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atorvastatin strontium (Newvast)

✓ Approved

Hanmi Pharmaceutical · HMGCR · Small Molecule

What is atorvastatin strontium?

atorvastatin strontium is a small molecule developed by Hanmi Pharmaceutical. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesNewvast
CompanyHanmi Pharmaceutical
Drug ClassSmall Molecule
Molecular TargetHMGCR
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Hanmi Pharmaceutical

Mechanism of Action

Molecular Targets

atorvastatin strontium acts on 1 molecular target:

HMGCR3-hydroxy-3-methylglutaryl-CoA reductase (LDLCQ3, LGMDR28)
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Therapeutic Indications

atorvastatin strontium is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersHypercholesterolaemia✓ Approved
Metabolism and nutrition disordersHyperlipidaemia✓ Approved

Related Research Articles

PubMedJournal of the American Heart Association2026-10-16

Association of Non-Cytochrome P450 3A4-Metabolized Statins Versus Atorvastatin With Major Adverse Cardiovascular Events in Patients With Cancer Receiving Tyrosine Kinase Inhibitors: A Propensity Score-Matched Target Trial Emulation.

Liao Jing-Huan JH, Chang Wei-Cheng WC, Jhou Hong-Jie HJ, Chen Hsin-Yu HY et al.

Tyrosine kinase inhibitors (TKIs) often undergo CYP3A4 (cytochrome P450 3A4) metabolism. Atorvastatin is a CYP3A4 substrate, whereas rosuvastatin and pitavastatin largely bypass this pathway. We evaluated whether statin choice was associated with major adverse cardiovascular events in TKI-treated patients with cancer. Using TriNetX, we conducted an active-comparator, new-user target trial emulation among adults with cancer receiving their first TKI. The index date was the first statin dispensation; outcome ascertainment began on Day 30 and continued up to 3 years. Separate 1:1 propensity score-matched comparisons included rosuvastatin versus atorvastatin (primary; 2215 per group), pitavastatin comparisons, and a pooled non-CYP3A4 statin comparison. Among 10 843 eligible patients (mean age, 66.7 years; 60.7% male), rosuvastatin was associated with a lower major adverse cardiovascular events rate than atorvastatin (624 versus 769 events; hazard ratio [HR], 0.84 [95% CI, 0.76-0.93]). The proportional-hazards assumption was violated (P=0.042), so the HR was interpreted as a time-averaged association. The pooled comparison was concordant (HR, 0.87 [95% CI, 0.78-0.96]). The early-persistence Day-180 estimate was imprecise (HR, 0.90 [95% CI, 0.73-1.09]). Rosuvastatin use was associated with lower major adverse cardiovascular events than atorvastatin in TKI-treated patients with cancer. This observational finding is compatible with, but does not establish, a CYP3A4-mediated interaction. Residual confounding, nonaligned TKI and statin timing in part of the primary cohort, and lack of individual-level event-time data require prospective confirmation.

PMID 42885792
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PubMedCancer gene therapy2026-10-16

Restoration of p53 function via hybrid strontium sulfite nanoparticles modified LNP improves the antitumor efficacy in breast cancers.

Karim Md Emranul ME, Holl Mark M Banaszak MMB, Corrie Simon S, Chowdhury Ezharul Hoque EH

