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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

PubMedBiomechanics and modeling in mechanobiology2026-08-30

Calcium-mediated force-interval relationship drives post-extrasystolic potentiation in premature ventricular complexes: a computational study.

Vossen Sjoerd S, van Osta Nick N, Lourenço Guilherme Pedro Carvalho GPC, Laranjo Sérgio Matoso SM et al.

Premature ventricular complexes (PVCs) are common cardiac arrhythmias that can lead to cardiomyopathy when frequent. Post-extrasystolic potentiation (PESP), which is the transient increase in contractility following a PVC, may serve as a predictive marker for heart failure risk; yet, the underlying calcium-mediated mechanisms and their relative contribution compared to loading conditions remain poorly understood. We integrated a mechanochemical model coupling intracellular calcium dynamics to sarcomere mechanics within the CircAdapt closed-loop cardiovascular framework. A novel calcium source model incorporating the force-interval relationship was calibrated using experimental canine data. We simulated single PVCs across varying coupling intervals and systematically investigated the contributions of calcium dynamics versus loading conditions to PESP, quantified as changes in systolic blood pressure (∆SBP), maximum rate of left ventricular pressure rise (∆max(dPLv/dt)), and left ventricular ejection fraction (∆LVEF). The calcium-based force-interval relationship reproduced experimental mechanical restitution curves with high accuracy (RMSE 9.59 ± 0.08%). Shorter coupling intervals reduced premature beat contractility while enhancing PESP in subsequent beats. Systematic variation of preload, afterload, and intrinsic contractility revealed that calcium dynamics reproduce the observed PESP patterns, with loading conditions as modulators. Notably, ∆max(dPLv/dt) and ∆SBP responded differently, with ∆SBP exhibiting complex non-monotonic behavior. The model qualitatively reproduced pressure-volume patterns from a single clinical quadrigeminy case. This study demonstrates that a calcium-based force-interval formulation reproduces the qualitative features of PESP within this framework, with preload and afterload modulating the pattern of beat-to-beat pressure response. The divergent behavior among contractility metrics emphasizes the need for multimetric assessment. This framework enables distinguishing intrinsic myocardial dysfunction from extrinsic loading effects, facilitating patient-specific risk stratification in PVC-induced cardiomyopathy.

PMID 42669085
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PubMediScience2026-08-30

Claudin-12 sustains urothelial barrier defense against uropathogenic E. coli via calcium-dependent immunomodulation.

Tian Yanpeng Y, Tong Hongping H, Sun Yinhui Y, Hong Longcheng L et al.

Urothelial barrier compromise defines inflammatory cystitis, though molecular regulators remain elusive. We identify claudin-12-a bladder-enriched tight junction protein-as an essential barrier component against uropathogenic E. coli (UPEC) invasion. At 72 h post-infection in the murine model of UPEC-induced cystitis, infection triggered dysregulation of canonical tight junction components (claudin-12, ZO-1, occludin), with claudin-12 exhibiting maximal depletion. Immunofluorescence confirmed profound tight junction disassembly in infected bladders. Consistent with this structural defect, claudin-12-knockout mice developed exacerbated acute cystitis, manifesting elevated bacterial colonization, neutrophil/monocyte infiltration, pro-inflammatory gene upregulation, and epithelial denudation. Mechanistically, claudin-12 loss increased calcium permeability in urothelial cells during UPEC infection, driving intracellular calcium accumulation and subsequent activation of apoptosis-related pathways. Notably, pharmacological inhibition of calcium accumulation by TMB-8 reversed both UPEC-induced apoptosis and claudin-12 depletion. Thus, claudin-12 emerges as a pivotal orchestrator of urothelial defense, wherein its regulation of calcium flux restrains UPEC-driven inflammation-revealing therapeutic potential for barrier-repair strategies.

PMID 42668535
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PubMedPakistan journal of medical sciences2026-08-30

Evaluation of serum antioxidant markers and calcium levels in women with Arthritis.

Rehman Abdul A, Jamil Muhammad M, Farhan Maham M, Khan Amna Saleem AS et al.

Osteoarthritis (OA) and Rheumatoid Arthritis (RA) are chronic, degenerative and inflammatory joint diseases, aggravated by reactive oxygen species (ROS) and impaired antioxidant defense system. However, gender based oxidative stress analysis remain under-examined, despite increasing evidence points towards sex-based biochemical changes in arthritis patients. The study aimed to measure the antioxidant activities of enzymes including superoxide dismutase (SOD), Glutathione reductase (GR) alongside reduced glutathione (GSH), and catalase (CAT) in female arthritis patients. Calcium balance is also estimated in order to analyze the bone demineralization. The case-control study was designed and conducted at the Orthopedic Department of a Dr. Ruth K. M. Pfau, Civil hospital, Karachi. Serum levels of GSH, GR, SOD, CAT, and calcium were evaluated in 42 arthritis patients and 16 age matched healthy female controls by using standard spectrophotometric and biochemical assays. Data was expressed as mean ± SD and analyzed statistically to compare both the groups. Arthritis patients in comparison with healthy controls showed significant decrease in GSH (p < 0.001) and GR (p < 0.01) levels, while SOD and CAT levels were slightly reduced but non-significant. Similarly, slightly higher calcium levels were also observed, suggesting altered mineral homeostasis associated with inflammatory conditions. The simultaneous decrease in antioxidant enzyme activities suggests the impaired redox homeostasis in female patients. The study highlights an altered antioxidant status and disturbed calcium homeostasis in female patients. These alterations in biochemical system suggest the therapeutic potential of antioxidant and calcium modulating interventions as effective treatment for managing and slowing disease progression in females.

