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sultosilic acid piperazine (Mimedran)

✓ Approved

Esteve · LPL · Small Molecule

What is sultosilic acid piperazine?

sultosilic acid piperazine is a small molecule developed by Esteve. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesMimedran
CompanyEsteve
Drug ClassSmall Molecule
Molecular TargetLPL
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Esteve

Mechanism of Action

Molecular Targets

sultosilic acid piperazine acts on 1 molecular target:

LPLlipoprotein lipase (HDLCQ11, LIPD)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

sultosilic acid piperazine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersHyperlipidaemia✓ Approved

Related Research Articles

PubMedMedicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents2026-07-17

Design and synthesis of pyrrolo[2,3-d]pyrimidine linked diazospiro and piperazine - piperidine libraries as anticancer agents.

Guda Sridhar S, Patri Srilakshmi V SV, Reddy V Krishna K, Thumma Vishnu V et al.

Three libraries containing pyrrolo[2,3-d]pyrimidine moiety linked to diazospiro[3.5]nonane, diazospiro[5.5]undecane and piperazine - piperidine hybrid derivatives were synthesized involving various N-deprotection and acid amine coupling reactions. They were tested for their invitro cytotoxicity against triple negative human breast cancer cells MDA-MB-231 and BT-549. Promising results were obtained by pyrrolo[2,3-d]pyrimidine linked diazospiro[3.3]nonane compounds (7a and 7c) containing ortho-trifluoro and meta-bromo functional groups against MDA-MB-231 cells. Their dose response curves were plotted and their IC50 value found to be 11.66 µM (7a) and 10.37 µM (7b). Additionally, performed acridine orange and rhodamine 123 straining tests to study the cell deformation at various dosages, which garnered promising results.

PMID 42467191
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PubMedWorld journal of microbiology & biotechnology2026-07-17

Staphylococcus cohnii mediated production of perillic acid from limonene and synthesis of its amide derivatives for the induction of apoptosis in TNBC Cells.

Ayoub Nargis N, Singh Ajay A, Lone Bashir Ahmad BA, Shafeeq Haseena H et al.

Perillic acid (PA), an oxygenated monoterpenoid derived from limonene, has attracted significant attention owing to its wide range of biological activities, especially its promising anticancer properties. However, its limited availability and inefficient chemical synthesis routes restrict its broader therapeutic exploration. In the present study, perillic acid was produced through microbial biotransformation of R-(+)-limonene using Staphylococcus cohnii IIIMB2707, which showed the highest oxidation efficiency among eleven screened microbial strains. Under simplified and scalable operating conditions (pH 7.0, 28 °C, 48 h), the strain achieved a conversion yield of 77.91%, demonstrating an efficient, scalable biocatalytic process for perillic acid production. The product was isolated and structurally confirmed by GC-MS, NMR, and LC-MS analysis. To enhance the anticancer potential of PA, a series of novel piperazine-based amide derivatives C1-C8 were synthesized and characterized using NMR and HRMS techniques. Cytotoxicity evaluation revealed compound C-1 as the most potent derivative, exhibiting selective activity against MDA-MB-231, triple-negative breast cancer cells (TNBC), with a selectivity index (SI) of 6.24, indicating favorable selectivity toward cancer cells. Mechanistic investigations demonstrated that C-1 induces apoptosis through a reactive oxygen species (ROS)-mediated intrinsic mitochondrial pathway. Overall, this study establishes Staphylococcus cohnii IIIMB2707 as a new microbial biocatalyst for efficient perillic acid production and identifies C-1 as a promising hit for further mechanistic elucidation.

PMID 42463596
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PubMedThe Journal of biological chemistry2026-07-17

Lauric acid engages an O-GlcNAc-sensitive BCKDH regulatory node to modulate branched-chain amino acid oxidation in skeletal myotubes.

Sumi Koichiro K, Shioyama Miho M, Munakata Kinuyo K, Takasugi Satoshi S et al.

Branched-chain amino acid (BCAA) catabolism is controlled by the phosphorylation state of the branched-chain α-ketoacid dehydrogenase (BCKDH) complex, which is regulated by the opposing actions of BCKDH kinase (BDK) and the phosphatase PPM1K. Although fatty acids and amino acids both contribute to skeletal muscle energy metabolism, how fatty acid availability influences BCAA catabolic regulation remains incompletely understood. Here we examined the effects of lauric acid (C12), a medium-chain fatty acid abundant in dietary lipids, on BCAA metabolism in differentiated skeletal myotubes. Lauric acid increased phosphorylation of the BCKDH E1α subunit at Ser293 during nutrient perturbation in both mouse and human skeletal myotubes. Stable isotope tracing with U-[ˆ13C6]-leucine revealed that C12 reduced incorporation of leucine-derived carbon into downstream tricarboxylic acid (TCA) cycle-associated metabolites, indicating suppression of BCAA oxidative flux, whereas incorporation of labeled leucine into protein was not significantly altered. Mechanistically, genetic and pharmacological perturbation experiments indicated that the C12 effect requires PPM1K and is sensitive to O-GlcNAc cycling. Knockdown of O-GlcNAc transferase attenuated the C12-induced increase in BCKDH phosphorylation and reversed suppression of leucine-derived carbon flux. Dual-tracer experiments further showed that carbon derived from lauric acid and leucine converges in shared TCA cycle-associated metabolite pools, including glutamate and glutamine. Together, these findings identify a nutrient-sensitive regulatory node linking fatty acid availability, O-GlcNAc signaling, and BCKDH phosphorylation that modulates BCAA oxidation in skeletal myotubes.

