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calcium polycarbophil (Polyful / Colonel)

✓ Approved

Astellas Pharma · Small Molecule · Small Molecule

What is calcium polycarbophil?

calcium polycarbophil is a small molecule developed by Astellas Pharma. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesPolyful, Colonel
CompanyAstellas Pharma
Drug ClassSmall Molecule
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Astellas Pharma

Therapeutic Indications

calcium polycarbophil is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Gastrointestinal disordersIrritable bowel syndrome✓ Approved

Related Research Articles

PubMedEsophagus : official journal of the Japan Esophageal Society2026-09-20

Tumor-associated calcium signal transducer 2 expression as a promising therapeutic target in esophageal squamous cell carcinoma: a combined the Cancer Genome Atlas and an institutional cohort.

Inagaki Chiaki C, Kawakami Hisato H, Mitani Seiichiro S, Iijima Hiroshi H et al.

Esophageal squamous cell carcinoma (ESCC) has a poor prognosis, and new therapeutic targets are required. Antibody-drug conjugates (ADCs) are a promising therapeutic modality that selectively delivers cytotoxic payloads to tumors via cell-surface antigens. Tumor-associated calcium signal transducer 2 (TROP2, TACSTD2) has shown therapeutic potential as an ADC target in several malignancies; however, its clinical significance in ESCC remains unclear. An institutional cohort of ESCC patients treated at Kindai University was retrospectively evaluated by immunohistochemistry (n=70) and RNA sequencing (n=27). TACSTD2 copy number alterations, RNA expression, and survival were analyzed using the Cancer Genome Atlas (TCGA) ESCC dataset. IHC was assessed in both resected and biopsy specimens, including metastatic lesions. Survival analyses were performed, stratifying patients by cohort-specific median TACSTD2 expression levels. Immunohistochemistry analysis demonstrated uniformly strong TROP2 expression in all evaluable primary and metastatic lesions. In the TCGA dataset, TACSTD2 mRNA expression was consistently high, irrespective of copy-number status, and was comparable to or higher than that observed in non-small cell lung cancer and breast cancer, tumor types in which TROP2-targeted ADCs are clinically active. The TACSTD2 high-expression group showed a trend toward worse overall survival in both the institutional and the TCGA cohort, whereas disease-free survival was similar. TROP2/TACSTD2 is strongly and consistently expressed in ESCC at the protein and RNA levels, despite infrequent gene amplification, supporting its feasibility as a therapeutic target. High expression shows a trend toward poorer overall survival, warranting validation in larger cohorts.

PMID 42763384
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PubMedCureus2026-09-20

Noncanonical Splice Site Disruption: +4 Intronic Variant in Phosphate-Regulating Endopeptidase Homolog, X-linked (PHEX Gene) Supported by In Silico Analysis in X-linked Hypophosphatemic Rickets.

Panqueba Arias Carlos F CF, Rojas Rodriguez Ingry K IK, Quero Rossi I RI, Baez Cielo C CC

X-linked hypophosphatemic rickets (XLH) is the most common inherited cause of renal phosphate wasting. It is typically caused by pathogenic variants in the phosphate-regulating endopeptidase homolog, X-linked (PHEX gene), which lead to increased levels of fibroblast growth factor 23 (FGF23). However, noncanonical intronic variants represent a significant diagnostic challenge, as they may not be detected by conventional genetic studies and require interpretation supported by bioinformatic tools. We present the case of a pediatric patient with postnatal short stature and progressive genu varum. Biochemical studies revealed hypophosphatemia with reduced tubular reabsorption of phosphate, while calcium, parathyroid hormone (PTH), and vitamin D levels were within normal ranges. Radiological findings were consistent with rickets. Initial clinical exome sequencing was negative. Subsequently, a targeted gene panel identified a previously unreported intronic variant in the PHEX gene (c.1768+4dup; chrX:22,219,105 T>TA). In silico analysis using SpliceAI demonstrated a high probability of donor splice site loss (DS_DL = 0.80), while Pangolin predicted a splice-disrupting effect (score = 0.72); collectively, these findings support a deleterious effect on mRNA splicing. This case highlights the importance of integrating clinical, biochemical, genetic, and computational data for the interpretation of noncanonical intronic variants, expanding the mutational spectrum described for PHEX in XLH.

PMID 42763725
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PubMedOpen life sciences2026-09-20

Comparative analysis of vitamin C derivatives on ATP homeostasis across diverse cell types.

Goc Anna A, Sumera Waldemar W, Niedzwiecki Aleksandra A

Cellular energy homeostasis is tightly regulated by mitochondrial function and substrate availability. Vitamin C is a redox-active molecule with emerging roles in cellular metabolism; however, the metabolic impacts of structurally distinct vitamin C derivatives remain incompletely defined. In this study, we systematically compared l-ascorbic acid, dehydroascorbic acid, 6-O-palmitoyl-l-ascorbate, and mineral ascorbates (calcium, magnesium, sodium, and potassium salts) across multiple mammalian cell types. Cells were exposed to concentrations ranging from 60 to 500 µM, encompassing physiologically and pharmacologically relevant levels. The vitamin C derivatives induced cell type- and concentration-dependent modulation of intracellular ATP levels. Notably, HepG2 and renal epithelial cells exhibited robust ATP increases, whereas fibroblasts, myocytes, microglia, and skeletal muscle models displayed variable responses depending on the derivative and dose. Moreover, in skeletal muscle cells, co-treatment of standard l-ascorbic acid with select fatty acids did not yield additive bioenergetic effects, suggesting a localized, substrate-specific plateau or shared regulatory step in this specific cell model. Exposure to l-ascorbic acid induced selective increases in COX-1 without changes in SDH-A, consistent with rapid functional modulation of mitochondrial activity in myocytes and microglial cells only. Collectively, these findings demonstrate that vitamin C derivatives modulate cellular ATP levels within existing metabolic networks in a context-dependent manner, consistent with the modulation of mitochondrial-associated energy metabolism.