The astounding success of mRNA empowers the diverse application of mRNA therapeutics in multiple genetic disorders. Besides the vaccines, the rational design of mRNA drugs has been explored widely to target the undruggable gene therapy for managing cancer. Restoration of the p53 tumor suppressor gene via introducing foreign p53-mRNA therapeutics may inhibit the growth and development of tumors. Since the development of mRNA transporting vehicles, liposome-based nanoparticles are the mainstay and are widely used in several ex vivo and clinical studies. But the delivery of mRNA outside the immune cells and hepatocytes for protein replacement therapy through systemic administartion is very limited and requires additional optimization. Here, we modified classical LNP (lipid nanoparticles) with SSNs (strontium sulfite nanoparticles) and complexed the LNP with p53 mRNA to improve the delivery efficiency of p53 mRNA. We assumed that restoration of p53 function in breast tumor cells might improve antitumor efficacy against breast cancer. We screened the SSNs-LNP to get the favorable physicochemical properties and to improve the delivery efficiency. The SSNs-LNP showed a threefold increase of luciferase gene expression in breast cancer cell lines compared to the classical LNP. In the animal model, the SSNs-LNP improved the biological stability and tumor targeting efficiency and restored the expression of p53, resulting in a significant reduction of tumor volume. Thus, we anticipate that the hybrid SSNs-LNP particles could be a translatable nanocarrier system in transporting mRNA drugs for the treatment of cancers.

PMID 42881229
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PubMedAdvanced materials (Deerfield Beach, Fla.)2026-10-16

Tuning N-Species Adsorption/Desorption Equilibrium by Ni1Aun-SrTiO3 for Artificial Urea Photosynthesis.

Li Dong D, Zhai Shaochuan S, Wang Jinhu J, Gao Junyu J et al.

Inefficient generation of N-related intermediates, stemming from inert adsorption/photoactivation of N2, has hindered efficient artificial photosynthesis of urea from N2, CO2, and H2O. To overcome this bottleneck, we herein propose a strategy for modulating the adsorption/desorption equilibrium of N-related species using precisely designed bimetallic Ni1Aun active sites supported on a strontium titanate (NiAu-STO) semiconductor photocatalyst. This strategy significantly enhances N2 adsorption/activation and effective generation of N-related intermediates to facilitate C-N coupling for the photocatalytic urea synthesis, affording a considerable urea production rate of 1333.63 µg gcat. -1, with successful crystallization of a collectible solid-phase urea product. Furthermore, we developed a novel reaction-temperature programmed desorption-mass spectrometry tandem monitoring system to elucidate the adsorption behavior of N2, which can clarify the adsorption behavior of N2 and confirm the formation of critical N-related intermediates (e.g., *NH2) on the NiAu-STO photocatalyst. In addition, in situ Raman spectroscopy results further validated the formation of a distinctive C-N coupling intermediate (*NH2COO-) on the photocatalyst surface, providing mechanistic insights into urea photosynthesis from N2, CO2, and H2O.

PMID 42885862
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PubMedMolecules (Basel, Switzerland)2026-10-16

Distinct Inhibitory Effects of Statin Lactones on Ca2+- and Na+/K+-ATPases.

Cruz-Cortés Carlos C, Šeflová Jaroslava J, Espinoza-Fonseca L Michel LM

P-type ATPases share a conserved catalytic architecture but have different sensitivities to small-molecule inhibitors. We previously identified several statins as inhibitors of the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA), but the extent to which this inhibitory activity reflects broader pharmacological cross-reactivity among P-type ATPases remains unknown. Here, we compared the effects of seven structurally diverse statin lactones, which share a common δ-lactone moiety but contain distinct core scaffolds, including hexahydronaphthalene-based and aromatic heterocyclic ring systems, on SERCA and the Na+/K+-ATPase (NKA). The structurally related lovastatin and simvastatin produced similar concentration-dependent inhibitory profiles toward SERCA and NKA, despite the otherwise distinct pharmacological sensitivities of these pumps. In contrast, atorvastatin, rosuvastatin, and pitavastatin showed more divergent inhibitory profiles, generally with greater inhibition of SERCA than NKA at higher concentrations. Pravastatin and fluvastatin, however, had minimal effects on either ATPase over the concentration range examined. These findings build on our previous identification of selected statins as SERCA inhibitors by demonstrating that their activity can extend to NKA. Overall, the results reveal substantial structure-dependent variation in the effects of statin lactones on these P-type ATPases, ranging from convergent inhibition to differential inhibition and minimal activity.

