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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

PubMedSkeletal muscle2026-11-11

MFN2 alleviates mitochondrial calcium overload in sepsis-induced myopathy by modulating GRP75-VDAC1 interaction.

Li Xuexin X, He Fei F, Wang Yun Y, Sun Bowen B et al.

Sepsis-induced myopathy (SIM) is characterized by skeletal muscle dysfunction associated with mitochondrial calcium overload. The mitochondria-associated endoplasmic reticulum membrane (MAM) plays a crucial role in mediating mitochondrial calcium uptake. Although MFN2 and the IP3R-GRP75-VDAC1 complex have each been implicated in mitochondrial calcium regulation, their respective contributions and potential interplay in the pathogenesis of SIM remain poorly understood. A murine sepsis model was established by cecal ligation and puncture (CLP). Skeletal muscle function was assessed by compound muscle action potential (CMAP) recording and forelimb grip strength testing. Gastrocnemius muscle histology was evaluated by H&E and WGA staining. Tibialis anterior muscles were analyzed by immunofluorescence and transmission electron microscopy (TEM) to characterize MAM ultrastructure. Protein expression was quantified by western blotting, and MFN2 mRNA levels were measured by qPCR. Co-immunoprecipitation was performed to assess GRP75-VDAC1 protein interaction. Mitochondrial and cytoplasmic calcium levels were monitored using Rhod-2 AM and Fluo-4 AM, respectively. Sepsis induced skeletal muscle atrophy and dysfunction both in vivo and in vitro. IP3R-dependent calcium transfer at MAM was associated with pathological mitochondrial calcium overload, and pharmacological IP3R inhibition with 2-APB attenuated mitochondrial calcium uptake and ameliorated muscle atrophy. Concurrently, sepsis-induced MFN2 downregulation was associated with reduced ER-mitochondria distance, further promoting mitochondrial calcium overload. AAV-mediated MFN2 overexpression restored ER-mitochondria distance and was associated with reduced VDAC1 protein expression, attenuated GRP75-VDAC1 interaction, collectively contributing to mitigation of mitochondrial calcium overload and amelioration of skeletal muscle atrophy. MFN2 attenuates sepsis-induced mitochondrial calcium overload through two complementary mechanisms: increasing ER-mitochondria distance and modulating GRP75-VDAC1 interaction and IP3R-GRP75-VDAC1 complex assembly. These findings identify MFN2 as a potential regulator of MAM-mediated mitochondrial calcium homeostasis in SIM and suggest it may represent a therapeutic target for sepsis-induced skeletal muscle dysfunction.

PMID 43010086
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PubMedInternational journal of endocrinology2026-11-11

Denosumab and Calcium Homeostasis in Hypercalcaemia of Malignancy and Primary Hyperparathyroidism.

Zhou Fengye F, Liu Ying Y, Liang Chunfang C, Yun Sufang S

To evaluate short-term changes in serum calcium and the occurrence of values below prespecified thresholds after denosumab treatment in institutional oncology and primary hyperparathyroidism (PHPT) cohorts, and to interpret these findings within the context of FAERS reporting patterns and published PHPT evidence. We retrospectively analysed denosumab-treated patients at the Affiliated Hospital of Inner Mongolia Medical University; the retrospective study was performed in the Department of Clinical Pharmacy (oncology cohort, 2024; PHPT cohort, 2022-April 2025). Total serum calcium was evaluated at baseline and around Days 3 and 7. A downstream FAERS reanalysis used the fixed 2014Q1-2023Q2 dataset, and published PHPT reports were re-extracted for actual follow-up and complications. In the oncology subgroup with baseline calcium > 2.55 mmol/L, mean paired calcium changed from 3.101 to 2.278 mmol/L at Day 3 (n = 12; p = 0.0002) and from 3.158 to 1.990 mmol/L at Day 7 (n = 11; p < 0.0001). In PHPT, the corresponding changes were 3.376 to 2.661 mmol/L at Day 3 (n = 9; p = 0.0038) and 3.351 to 2.289 mmol/L at Day 7 (n = 8; p = 0.0013). During Days 1-10, calcium < 2.10 mmol/L occurred in 57/102 oncology patients with non-low baseline calcium and 4/9 PHPT patients; values < 1.60 mmol/L occurred in 3/102 and 0/9, respectively. Among 1433 FAERS hypocalcaemia reports, 1186 (82.76%) had at least one serious-outcome code, most often hospitalisation/prolonged hospitalisation (769; 53.66%) or another medically important condition (725; 50.59%). Crude hypocalcaemia reporting proportions were higher for 120 mg than 60 mg, for male than female reports, and for tumour-related than osteoporosis indications; the youngest evaluable age strata also had higher proportions, but denominators were small, and the comparisons were unadjusted. In the analysed cohorts, denosumab was followed by short-term calcium reduction in patients with baseline hypercalcaemia and in the small PHPT cohort. Values below 2.10 mmol/L were common in early follow-up, whereas values below 1.60 mmol/L were uncommon, and clinical hypocalcaemia was not systematically adjudicated. FAERS hypocalcaemia reports often carried serious-outcome codes, mainly hospitalisation and other medically important conditions, without establishing incidence, causality or independent risk factors.

