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calcitonin (Calsynar / calcitonin, Aventis / Calcin)

✓ Approved

Sanofi S.A · CALCR · Polypeptide

What is calcitonin?

calcitonin is a polypeptide developed by Sanofi S.A. It is approved for therapeutic indications via inhaled.

Drug Profile

Brand NamesCalsynar, calcitonin, Aventis, Calcin
CompanySanofi S.A
Drug ClassPolypeptide
Molecular TargetCALCR
RouteInhaled
StatusApproved
Sources: ClinicalTrials.gov, Sanofi S.A

Mechanism of Action

Molecular Targets

calcitonin acts on 1 molecular target:

CALCRcalcitonin receptor (CT-R, CTR)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

calcitonin is developed for 3 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Surgical and medical proceduresHypercalcaemia therapy✓ Approved
Musculoskeletal and connective tissue disordersOsteitis deformans✓ Approved
Musculoskeletal and connective tissue disordersOsteoporosis✓ Approved

Related Research Articles

PubMedNeurogastroenterology and motility2026-07-17

Transient Receptor Potential Melastatin 8 Plays a Key Role in Dextran Sulfate Sodium-Induced Murine Colitis via Regulating Extrinsic Sensory Neurons and Enteric Macrophage Secretory Activities.

Matsumoto Kenjiro K, Nakamoto Tomohiro T, Sato Akari A, Utsumi Daichi D et al.

Transient receptor potential melastatin 8 (TRPM8) is a cold-sensitive Ca2+-permeable ion channel that regulates intestinal inflammation. This study was aimed to elucidate the role of TRPM8 in enteric macrophages and spinal afferent sensory neurons during dextran sulfate sodium (DSS)-induced colitis. The role of TRPM8 in the progression of colonic inflammation was examined in 2% DSS-induced colitis by immunohistochemistry, reverse transcription-polymerase chain reaction, visceral sensing assessment, and flow cytometry. The role of TRPM8 in sensory neurons and macrophages was investigated using primary cultured dorsal root ganglion (DRG) neurons and bone marrow-derived macrophages (BMDMs). DSS-induced colitis was significantly aggravated in TRPM8-deficient (KO) mice compared with that in wild-type (WT) mice. In the colitis model, KO mice showed lower IL-10 mRNA levels than WT mice, but IL-6, IL-1β, and TNF-α levels were not affected. TRPM8 expression was upregulated in the distal colon and DRG following DSS administration. In the distal colon, TRPM8-immunoreactive cells and nerve fibers colocalized with F4/80 and substance P/calcitonin gene-related peptide (CGRP), respectively. In the DRG, TRPM8 neuron subtypes were labeled by neurofilament 200, substance P, CGRP, and tyrosine kinase receptor A. In cultured DRG neurons, TRPM8 deficiency attenuated lipopolysaccharide (LPS)-elicited CGRP release but did not affect substance P release. In BMDMs, TRPM8 deficiency significantly decreased LPS- and LPS/CGRP-elicited upregulation of IL-10 mRNA compared with that in WT animals. TRPM8 protects against DSS-induced experimental colitis via regulating CGRP release from sensory neurons and IL-10 production in enteric macrophages during intestinal inflammation.

PMID 42464071
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PubMedBMC oral health2026-07-16

Association between calcitonin gene-related peptide and substance P in saliva and pulp according to anxiety levels in patients with dental pain: a cross-sectional study.

Kamalak Aliye A, Balkanlıoğlu Esra E, Taş Hilmi H, Hurşitoğlu Rabia R et al.