PMID 42668919
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PubMedKidney medicine2026-08-30

Calcium Crystal Deposits in Kidney Allografts: The Interplay of PTH Levels and Phosphaturia.

Barbuto Simona S, Vischini Gisella G, Magagnoli Lorenza L, Provenzano Michele M et al.

Hyperparathyroidism is common in kidney transplant recipients and may contribute to graft injury through calcium crystal deposition. We investigated the association between pretransplant parathyroid hormone (PTH) levels and calcium crystal deposits (CCDs) and whether fractional excretion of phosphate (FePi) mediates this relationship. Retrospective single-center observational study. Forty-one kidney transplant recipients undergoing protocol biopsies at 3 and 12 months posttransplantation. Pretransplant PTH levels. Presence of calcium crystal deposits in graft biopsies. Logistic regression models and mediation analysis were used to evaluate associations between PTH levels, FePi, and CCDs. CCDs were detected in 33% of biopsies at 3 months and 45% at 12 months. Higher pretransplant PTH levels were associated with increased odds of CCDs. Mediation analysis showed that approximately 72% of this effect was explained using FePi levels. At 24 months posttransplantation, no meaningful difference in estimated glomerular filtration rate was observed between patients with and without CCDs. Retrospective design, small sample size, absence of fibroblast growth factor 23 level measurements, and limited adjustment for potential confounders. Elevated pretransplant PTH levels are associated with calcium crystal deposition in kidney allografts, largely mediated by phosphate wasting. However, no clear impact on graft function was observed within the first 2 years posttransplantation.

PMID 42668546
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PubMedBiochemistry. Biokhimiia2026-08-30

EF-Hand Calcium-Binding Motif: Novel Structural and Functional Insights.

Denessiouk Konstantin A KA, Permyakov Evgeny A EA, Denesyuk Alexander I AI, Permyakov Sergey E SE

The EF-hand motif is one of the most widespread calcium-binding protein motifs in nature, mediating calcium signaling across a variety of biological processes. While structural and functional properties of the individual proteins within the EF-hand superfamily are well studied, general principles governing organization and function of these proteins are only now being elucidated. This review examines some of these emerging patterns, including recently discovered structural elements of the EF-hand motif (EF-hand zone, one-residue and three-residue units, local "Clamp" units, and "black" and "gray" clusters). Additionally, we discuss the ability of certain EF-hand proteins to recognize a broad spectrum of protein targets, as well as their zinc-binding properties. New structural data on the EF-hand domain allow proposing a structural-functional classification for the proteins in this family. Furthermore, tendency of some EF-hand proteins toward promiscuity and zinc binding significantly expands their functional importance.

PMID 42669557
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PubMedNutrition (Burbank, Los Angeles County, Calif.)2026-08-30

Effect of a web-based nutrition intervention among families to increase regular-fat and low-fat dairy products: a randomized controlled trial.

Lemay Juliette J, Provencher Véronique V, Tremblay Angelo A, Panahi Shirin S et al.

This study evaluated the effect of a family- and web-based nutrition intervention, "Dairyathlon," promoting regular- or low-fat dairy consumption on dairy and calcium intakes, diet quality, and weight outcomes. Fifty-seven families, 108 parents and 109 children participated in an 8-week web-based nutrition intervention. They were randomly assigned to either Control, Low-fat dairy, or Regular-fat dairy group. All groups received education based on the 2019 Canada's Food Guide. Intervention groups were asked to include four daily servings of dairy (milk, cheese, and two yogurt servings). Three assessments were completed at baseline (T0), postintervention (T1), and 4-6 months follow-up (T2) for dietary intake via three 24-hour web-based dietary recalls and anthropometric. In parents, a significant effect of the intervention was observed, indicating differential changes over time across groups. Post hoc analyses showed that both intervention groups increased dairy consumption and calcium intake at T1. Specifically, Low-fat group increased dairy intake from 2.1 ± 0.2 to 3.1 ± 0.3 servings/day (P = 0.03) and calcium intake (P = 0.04), while dairy intake in Regular-fat group increased from 2.3 ± 0.2 to 3.5 ± 0.3 servings/day (P = 0.006) and calcium intake (P = 0.02). Only dairy consumption remained elevated at follow-up in the Low-fat group, which was significantly higher than in the Control group (2.7 ± 0.2 versus 1.6 ± 0.2 servings/day, P = 0.04). A significant interaction was also observed for diet quality; C-HEI was significantly higher at follow-up compared to baseline among parents in the Low-fat group. No significant changes were observed in children. Dairy and calcium intake improved among parents in the intervention groups during the program's active phase; however, sustained effects were limited. A significant effect at follow-up was observed only for the low-fat dairy intake group among parents. Web-based, family-centered approaches may facilitate targeted dietary changes, but additional strategies are necessary to achieve lasting, clinically meaningful impacts. ClinicalTrials.gov [Full-fat Dairy Products, Body Weight Control and Metabolic Health]; [NCT05417347]; [https://clinicaltrials.gov/study/NCT05417347?titles=NCT05417347&rank=1].

PMID 42669255
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