PMID 43011605
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PubMedFrontiers in behavioral neuroscience2026-11-11

Distinct calcium responses distinguish itch- and pain-associated neurons in the anterior cingulate cortex.

Lee Chiwoo C, Ko Hyoung-Gon HG

Itch and pain are distinct aversive sensations. We previously identified segregated neuronal populations in the anterior cingulate cortex (ACC) that selectively respond to pain and itch stimuli and reported full-trace classification with a mean-frequency difference, leaving the broader calcium-transient properties associated with this separation unresolved. Here, we reanalyzed denoised in vivo calcium traces from stimulus-responsive ACC neurons and quantified interpretable response features, including peak rate, peak interval, rise and decay area under the curve (AUC), and rise and decay slope. Pain- and itch-associated neurons differed across multiple single-neuron calcium features. Trace-based stochastic gradient descent (SGD) classification separated the two groups, indicating that their response profiles contain label-discriminative information. Notably, classification performance was only weakly affected by neuron-wise z-scoring, suggesting that separation is not explained solely by simple amplitude scaling. A mouse-constrained shuffled-label control reduced classification performance, supporting the contribution of within-mouse label-associated structure while also highlighting mouse-level sampling constraints. Paired mouse summaries and mouse-exclusive validation showed limited cross-animal consistency, whereas within-mouse neighborhood analysis retained local label-associated organization. UMAP of full traces provided descriptive visualization of neuron-level response organization. Together, these results show that interpretable calcium response features carry meaningful itch-/pain-associated structure among the analyzed responsive ACC neurons.

PMID 43011375
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PubMedEuropean journal of case reports in internal medicine2026-11-11

Combined Calcium Channel Blocker And Angiotensin-Converting Enzyme Inhibitor Overdose.

Kahal Fares F, Guérard-Poirier Natasha N, Ji Cheng C, Gursahaney Ashvini A et al.

Combined overdoses of angiotensin-converting enzyme inhibitors and calcium channel blockers are rare but associated with more severe toxicity than either agent alone. A 48-year-old woman presented to the emergency department nine hours after intentionally ingesting 40 tablets of amlodipine (10 mg) and 40 tablets of ramipril (10 mg). On arrival, she was hypotensive and tachycardic. Initial management included fluids, intravenous calcium and insulin bolus followed by high-dose insulin euglycaemic therapy (HIET). Despite escalating vasopressor support, she developed mixed vasoplegic and cardiogenic shock complicated by acute kidney injury, fluid overload, respiratory failure and metabolic acidosis, necessitating intubation and continuous renal replacement therapy. Improvement in haemodynamics was only achieved by day 9. She was transferred from the intensive care unit (ICU) on day 20 with residual weakness from ICU-acquired myopathy and was ultimately discharged after 66 days, with a prolonged hospitalisation attributed to delirium and deconditioning. Severe combined angiotensin-converting enzyme inhibitors (ACEI) and calcium channel blockers (CCB) overdose may cause prolonged, refractory haemodynamic instability requiring extended high-dose insulin euglycaemic therapy (HIET), vasoactive support and fluid administration. Concentrated insulin, dextrose and vasopressor preparations may help mitigate fluid overload. Angiotensin II may be a potential treatment for refractory vasoplegia, although evidence and availability remain limited. Secondary complications can prolong recovery beyond the duration of drug toxicity. This case highlights the need for individualised, multidisciplinary management, early HIET, vasoactive support and fluid-sparing strategies in severe combined ACEI and CCB overdose. Management of severe combined calcium channel blocker and angiotensin-converting enzyme inhibitor overdose may require prolonged resuscitation with high-dose insulin euglycaemic therapy, vasoactive support and fluid administration. The cumulative fluid requirements of these therapies, combined with complications such as acute kidney injury, can contribute to severe fluid overload. The use of concentrated insulin, dextrose and vasopressor preparations may help limit the iatrogenic fluid accumulation.Clinicians should anticipate and proactively manage secondary complications, including acute kidney injury, volume overload, respiratory failure and infection, as these complications may independently prolong recovery beyond the expected duration of drug toxicity.Combined angiotensin-converting enzyme inhibitor and calcium channel blocker overdose lacks established management guidelines and requires individualised, multidisciplinary care based on clinical severity and response to therapy.

