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calcium acetate (PhosLo Gelcaps / PhosLo Tablets / Phoslyra)

✓ Approved

Vaxart, Inc. · 小分子 · 小分子

什么是 calcium acetate？

calcium acetate 是一种小分子，由Vaxart, Inc.研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名PhosLo Gelcaps, PhosLo Tablets, Phoslyra
公司Vaxart, Inc.
药物类别小分子
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Vaxart, Inc.

治疗适应症

calcium acetate 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersHyperphosphataemia✓ Approved

相关研究文献

PubMedMicrobial biotechnology2026-10-26

Adaptive Laboratory Evolution Rewires Pseudomonas putida for Resource-Efficient Acetate Assimilation.

Gurdo Nicolás N, Srinivasan Aparajitha A, Tagliani Tommaso T, Filbig Melanie M et al.

Acetate is an attractive renewable two-carbon substrate for microbial biotechnology, but toxicity limits growth and carbon-use efficiency at process-relevant concentrations. Here, we used adaptive laboratory evolution to improve acetate tolerance in a genome-reduced strain of Pseudomonas putida and combined whole-genome sequencing, quantitative physiology, reverse engineering, transcriptomics, proteomics and 13C-acetate fluxomics to resolve the underlying adaptation mechanisms. Evolution under increasing acetate concentrations selected recurrent mutations in gacA and fabB, which encode a global response regulator and a fatty acid biosynthesis enzyme, respectively. Reverse engineering of these mutations recapitulated most of the evolved phenotype, including shorter lag phase and substantially higher biomass yield from acetate. Multi-omic analyses showed repression of type VI secretion systems, carbohydrate storage functions, fatty acid metabolism and oxidative stress-associated proteins, indicating resource reallocation away from costly stress and non-essential programs. Fluxomics further revealed reduced carbon cycling and increased glyoxylate shunt flux, consistent with improved acetate-carbon retention in biomass. These results establish acetate tolerance in P. putida as a resource-efficiency phenotype and identify gacA and fabB as actionable targets for acetate-based bioproduction.

PMID 42929247
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PubMedCardiovascular research2026-10-26

NOR-1 is an upstream regulator of Ca2+ homeostasis and calmodulin kinase II-dependent arrhythmogenesis.

Vázquez-Sufuentes Paula P, Jiménez-Sábado Verónica V, Ballester-Servera Carme C, Casabella-Ramón Sergi S et al.

Dysregulation of NOR-1 has been reported in cardiovascular diseases associated with altered calcium handling. We therefore investigated how NOR-1 affects calcium homeostasis and arrhythmogenesis to identify the underlying mechanisms. We assessed the expression of NOR-1 and calcium regulatory proteins in myocardial samples from humans and mice that overexpress human NOR-1 in the heart (TgNOR-1). Gene promoter activity was determined by transient co-transfection assays. Calcium imaging, patch-clamp recordings and immunofluorescent labeling was performed in mouse cardiomyocytes. Experimental data were used for mathematical modeling. Arrhythmias were induced in vivo by an epinephrine/caffeine challenge. In human cardiac samples, mRNA levels of genes coding for SERCA2a, CASQ2, TN-C1 and PLB correlated with those of NOR-1, while TgNOR-1 mice exhibited higher cardiac levels of these calcium regulatory proteins than wild-type animals (WT). NOR-1 increased luciferase activity driven by the proximal promoter of both human and mouse genes. Calcium transients were smaller in TgNOR-1 cardiomyocytes while L-type calcium current and SR calcium content were unchanged. Mathematical modeling revealed that more calcium binds to CASQ2 and is released from the SR in TgNOR-1 cardiomyocytes, but the resulting calcium transient is smaller because more calcium is buffered by TN-C1. Furthermore, NOR-1 transgenesis increased the level of reactive oxygen species and CAMKII oxidation, as well as RyR2 phosphorylation at Ser-2814, which led to a higher incidence of calcium waves and afterdepolarizations in resting TgNOR-1 cardiomyocytes. In electrically paced myocytes, NOR-1 transgenesis promoted extra-transients at low frequencies and calcium alternans at high frequencies. Importantly, these derangements in intracellular calcium handling concurred with a dramatic increase in epinephrine/caffeine-induced bidirectional ventricular tachycardia in TgNOR-1 mice. Moreover, the antioxidant N-acetylcysteine and the CAMKII inhibitor KN-93 attenuated arrythmia in TgNOR-1 mice and arrhythmogenic calcium release in isolated myocytes. Our findings highlight NOR-1 as an upstream regulator of CAMKII-oxidation underlying arrhythmia induced by defective calcium homeostasis, pointing to therapies targeting CAMKII as a means to attenuate arrhythmia triggered by pathological upregulation of NOR-1.

PMID 42929040
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PubMedTraffic (Copenhagen, Denmark)2026-10-26

TMEM55B Maintains Lysosomal Homeostasis and Promotes ER-Lysosome Calcium Signaling.