Dental pain is influenced by both local inflammatory processes and neurobiological and psychological factors. This study compared substance P (SP) and calcitonin gene-related peptide (CGRP) levels in pulp tissue and unstimulated saliva between patients with dental pain and painless controls, and investigated their relationships with pain severity, pulpal inflammation, and psychological distress. Fifty-two adult patients indicated for primary endodontic treatment were enrolled and allocated into two groups: 26 patients with dental pain and 26 painless controls with no pain complaint and a VRS score of 0. Pain intensity was assessed using the Verbal Rating Scale (VRS). Depression, anxiety, and stress were evaluated using the Depression Anxiety Stress Scale-21 (DASS-21). Pulp tissue and unstimulated saliva samples were collected and analyzed using enzyme-linked immunosorbent assay. Pulpal inflammation was graded histopathologically. Between-group comparisons were performed using independent samples t-tests or Mann-Whitney U tests, as appropriate. Effect sizes were calculated using eta squared (η²). Correlations were assessed using Pearson or Spearman coefficients to examine associations between neuropeptide levels, pain severity, and inflammation grade. Pulp calcitonin gene-related peptide levels were significantly higher in patients with dental pain than in painless controls (p = 0.007; η² = 0.146). Salivary substance P levels were also significantly increased in the painful group (p = 0.044; η² = 0.080). No significant between-group differences were observed for pulp substance P or salivary calcitonin gene-related peptide (p > 0.05). Depression, anxiety, and stress scores were all significantly higher in patients with dental pain (all p < 0.001). Pain severity showed positive correlations with pulp calcitonin gene-related peptide (r = 0.332) and salivary substance P (r = 0.324), whereas no significant association was found between pain severity and histopathological inflammation grade. Pulp calcitonin gene-related peptide may be associated with local neurogenic activation in symptomatic pulpal pain, while salivary substance P may represent a potential noninvasive candidate marker for pain-associated responses. However, the lack of consistent pulp-saliva correspondence indicates that salivary biomarkers should not be considered direct surrogates of pulpal neuropeptide activity. ClinicalTrials.gov Identifier: NCT07330024.

PMID 42458416
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PubMedThe European journal of neuroscience2026-07-16

Calcitonin Gene-Related Peptide (CGRP)-Containing Terminals in the Central Amygdala of Mice and Monkeys: Ultrastructural Analysis and Subsynaptic Expression of GluD1.

Choi Diane D, Villalba Rosa M RM, Dalal Karina K, Paré Jean-Francois JF et al.

The right central amygdala (CeA) is involved in the processing of emotional-affective dimensions of pain. Through the spino-parabrachio-amygdaloid pain pathway, the CeA receives nociceptive information from calcitonin gene-related peptide (CGRP) neurons in the parabrachial nucleus. Recent evidence indicates that the glutamate delta 1 (GluD1) receptor, an atypical ionotropic glutamate receptor that largely functions as a synaptogenic molecule involved in the formation and maintenance of synapses, regulates this projection in mice. Despite its strong cellular expression, little is known about the subsynaptic localization of GluD1, and its potential interaction with CGRP terminals, in CeA neurons. To address this issue and further characterize the ultrastructure and synaptic connectivity of CGRP terminals across species, we used single and double immuno-electron microscopy techniques in mice and monkeys. For all ultrastructural parameters examined, no species difference was found. In both species, CGRP-positive (CGRP+) terminals formed symmetric or asymmetric synapses with dendrites, symmetric synapses with soma, and less commonly, asymmetric synapses with spines. Almost 90% of CGRP+ terminals forming asymmetric or symmetric synapses expressed vGluT2 immunoreactivity confirming the glutamatergic and peptidergic nature of this projection. Confocal microscopic analyses confirmed the perisomatic association between CGRP+ and GluD1+ puncta in mice and monkeys. At the ultrastructural level, GluD1 was expressed in the core of symmetric axo-dendritic and axo-somatic synapses and perisynaptic to asymmetric synapses formed by CGPR+ terminals. These findings demonstrate that the CGRP+ PB-CeA projection mediates its effects through a heterogeneous population of terminals that display strong synaptic relationships with GluD1 in rodents and primates.

PMID 42460853
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PubMedImmunity2026-07-16

Activation of the auricular vagus nerve reflex suppresses airway inflammation.

Shibuya Rintaro R, Abe Nobuya N, Song Keaton K, Rossen Nathan D ND et al.

