABCC1, ABCC4 and/or ABCG2 mRNA levels with siRNA significantly increased intracellular accumulation of atorvastatin in differentiated myotubes. Interestingly, the siRNA targeting ABCG2 had a moderate effect on intracellular accumulation of atorvastatin in a volunteer expressing the ABCG2 variant rs2231142 (c.421C>A, p.Gln141Lys). This hypothesis was further validated in a HEK recombinant model overexpressing ABCG2 either wild‐type (421C) or variant (421A). Reduction of SLCO1B1 and SLCO2B1 mRNA levels significantly modified intracellular accumulation of atorvastatin in only some volunteers, depending on the expression levels of transporters.Conclusion and ImplicationsSilencing ABCC1, ABCC4 or ABCG2 expression alters accumulation of atorvastatin in myotubes, whereas the effect of silencing influx transporters depends on the expression of these transporters.

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