PMID 42463056
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PubMedMicrobiology spectrum2026-07-17

Antibacterial and antibiofilm effects of natural phenolic acids: Insights into structure-function relationships, extracellular pH, and morphological changes.

Bārzdiņa Ance A, Teterovska Renāte R, Prudņikova Daniela Paula DP, Broks Renārs R et al.

Wound infections are a challenging healthcare burden against which treatment is hindered by the presence of biofilms and the rise in antibacterial resistance. To date, the potential of natural phenolic acids as topical antibacterial agents is under-researched. The aim of this study was to investigate and compare the antibacterial and antibiofilm effects of 5 hydroxycinnamic acids (caffeic acid, chlorogenic acid, p-coumaric acid, ferulic acid, and rosmarinic acid), 4 hydroxybenzoic acids (gallic acid, salicylic acid, syringic acid, and vanillic acid), as well as 2 related compounds (tannic acid and quinic acid) against a panel of 10 bacterial strains. The tested phenolic acids showed a bactericidal action with minimum inhibitory concentration (MIC) values in the range of 0.625 to 10.0 mg/mL. A negative correlation between an increase in the polarity of the molecule and antibacterial effect was observed. At minimum bactericidal concentration (MBC), phenolic acids prevent an increase in extracellular pH by halting bacterial metabolism. Under bacterial metabolism-induced alkaline conditions, caffeic, chlorogenic, rosmarinic, and gallic acids change color to brown or green at sub-MIC concentrations. Caffeic and chlorogenic acids induce filamentation of planktonic P. aeruginosa. Tested phenolic compounds reduce biofilm biomass in the range of 10% to 90%, with Gram-positive biofilms being more susceptible. SEM imaging revealed a significantly diminished biofilm EPS with damaged cell structure after phenolic acid treatment. Out of the tested compounds, p-coumaric acid and salicylic acid show the most promise as antibacterial agents against bacterial species characteristic of wound infections. The search for new antibacterial agents is one of the highest healthcare priorities. Phenolic acids are increasingly researched alone and as part of various drug delivery systems for wound care applications. However, to date, the available literature on the antibacterial effects of these compounds is rather fragmented and outdated, with unreproducible results. In this study, we link the physicochemical properties and structure of the molecules with their antibacterial and antibiofilm potential, investigate phenolic acid's impact on the bacterial metabolism-induced extracellular pH change, and use SEM imaging to characterize the morphological changes of both planktonic bacteria and biofilms in response to phenolic acid treatment. Additionally, we provide an assessment of the compound ADMET properties with respect to their potential topical application. The data can be used in the future to test potential synergic effects with antibiotics, develop drug delivery systems, and investigate the efficacy of these agents against multi-resistant bacterial strains.

PMID 42466895
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PubMedPhysiological research2026-07-17

Impact of Co-Supplementation of Gallic Acid With Vitamin C on Oxidant Stress, Inflammation, Hepatic and Renal Histology of Type 2 Diabetic Rats Induced With Fructose and Streptozotocin.

Yan S S, Xiang X X, Hua W W

This study assessed the impact of gallic acid plus vitamin C on systemic oxidant stress, inflammation, hepatic and renal histology of rats with type 2 diabetes mellitus. Twenty five albino male rats were allotted into five categories of five rats each and treated hereafter as: control and diabetic group (fed rat diets and water), vitamin C (diabetic treated rats administered vitamin C, 50 mg/kg), gallic acid (diabetic treated rats administered gallic acid at 20 mg/kg), gallic acid plus vitamin C (diabetic treated rats administered 20 mg/kg gallic acid and 50 mg/kg vitamin C). The study duration was forty two days. The diabetic group had significant raise (P<0.05) of fasting glucose, glycated hemoglobin, insulin resistance scores, oxidative stress and inflammatory markers (in the liver, kidney and serum), alteration of relative liver and kidney weights, liver and kidney function indices, significant decrease (P<0.05) in total hemoglobin, serum insulin, insulin sensitivity and pancreatic beta cell function scores, body weights and pathological changes in their liver and kidney histology. These changes were ameliorated following supplementation of the diabetic group with gallic acid, vitamin C and gallic acid plus vitamin C combined treatment. Intervention with vitamin C was more efficacious than gallic acid. However, combined treatment of gallic acid plus vitamin C was more efficacious than the single treatments in modulating systemic and local oxidative stress, inflammation and in restoring the altered liver and kidney histology of the diabetic rats. Key words Antioxidants " Type 2 diabetes mellitus " Diabetic liver disease " Diabetic kidney complication " Natural products.

PMID 42466700
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PubMedThe Journal of steroid biochemistry and molecular biology2026-07-17

Gallic acid from Moutan Cortex promotes osteoblast differentiation and alleviates osteoporosis in mice by targeting HRAS and activating the ERK pathway.

Gu Weiwei W, Zhou Haiyan H, Sun Yongjin Y, He Xiaojing X et al.

Fracture healing is a complex process where osteoblasts appear as central players in restoring bone integrity through proliferation, differentiation, and mineralization. Previous studies have identified several compounds in cortex moutan, which have been testified to significantly expedite osteoblast proliferation and differentiation. In this study, cell experiments were utilized to screen gallic acid, the key active substance in Moutan Cortex that promote osteogenesis. Subsequently, the targets of gallic acid were analyzed through network pharmacology. As a result, HRAS was a potential target of gallic acid. We further verified the regulation of the RAS/ERK pathway by gallic acid through bioinformatics and Western blot (WB) experiments. Finally, through cell and animal experiments, we demonstrated that Moutan Cortex promoted osteoblast differentiation and relieved osteoporosis.

PMID 42463030
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