Drug Database
CA

calcium carbonate (Cimascal / Cimascal D Forte)

✓ Approved

CPEX Pharmaceuticals, Inc. · VDR

What is calcium carbonate?

calcium carbonate is a therapeutic agent developed by CPEX Pharmaceuticals, Inc.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesCimascal, Cimascal D Forte
CompanyCPEX Pharmaceuticals, Inc.
Molecular TargetVDR
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, CPEX Pharmaceuticals, Inc.

Mechanism of Action

Molecular Targets

calcium carbonate acts on 1 molecular target:

VDRvitamin D receptor (NR1I1, PPP1R163)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

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

Therapeutic AreaConditionPhase
Musculoskeletal and connective tissue disordersOsteoporosis✓ Approved

Related Research Articles

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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PubMedbioRxiv : the preprint server for biology2026-09-19

Cholesterol-Mediated Modulation of Collecting Lymphatic Vessel Contractility: Exploring Cholesterol Depletion as a Therapeutic Alternative to Improve Lymphatic Function in Hypercholesterolemia.

Keane Keith K, Castorena-Gonzalez Jorge A JA

Globally, hypercholesterolemia affects over 20% of the population; and while many studies have examined its impact on cardiovascular health, little is known about its effects on the lymphatic system. In mice, hypercholesterolemia has been linked to multiple aspects of lymphatic dysfunction; and a recent study demonstrated that cholesterol depletion by cyclodextrins promoted lymphatic vessel regeneration and restored lymphatic drainage in mouse models of lymphedema. Collecting lymphatic vessels rely on the spontaneous and highly entrained contractions of lymphatic muscle cells (LMCs) and competent unidirectional on-way valves to propel lymph forward. Critical to lymphatic pacemaking and contractility is the proper functioning of ion channels, which are known to be modulated by the cholesterol content in the plasma membrane. Therefore, we sought to understand the role cholesterol plays in regulating lymphatic contractility. The effects of cholesterol depletion by the cyclodextrins MβCD and HPβCD were assessed in cannulated and pressurized inguinal-axillary collecting lymphatic vessels (CLVs) from C57BL6/J (WT) mice. Noteworthy, studies have shown that HPβCD is safe for human use, and in fact, it is commonly used as a drug excipient. Acute treatment with both cyclodextrins significantly increased the pumping capacity of CLVs, as demonstrated by the increased contraction amplitudes by ~50±12% and calculated fluid volume displacement by each contraction by ~35±11%. Calcium imaging demonstrated that HPβCD increased the amplitude and duration of the large Cav1.2-mediated calcium events (termed calcium flashes. In contrast, cholesterol supplementation by incubation with BODIPY-cholesterol, which presumably incorporates cholesterol into the cell membrane, significantly impaired the contractile activity of CLVs compared to controls by decreasing contraction amplitude (control: 42±2 µm versus BODIPY-cholesterol: 20±7 µm) and calculated fluid volume displacement (control: 9.2±3.9 nL versus BODIPY cholesterol: 3.3±1.2 nL) which were significantly restored with subsequent cholesterol depletion using HPβCD (amplitude: 36±11 µm, volume displacement: 5.5±2.4 nL). Similarly, treatment with HPβCD significantly improved the contractile capacity of dysfunctional CLVs isolated from hypercholesterolemic ApoEKO mice. In conclusion, changes to cell membrane cholesterol content acutely and significantly altered CLV contractility with depletion improving contractility associated with recruitment of voltage-gated Cav1.2 channels in lymphatic muscle cells (LMCs). Future studies from our lab will determine whether pharmacological depletion of membrane cholesterol can be therapeutic strategy to improve and/or restore lymphatic contractile function in secondary lymphedema, including obesity/hypercholesterolemia-induced and cancer-related lymphedemas.

PMID 42760988
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PubMedFrontiers in immunology2026-09-19

α7nAChR alleviates cognitive impairment by promoting autophagy in astrocytes via CaMKK2/AMPK/mTOR pathway in sepsis-associated encephalopathy.

Liu Yuesong Y, Wang Fuhua F, Wang Lu L, Wang Siqing S et al.

