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Preterm Labor
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
Giving ambroxol to women at risk of PTB to prevent neonatal RDS is not supported by available evidence. Prenatal administration of ambroxol to reduce the risk of RDS in preterm infants has not been shown to reduce the incidence of RDS or perinatal mortality when compared to betamethasone or placebo. Maternal adverse effects were similar in ambroxol- and betamethasone-treated women. Since the trials included in the Cochrane systematic review were of very low to moderate quality, there is insufficient evidence to support or refute this intervention [35].
Ambroxol
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
Ambroxol is an aromatic amine and a metabolite of bromhexine that stimulates mucociliary action and clears the air passages in the respiratory tract. As a secretolytic agent it is indicated for treatment of bronchopulmonary diseases with abnormal or excessive mucus secretion and transport. It allows the mucus to be more easily cleared and eases a patient’s breathing. In pharmaceutical products, ambroxol is employed as ambroxol hydrochloride (CAS number 23828-92-4, EC number 245-899-2, molecular formula C13H19Br2ClN2O) (1).
Topical Pain Medications and Their Role in Pain Management
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Ambroxol is an agent that is most commonly used to treat respiratory diseases to combat excessive mucus production. Mechanistically, it acts as a voltage gated sodium channel blocker, blocking subtype Nav 1.8 expressed on nociceptive C fiber neurons.34
The discovery and development of transmembrane serine protease 2 (TMPRSS2) inhibitors as candidate drugs for the treatment of COVID-19
Published in Expert Opinion on Drug Discovery, 2022
Christiana Mantzourani, Sofia Vasilakaki, Velisaria-Eleni Gerogianni, George Kokotos
Bromhexine hydrochloride (6, Figure 3) is an orally bioavailable drug, which is used as a mucolytic cough suppressant, with few to no adverse effects [85]. This drug is further metabolized to ambroxol (7, Figure 3) by removal of a methyl group and hydroxylation on the cyclohexyl ring. Ambroxol is also a mucoactive agent, which is in use in cough syrup [86]. Bromhexine hydrochloride selectively inhibits TMPRSS2 activity with an IC50 value of 0.75 μM, while it is less active against hepsin, matriptase, trypsin and thrombin [87]. Furthermore, the efficacy of bromhexine against the cytopathic effect (CPE) of SARS-CoV-2 infection has been demonstrated by the National Institutes of Health (NIH), with an AC50 of 8.9 μΜ [88].
Current and emerging pharmacotherapy for Gaucher disease in pediatric populations
Published in Expert Opinion on Pharmacotherapy, 2021
Richard Sam, Emory Ryan, Emily Daykin, Ellen Sidransky
Already there is considerable anecdotal data regarding Ambroxol in the pediatric population from scattered case reports. One report described a 5-year-old female patient with GD1 (genotype p.Leu395Trpfs*8/p.Arg392Trp) with hepatosplenomegaly, anemia, thrombocytopenia, bone lesions including aseptic necrosis of the femoral heads bilaterally, and elevated plasma chitotriosidase activity. The authors reported that the administration of Ambroxol (10 mg/kg/day initially for 6 months, then increased to 15 mg/kg/day for 2.5 years) was safe, and resulted in remodeling of the sphericity of the femoral head bilaterally [105]. Ambroxol has also been administered in neuronopathic forms of GD with some indications of neurological improvement, particularly in seizure control and gait [103,104,106–109].
Therapeutic strategies for Parkinson’s disease: promising agents in early clinical development
Published in Expert Opinion on Investigational Drugs, 2020
Margherita Fabbri, Santiago Perez-Lloret, Olivier Rascol
GBA mutations are the largest risk factor for the development of PD [79]. The mechanism by which GBA1 mutations increase the risk of PD is still unknown, but there is evidence supporting changes in mutated GCase influencing α-synuclein aggregation [80], lysosomal-autophagy axis changes [81], and endoplasmic reticulum stress [82,83]. Increasing GCase activity might enhance α-synuclein degradation in neurons. Different mechanisms can be targeted for a therapeutic approach, including enzyme replacement therapy, drugs that modulate GCase activity, and glucosylceramide synthase inhibitors that block the formation of glucosylceramide and reduce α-synuclein aggregates [84]. Small-molecule chaperones can assist in the correct folding of mutant GCase molecules in the reticulum, contributing to their transport to the lysosomes and increasing GCase activity. Ambroxol, an orally active secretolytic agent licensed for respiratory diseases to reduce mucous production, is such a molecule, with encouraging preclinical tests. In an open-label pilot trial (NCT02941822), ambroxol showed its ability to penetrate cerebrospinal fluid, modify cerebrospinal fluid α-synuclein levels, and decrease mean MDS-UPDRS part III in patients with and without GBA1 mutations [85]. A randomized placebo-controlled Phase II trial aiming to evaluate its effect on motor and cognitive symptoms of patients with PD dementia is currently ongoing (NCT02914366).