PMID 43012017
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PubMedFrontiers in cardiovascular medicine2026-11-11

Balancing innovation and safety in percutaneous treatment of coronary artery calcification.

Helal Ayman A, Ladwiniec Andrew A, Mozid Abdul A, Malik Iqbal I et al.

Coronary artery calcification (CAC) is an independent predictor of adverse outcomes in percutaneous coronary intervention (PCI). Under-preparation of calcified plaque predisposes to stent under-expansion, mal-apposition, restenosis, and stent thrombosis, while over-aggressive debulking strategies carry risk of dissection, perforation, and no-reflow. The interventional armamentarium for calcium modification has expanded from high-pressure and non-high pressure specialty balloons including intravascular lithotripsy (IVL) to dedicated atherectomy devices i.e., rotational atherectomy (RA), orbital atherectomy (OA), and excimer laser coronary atherectomy (ELCA), each with a distinct mechanism, evidence base, and risk profile. Additionally, comprehensive assessment of coronary calcium is central to guiding lesion preparation and selecting treatment strategy, with IVUS and OCT providing detailed intravascular characterisation, and CT emerging as a complementary non-invasive tool for procedural planning. Appropriate procedural planning and judicious selection of calcium-modification tools are paramount to maximising procedural safety, minimising complications, and improving clinical outcomes. This review summarizes the pathophysiology of CAC, describes each modification technique, synthesizes the pivotal and recent randomised evidence, outlines current guideline position, and proposes a practical framework for balancing procedural innovation against patient safety. Current evidence supports an individualized, imaging-guided approach to calcium modification. Balloon-based strategies, IVL, atherectomy, and ELCA each have specific strengths and limitations, and no modality has demonstrated universal superiority across lesion subsets. Atherectomy and laser remain important for selected uncrossable, undilatable, or highly resistant lesions, whereas IVL and specialty balloons may provide effective alternatives in appropriately selected crossable lesions. Evidence for many technologies is stronger for procedural and imaging endpoints than for long-term clinical outcomes.

PMID 43011531
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PubMedEuropean journal of case reports in internal medicine2026-11-11

Iatrogenic Hypercalcemia in A Patient with Type 2 Diabetes and Chronic Kidney Disease.

Mačković Maja M, Marić Nikolina N, Kralj Ivan I, Bakula Miro M

The introduction of glucagon-like peptide-1 receptor agonists (GLP-1 RA) and non-steroidal mineralocorticoid receptor antagonists (nsMRA) has significantly improved outcomes in patients with type 2 diabetes, obesity and chronic kidney disease (CKD). However, the increasing use of combination therapies may result in previously unrecognized adverse drug interactions. We report the case of a 59-year-old man with obesity, type 2 diabetes, CKD stage 3b, albuminuria and established cardiovascular disease receiving optimized treatment with renin-angiotensin-aldosterone system blockade, sodium-glucose cotransporter-2 inhibition, semaglutide and finerenone. Mild finerenone-associated hyperkalaemia was treated with calcium polystyrene sulfonate. Several weeks later, the patient developed symptomatic severe non-parathyroid hormone-mediated hypercalcemia accompanied by acute kidney injury, fatigue, muscle weakness, constipation, polyuria and polydipsia. Extensive investigations excluded solid and haematological malignancy, granulomatous disease and endocrine disorders. Hypercalcemia was attributed to increased calcium absorption from calcium polystyrene sulfonate, likely facilitated by prolonged gastrointestinal transit secondary to semaglutide-induced constipation. Treatment consisted of withdrawal of the offending medications, aggressive intravenous hydration, loop diuretics and a reduced dose of intravenous zoledronic acid, resulting in normalization of serum calcium and recovery to baseline kidney function. Semaglutide and finerenone were subsequently reintroduced without recurrence of hyperkalaemia or hypercalcemia, eliminating the need for potassium binders. This case highlights a previously unreported mechanism of iatrogenic hypercalcemia resulting from the interaction between contemporary cardio-renal-metabolic therapies and underscores the importance of careful monitoring for unexpected adverse effects when combining newer agents with established treatments. Patients treated for cardiovascular-kidney-metabolic syndrome require several lines of pharmacological therapy with potential for developing side-effects.The diagnostic algorithm for non-parathyroid hormone-mediated hypercalcemia should always include thorough investigation of medications and their potential for interactions.

PMID 43012014
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