Sepsis-associated encephalopathy (SAE) is a syndrome of cerebral dysfunction secondary to sepsis. Although the α7 nicotinic acetylcholine receptor (α7nAChR) plays a pivotal role in the SAE, the specific mechanisms by which it mediates neuroinflammatory responses and contributes to pathological injury in SAE remain unclear. The serum α7nAChR level was measured in all included patients. The ROC curve was used to analyze the α7nAChR level for predicting the risk of SAE. The sepsis rat model was constructed by cecal ligation puncture (CLP). The α7nAChR was activated and inhibited by PNU282987 and Methyllycaconitine (MLA) respectively. Cognitive function and neuronal damage were evaluated using behavioral experiment, Nissl staining, Golgi staining and Electron microscopy. Autophagy was examined by Western blot (WB) and transmission electron microscope (TEM). In vitro experiments, lipopolysaccharide (LPS) was used to construct the model of U118. After knockdown and overexpression of α7nAChR, the autophagy proteins level was detected by western blot and the level of cell supernatant inflammatory factors were detected by ELISA. Intracellular calcium concentration was evaluated by flow cytometry. The serum α7nAChR levels in SAE patients were lower than that in the healthy controls and sepsis patients, and the its AUC for predicting the risk of SAE was 0.79 (95% CI, 0.68-0.90). Activation of the α7nAChR elevated neurobehavioral scores, increased the number of Nissl bodies and synapses, and improved dendritic spine morphology in rats. Activation of α7nAChR weakened the activation of astrocytes, thereby reducing the release of IL-1β, IL-6 and TNF-α. The activation of α7nAChR inhibited the level of P62, up-regulated the expression of LC3. In vitro, α7nAChR promoted LPS-induced autophagy in U118 cells, increased intracellular calcium (Ca2+) concentrations, elevated p-CAMKK2/CAMKK2 and p-AMPK/AMPK levels, and decreases p-mTOR/mTOR levels. α7nAChR can alleviate cognitive dysfunction in SAE by activating the Ca2+/CaMKK2/AMPK/mTOR signaling pathway and promoting autophagy in astrocytes.

PMID 42760969
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PubMedJournal of biophotonics2026-09-19

Enhancement of Harvested Islet Functionality Through Photostimulation.

Fowlds Kelli K, Darden Carly M CM, Lawrence Michael C MC, Cho Michael M

Allogeneic islet transplantation is a promising treatment for Type I diabetes, but its success is limited by islet loss during isolation, purification, and engraftment, resulting in variable long-term insulin independence. Our previous studies demonstrated that photobiomodulation (PBM) significantly enhances insulin and glucagon secretion in pancreatic cells, likely through modulation of ATP production and calcium signaling pathways involved in hormone release. Building on these mechanistic findings, we investigated whether PBM could similarly improve the functionality of whole islets before transplantation. Mouse islets were isolated by pancreatectomy, cultured ex vivo, and treated daily with PBM for 7 days. Fluorescence imaging and functional assays were used to assess insulin expression and secretion. PBM significantly enhanced insulin secretion, with an approximately twofold increase observed after 3 days of treatment. These findings support PBM as a promising, noninvasive approach for improving islet function before transplantation.

PMID 42760903
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PubMedCardiovascular research2026-09-19

Lysosomal signaling pathways influence heart rhythm, and regulate atrial function.

Akerman Emily E, Capel Rebecca A RA, Rog-Zielinska Eva A EA, Winbo Annika A et al.

In the heart, endogenous nicotinic acid adenine dinucleotide phosphate (NAADP) triggers lysosomal calcium (Ca2+) release to augment sarcoplasmic reticulum (SR) Ca2+ sequestration, producing larger Ca2+ transients. However, the role of lysosomal Ca2+ signals in pacemaker activity, a distinct Ca2+-operated function of the sinoatrial node (SAN), or in the atrial myocardium has not been investigated. Pharmacological or genetic ablation of the NAADP pathway inhibits the spontaneous beating rate response to β-adrenergic stimulation in intact SAN. We found intracellular signaling microdomains between lysosomes and neighboring SR or mitochondria in mouse, and goat tissue. The spatial relationship between lysosomes and other Ca2+-handling organelles are altered in goat atrial fibrillation. Furthermore, we demonstrate atrial myocytes produce 3'-5'-cyclic adenosine monophosphate (cAMP) in response to lysosomal signaling, adding a novel trigger for cyclic nucleotide signaling. Our findings support the hypothesis that lysosomal Ca2+ signaling contributes to regulation of cardiomyocyte cAMP levels and pacemaker activity.

PMID 42760609
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PubMedNature neuroscience2026-09-19

Serotonin neurons in the dorsal raphe control food-craving-like behavior during pregnancy in mice.

Zhao Qianru Q, Feng Bing B, Dong Vicky V, Lau Lee How LH et al.

During pregnancy, physiological changes can alter food intake behaviors. However, the underlying neural mechanisms remain unclear. Here we show that female mice exhibit food-craving-like behavior during pregnancy, mirroring many patterns described in humans. We show that 5-HTDRN neuronal firing activity is reduced during pregnancy through increased small-conductance calcium-activated potassium type 3 (SK3) ion-channel activity. Genetic knockout of SK3 ion channels from 5-HTDRN neurons abolishes the pregnancy-associated suppression in 5-HTDRN neuronal firing activity and reduces food-craving-like behavior in pregnant mice. Conversely, overexpression of SK3 in 5-HTDRN neurons mimics pregnancy-induced food-craving-like behavior in virgin female mice. Moreover, activation of 5-HTDRN projections to ventral tegmental area inhibits food-craving-like behavior in pregnant mice. These findings provide novel insights into the role of 5-HT signaling in modulating food cravings during pregnancy and highlight potential targets for managing pregnancy-associated appetite dysregulation and maternal obesity in humans.

PMID 42760322
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