PMID 42883189
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PubMedACS applied materials & interfaces2026-10-15

Functionalizing Robust (La,Sr)(Cr,Fe,Ni)O3 Mixed Ionic-Electronic Conducting Electrocatalysts through Bimetallic FeNi-Based Exsolution for Solid Oxide Electrolysis.

Zarkadoulas Athanasios A, De Gregorio Alessia A, Marousiadou Eirini E, Li Nannan N et al.

Solid oxide electrolysis cells (SOECs) are a promising alternative for highly efficient syngas production due to their ability to couple with renewable electricity (e.g. solar or wind power) and utilization of waste heat from industrial processes. To unlock their full potential a primary challenge is the development of redox stable, coking tolerant and catalytically active mixed ionic and electronic conducting (MIEC) materials. Here, we have functionalized a robust lanthanum strontium iron chromate by introducing both A-site deficiency to increase the number of oxygen vacancies and surface exchange kinetics, as well as Ni-doping at the B-site to boost catalytic properties by exsolving FeNi-based alloy nanoparticles. The morphological analysis revealed the high thermal stability of the host perovskite and the successful decoration of its surface with an Fe-rich, FeNi alloy as identified by the HRTEM analysis after reduction at 900 °C for 12 h. The physicochemical characterizations revealed a significant enhancement of the electrocatalytic properties of the modified samples that resulted in an >40% decrease in electrode polarization resistance in CO2/H2O co-electrolysis conditions. Our approach shows that simple yet rational modifications of highly stable perovskite oxides in combination with nano-engineering through exsolution could have a significant effect for advancing MIEC electrodes in SOECs.

PMID 42878070
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PubMedCureus2026-10-15

Persistent HyperCKemia Beyond Post-Viral Myositis: A Case of Anti-HMGCR Immune-Mediated Necrotizing Myopathy.

Xavier Rita R, Silva Sara S, Cunha Rita R, Coelho Angela A et al.

Anti-3-hydroxy-3-methylglutaryl-coenzyme A reductase (anti-HMGCR) immune-mediated necrotizing myopathy (IMNM) is a rare autoimmune myopathy that should be suspected in patients with progressive proximal muscle weakness and marked creatine kinase (CK) elevation persisting despite statin discontinuation, although distinguishing it from more common conditions such as post-viral myositis and toxic statin-associated myopathy remains a major diagnostic challenge. We report the case of a 64-year-old man receiving long-term atorvastatin therapy who presented with progressive proximal muscle weakness, dysphagia, and severe hyperCKemia following a self-limited flu-like illness, initially raising post-viral myositis as the leading hypothesis. Despite immediate statin discontinuation and aggressive intravenous hydration, severe hyperCKemia persisted during the first week of supportive management alone, and the neurological deficits did not improve, prompting further investigation and empirical immunosuppression. Muscle magnetic resonance imaging demonstrated multifocal inflammatory muscle edema, while extensive investigation for infectious, metabolic, endocrine, neoplastic, and autoimmune causes was unrevealing. Muscle biopsy showed a necrotizing myopathy with pauci-inflammatory features, and anti-HMGCR antibodies, which had not been included in the initial extended myositis panel and required a dedicated request, were subsequently identified, confirming statin-associated IMNM. Treatment with high-dose corticosteroids followed by methotrexate produced progressive biochemical improvement and complete recovery of muscle strength and swallowing function, with CK falling to 376 U/L (N 30-200 U/L) at the last follow-up (four months after admission). The principal educational value of this case lies in the diagnostic reasoning rather than in the diagnosis itself: it was the failure of the clinical and biochemical course to follow the anticipated trajectory, rather than the initial presentation, that prompted reconsideration of the working hypothesis. Dysphagia, less commonly reported in post-viral myositis and toxic statin-associated myopathy, together with persistent severe hyperCKemia despite statin withdrawal, should prompt evaluation for anti-HMGCR IMNM.

PMID 42877551
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