PMID 42763556
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PubMedFASEB bioAdvances2026-09-20

The Human PNPLA3I148M Polymorphism Alters the Renal Kinome and Transporters to Cause Hyperfiltration and Hypertension.

Arthur Gertrude G, Adenawoola Michael I MI, Wahba Sally S, Montgomery Bentley S BS et al.

The patatin-like phospholipase domain-containing protein 3 (Pnpla3) I148M polymorphism is a well-established genetic determinant of metabolic dysfunction-associated steatotic liver disease (MASLD), and emerging evidence links it to chronic kidney disease (CKD) and cardiovascular disease (CVD). However, the mechanisms underlying this relationship remain unclear. The goal of this study was to investigate the role of the Pnpla3I148M polymorphism on kidney function, blood pressure, and cardiac function in a mouse model carrying the identical human polymorphism. Male and female Pnpla3I148M knock-in and control C57BL/6 mice were fed either a normal sucrose diet (NSD) or a high sucrose diet (HSD) for 8 weeks. Glomerular filtration rate (GFR), blood pressure, cardiac, and vascular function were measured in each group. Renal cortical protein expression and kinome profiles were analyzed to identify pathways associated with hyperfiltration and renal injury. Pnpla3I148M mice exhibited increased renal sodium transporter levels and hyperfiltration, which was compounded by albuminuria in HSD mice. Pnpla3I148M mice were also hypertensive and exhibited impaired systolic function, consistent with pressure-overload-induced cardiac remodeling. Renal kinome profiling revealed sex- and diet-dependent alterations in serine/threonine kinases, primarily involving isoforms of protein kinase C (PKC), protein kinase A (PKA), cGMP-dependent protein kinase (PRKG), and calcium/calmodulin-dependent protein kinase (CaMK). Our findings suggest that Pnpla3I148M acts as a systemic cardio-renal risk allele that links metabolic dysregulation to progressive end-organ damage via renal kinase remodeling in a sex- and diet-dependent manner.

PMID 42763592
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PubMedMolecular psychiatry2026-09-20

A circuit dissection of perception-action decoupling in S-ketamine-induced hallucination-like states.

Wang Dijia D, Xu Junnan J, Wang Zhaoran Z, Liu Zhirui Z et al.

Hallucinations are a core feature of several psychiatric disorders, but the circuit mechanisms that separate perception from behavioral output remain poorly defined. Here, we combined an auditory discrimination task with AI-based pose analysis to quantify S-ketamine-induced false auditory threat responses and behavioral disorganization in mice. Control assays, including sucrose preference, loss of righting reflex, and prepulse inhibition, indicated that these effects were not explained by anhedonia, anesthesia, or basic auditory deficits. Using in vivo fiber photometry, single-cell miniscope calcium imaging, and pathway-specific chemogenetic and optogenetic manipulations, we identified dissociable circuit contributions within convergent striatal pathways. The basolateral amygdala to caudal striatum pathway (BLA→TS) supported salience-weighted perceptual decisions and, when aberrantly recruited by S-ketamine, promoted auditory false alarms. In contrast, the medial prefrontal cortex to caudal striatum pathway (mPFC→TS) primarily shaped behavioral expression and, when dysregulated, generated disorganized action patterns. At the network level, S-ketamine shifted TS activity from a sparse, high-contrast state to a high-frequency, low-amplitude, diffusely coupled state, consistent with reduced integrative precision. Auditory cortex to TS inputs were not broadly suppressed, supporting pathway specificity. Bidirectional chemogenetic manipulation of BLA→TS and mPFC→TS pathways in drug-naive mice further supported the TS as an integrative node linking perceptual evaluation to behavioral output. Dexmedetomidine co-administration restored pathway-level temporal dynamics and reorganized TS network coupling without simply suppressing activity. Together, these findings define a circuit framework for NMDAR-antagonist-induced hallucination-like states and provide a mechanistic rationale for dexmedetomidine-mediated mitigation of S-ketamine-associated perceptual and behavioral disruption.

PMID 42763341
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PubMedBiomaterials translational2026-09-19

Shellac-based encapsulation model incorporating calcium fluoride for oral care applications.

Dissara Piyada P, Sukcheep Chompunuch C, Ekgasit Sanong S, Pienpinijtham Prompong P et al.

Fluoride-releasing systems are widely incorporated into dental products to prevent caries; however, fluoride ions readily interact with calcium compounds in oral formulations, resulting in deactivation and reduced effectiveness. To overcome this limitation, a simple extrusion method was designed to fabricate shellac-based biopolymer beads capable of encapsulating fluoride. The resulting beads had an average diameter of 2.54 ± 0.22 mm, with theoretical analysis supporting particle size dependence on extrusion tube diameter. Structural and stability characterization was conducted using optical and electron microscopy, elemental analysis, vibrational spectroscopy, and thermal profiling, confirming in situ calcium fluoride formation and effective pore sealing. Key formulation parameters-including shellac concentration, dissolution time, bead formation time, and hardening time-were optimized to improve bead morphology and fluoride retention. An in situ blocking strategy, involving controlled precipitation of calcium fluoride within the bead matrix during formulation, was implemented to minimize fluoride diffusion and enhance long-term stability. This approach achieved 70% active fluoride retention over 90 days. The proposed encapsulation model holds promise for applications in toothpaste and other dental care products.

PMID 42760917
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