The vagus nerve regulates inflammation via sensory-motor arcs. While vagal sensory neurons relay signals from within the body (interoception), whether external inputs can regulate visceral neuroimmune responses (exteroception) remains poorly understood. We unveiled a skin-lung reflex by which sensory neurons from the auricular skin suppressed Alternaria alternata-induced allergic airway inflammation. Viral and chemical neural tracing revealed distinct sensory projections from the vagal ganglia to the auricular skin. Pharmacologic, chemogenetic, and optogenetic activation of auricular transient receptor potential vanilloid 1 (TRPV1)+ afferents attenuated type 2 allergic lung inflammation, including group 2 innate lymphoid cell, eosinophil, and type 2 cytokine responses in the airway. Conversely, silencing of these sensory neurons via the skin exacerbated lung inflammation, and immunosuppression of airway inflammation was dependent on the neuropeptide calcitonin gene-related peptide (CGRP)β. These findings reveal an evolutionarily conserved somato-visceral reflex by which exteroceptive inputs impact visceral inflammation. Thus, transcutaneous neuromodulation may represent a therapeutic strategy to treat visceral inflammation.

PMID 42456661
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PubMedFrontiers in pharmacology2026-07-16

Chronic migraine management with onabotulinumtoxinA and anti-CGRP/R monoclonal antibodies in an Italian real-world setting: update on therapeutic appropriateness and an emerging role of pharmacy.

Scuteri Damiana D, Naturale Maria Diana MD, Pagliaro Martina M, Brescia Amelia A et al.

Migraine is a disabling neurovascular disorder that may evolve from episodic to chronic forms, often complicated by medication-overuse headache (MOH). It generates substantial healthcare expenditures and indirect societal costs. Pharmacological constraints and resistance to acute therapies contribute to the development of MOH and increase the need for preventive treatments such as onabotulinumtoxin A (BoNT/A) and monoclonal antibodies (mAbs) targeting the calcitonin gene-related peptide (CGRP) pathway. This pharmacoepidemiology retrospective study aimed to evaluate real-world prescription patterns of BoNT/A and anti-CGRP/R mAbs in an Italian regional setting and to compare current data (2023-2024) with previously observed patterns (2020-2022) before the integration of pharmacists as outpost in migraine man-agement. Anonymized data were obtained from the regional drug reimbursement and prescription database. A total of 9,012 and 9,705 prescriptions were recorded in 2023 and 2024, respectively, indicating an increasing trend in the use of innovative preventive therapies. A gradual increase in the use of eptinezumab and BoNT/A appears to be associated with regional organizational measures aimed at improving access to care, adherence to clinical guidelines, and integrated management across healthcare levels. Therapeutic appropriateness is far from reaching the gold standard and an increasing role of pharmacists could improve clinical outcomes.

PMID 42460013
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PubMedInvestigative ophthalmology & visual science2026-07-16

Novel Role for CGRP in Aqueous Humor Outflow.

Mavlyutov Timur A TA, Bilal Samer E SE, Sharmin Tania T, McDowell Colleen M CM

Calcitonin gene related peptide (CGRP)-positive nerve fibers are the major type of sensory neurons innervating the trabecular meshwork (TM) and Schlemm's canal (SC). Upon activation, these neurons secrete CGRP locally. Here, we determined the role of CGRP in regulating homeostatic TM functions and the relation of CGRP-positive neurite innervation to segmental outflow regions. CGRP receptor expression in primary human TM (HTM) and primary human SC (HSC) cells in culture was determined by western blot analysis. HTM cells were treated with CGRP (0.1-3 µM) and fluorescent beads for 24 hours or were treated with CGRP (1 µM), TGFβ2 (5 ng/mL), and CGRP+TGFβ2 for 48 hours and processed for western blot analysis of alpha-smooth muscle actin (α-SMA) and collagen type 1 alpha 1 (COL1A1) expression. Segmental flow regions were determined in 9-month-old C57BL/6J mice using fluorescent tracer beads. Anterior segment flatmounts were co-labeled with antibodies against CGRP, CALCRL (CGRP receptor), and PECAM-1 (SC endothelium) and imaged by confocal microscopy. The density of CGRP neurites and CALCRL expression in each flow region were quantified by ImageJ analysis. CGRP receptors are expressed in human TM and SC cells. CGRP treatment significantly increased phagocytosis and blocked TGFβ2-induced COL1A1 and α-SMA expression. Significantly more CGRP-positive neurites were identified in high-flow regions compared to all other flow regions. CALCRL expression was significantly associated with high-flow and moderate-flow regions compared to no-flow regions. These data suggest that CGRP modulates important homeostatic mechanisms of TM function and may influence the development and regulation of segmental regions of aqueous humor outflow.

PMID 42461077
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