Mukae Nagi N, Maki Honoka H, Shirane Michiko M

At membrane contact sites (MCSs) between the endoplasmic reticulum (ER) and endolysosomal compartments, the Protrudin-PDZD8 complex promotes the maturation of endosomes into lysosomes, a process accompanied by acidification. Endosomal maturation is closely associated with both lysosomal acidification and calcium signaling; however, the molecular mechanisms linking the Protrudin-PDZD8 complex to these processes remain unclear. Here, we identified TMEM55B, a lysosome-localized protein, as a binding partner of the Protrudin-PDZD8 complex. TMEM55B has been reported to interact with the v-ATPase complex, suggesting a role in lysosomal function. Suppression of TMEM55B expression reduced the fluorescence of a lysosomal acidification probe, suggesting impaired lysosomal acidification. In addition, TMEM55B depletion attenuated lysosomal Ca2+ release and reuptake and reduced ATP-induced Ca2+ responses in the ER. These findings suggest impaired calcium-induced calcium release (CICR) at ER-lysosome MCSs. By contrast, mitochondrial Ca2+ dynamics were unaffected. Together, these results identify TMEM55B as a factor involved in maintaining lysosomal homeostasis and regulating calcium dynamics. Our findings suggest that TMEM55B cooperates with the Protrudin-PDZD8 complex to contribute to the regulation of lysosomal function at ER-lysosome MCSs.

PMID 42928446
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PubMedJournal of medical case reports2026-10-26

High-dose regular insulin as a potential rescue therapy in severe aluminum phosphide poisoning: a case report.

Sedaghattalab Moslem M, Akbari Ghaidafeh G

Aluminum phosphide (rice tablet) can cause cardiocirculatory collapse and has negative cardiac inotropic effect. Positive inotropic effect of insulin on the cardiac myocytes is through calcium flux. Insulin increases the intramyocytes calcium concentration by increasing conductance of calcium through the L-type calcium channels and by increasing intramyocytes concentration of cyclic adenosine monophosphate. In addition to increasing the intramyocytes calcium level, insulin also enhances the responsiveness of the cardiac cells to calcium. High-dose insulin is a potential therapy for hypodynamic and hypotensive septic shock due to its positive inotropic qualities. In this paper, a critical aluminum phosphide poisoning patient (a 25-year-old Iranian young woman), presented with mixed severe metabolic acidosis and respiratory alkalosis, tachypnea, tachycardia, and hypotension. In contrast to our previous experiences that ingestion of aluminum phosphide tablets associated with multiple organ failure and severe shock in approximately all critical poisoning patients, early initiation of high-dose intravenous regular insulin for this patient prevented multiorgan dysfunction and death. Treatment with high-dose intravenous insulin associated with IV fluids, sodium bicarbonate, hydrocortisone, potassium, dextrose therapy and supportive care resolved completely signs and symptoms of patient after 3 days in ICU. High-dose intravenous regular insulin may be act as a rescue therapy for aluminum phosphide poisoning patients. While this single case suggests a potential benefit, further studies are required to confirm these findings.

PMID 42928247
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PubMedCells2026-10-26

RapC Is Involved in the Development of Dictyostelium Through the Regulation of Autophagy and Calcium Signaling.

Han Nara N, Han Uri U, Kim Dahyeon D, Kim Wonbum W et al.

RapC is a Rap-subfamily small GTPase in Dictyostelium whose developmental function remains largely uncharacterized. Upon starvation, individual amoebae aggregate and undergo morphogenetic transitions to ultimately produce a fruiting body, a process requiring precise spatiotemporal regulation of a single apical tip as the primary organizing center. Here, we report that RapC is required for tip organizer formation during multicellular development by modulating autophagy and intracellular calcium signaling. rapC null cells develop normally through aggregation but consistently form three to four apical tips per aggregate rather than the single organizer tip characteristic of wild-type cells. Pharmacological phenocopy experiments revealed that caffeine and the selective TORC1 inhibitor rapamycin recapitulate the multi-tip phenotype, whereas the PI3K inhibitor LY294002 and the pan-TOR inhibitor Torin2 do not, implicating TORC1 signaling as the relevant downstream effector. In line with this, rapC null cells exhibit normal GFP-PH:CRAC translocation kinetics and slightly elevated PKB/PKBR1 phosphorylation, ruling out defects in the PI3K-TORC2-PKB signaling axis. Instead, rapC null cells display markedly elevated autophagic flux as assessed by the tandem RFP-GFP-Atg8 reporter assay, consistent with attenuated TORC1-mediated autophagy suppression. Furthermore, aggregation-competent rapC null cells show increased intracellular calcium ([Ca2+]i) upon external calcium stimulation, a response absent in wild-type cells and not reproduced by rapamycin, indicating a TORC1-independent role for RapC in calcium homeostasis. Together, our findings establish that RapC promotes normal Dictyostelium development by supporting TORC1 activity to suppress excessive autophagic flux and by maintaining [Ca2+]i homeostasis through a TORC1-independent mechanism.

PMID 42929849
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PubMedBiochemical Society transactions2026-10-26

Novel chemogenetic approaches in modulating calcium signaling.

Price Anna A, Lan Tien-Hung TH, Zhou Yubin Y

Calcium (Ca2+) signals regulate diverse processes ranging from neurotransmission and muscle contraction to gene expression, immune response, and cell death. Conventional pharmacological agents are readily applied but often lack molecular and cell-type specificity, whereas genetic perturbations offer greater precision but are typically slow and difficult to reverse. Chemogenetic systems bridge these approaches by combining genetically encoded protein actuators with exogenous chemical ligands. The present review summarizes emerging chemogenetic strategies that modulate Ca2+ signaling at distinct steps of the signaling cascade. These include engineered G protein-coupled receptors, chemically inducible receptor tyrosine kinases, direct actuators and inhibitors of STIM-ORAI coupling, genetically encoded blockers of voltage-gated Ca2+ channels, and engineered ligand-gated ion channels. We also discuss prospective designs targeting the phospholipase C signaling axis. Collectively, these approaches enable reversible and cell-specific modulation of Ca2+ dynamics.

PMID 42929082
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