Drug Database
CA

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

PubMedSleep medicine reviews2026-09-18

Beyond pain relief: rethinking sleep outcomes in CGRP-targeted migraine therapy.

Daou Marc M, Lee-Iannotti Joyce K JK, Robblee Jennifer J

Calcitonin gene-related peptide (CGRP)-targeted therapies have changed migraine treatment, but their effects on sleep remain incompletely understood. This review summarizes the emerging evidence on sleep outcomes with CGRP-targeted therapies, including monoclonal antibodies and gepants. Available studies suggest improvement in subjective sleep measures and few reported sleep-related adverse events, but the data are limited. Current findings do not establish whether sleep improvements reflect direct CGRP pathway modulation or improved migraine control. Interpretation is further complicated by patient heterogeneity, including comorbid sleep disorders, psychiatric symptoms, chronic pain, autonomic dysfunction, and concomitant medications. Future studies should use multidimensional sleep assessment and longitudinal objective measures to clarify whether CGRP-targeted therapies influence sleep physiology, sleep perception, or both.

PMID 42759069
Read full article →
PubMedJournal of neurophysiology2026-09-18

Resistance training for migraine in females: mechanistic review of hormonal, CGRP, autonomic, vascular and nociceptive pathways.

Tornero-Aguilera José Francisco JF, Muñoz-López Mario M, Casas-Gómez María M, Zabaleta-Korta Aitor A et al.

Migraine is the second leading cause of years lived with disability worldwide and disproportionately affects women, in whom the disorder tends to be more frequent, longer-lasting and functionally more disabling than in men. This female preponderance, which emerges after menarche, is tightly linked to changes in estrogen levels, reproductive phases and sex-specific responsiveness of the trigeminovascular and calcitonin gene-related peptide (CGRP) systems. Against this backdrop, non-pharmacological interventions that modulate the same physiological processes involved in migraine are particularly attractive. Resistance training (RT) has emerged from recent systematic reviews and network meta-analyses as one of the exercise modalities with the largest effect sizes on monthly migraine frequency, yet its mechanistic rationale in women is rarely addressed as a coherent biological argument. In this narrative review we integrate the pathophysiology of migraine in females with the adaptations induced by structured RT across four convergent axes: autonomic regulation, neurovascular and endothelial function, systemic and neurogenic inflammation, and endogenous pain modulation. We interpret the current clinical evidence in light of these mechanisms, outline how the hormonal milieu in females may shape individual responsiveness, and propose a translational framework for prescribing RT as part of a comprehensive, sex-informed migraine management plan. We explicitly distinguish between robust findings, emerging signals and hypotheses that remain to be tested, and highlight the main methodological barriers that should be addressed before RT can be firmly embedded in clinical guidelines for women with migraine.

PMID 42757466
Read full article →
PubMedJCEM case reports2026-09-17

Phenotype-driven cascade screening in a Syrian family with clinically consistent multiple endocrine neoplasia type 2A.

Hraib Munawar M, Alturun Mona M, Al Kheder Taim T, Alonainy Faozat F

Multiple endocrine neoplasia type 2A (MEN2A) is an autosomal dominant hereditary endocrine tumor syndrome classically associated with medullary thyroid carcinoma (MTC), pheochromocytoma, and primary hyperparathyroidism. Early recognition is important because cascade screening may identify affected relatives before advanced disease develops. We report a Syrian family with a clinically MEN2A-consistent phenotype. The index patient, a 37-year-old male, presented with a large multinodular thyroid mass and was found to have markedly elevated plasma metanephrines, bilateral adrenal masses, and elevated serum calcitonin and carcinoembryonic antigen. He underwent bilateral adrenalectomy followed by total thyroidectomy with bilateral neck dissection. Histopathology confirmed bilateral pheochromocytoma and multifocal MTC with gross extrathyroidal extension and lateral cervical lymph-node metastasis. Phenotype-driven cascade screening identified a 39-year-old sister with elevated calcitonin, metanephrine, and normetanephrine levels, bilateral adrenal masses, bilateral pheochromocytoma, and MTC, representing a second first-degree relative with the MEN2A-defining combination of MTC and bilateral pheochromocytoma. A 26-year-old brother was found to have synchronous papillary thyroid carcinoma and oncocytic/Hürthle-cell carcinoma with negative calcitonin immunostaining. This family highlights the value of phenotype-driven cascade screening when rearranged during transfection (RET) proto-oncogene testing is unavailable and emphasizes the importance of precise pathological classification of nonmedullary thyroid tumors in individuals from MEN2A-consistent families.

PMID 42751026
Read full article →
PubMedArchive of clinical cases2026-09-17

Persistent elevation of procalcitonin following resolution of presumed community-acquired pneumonia revealing sporadic medullary thyroid carcinoma.

Tang Shin Yee SY, Mattar Shaikh Abdul Matin SAM

Procalcitonin (PCT) is widely utilized as a biomarker of bacterial infection and sepsis and is expected to decline following successful treatment. Persistent elevation in the absence of ongoing infection should prompt consideration of alternative diagnoses. Medullary thyroid carcinoma (MTC), a rare neuroendocrine malignancy arising from parafollicular C-cells, is increasingly recognized as a non-infectious cause of elevated PCT. A 67-year-old woman presented with palpitations, exertional dyspnea, and dizziness. Initial investigations demonstrated a markedly elevated PCT level of 11.7 ng/mL and chest radiographic findings suggestive of community-acquired pneumonia. She responded well to antibiotic therapy; however, serial monitoring over seven months revealed persistently elevated PCT ranging from 9.5-12.9 ng/mL, despite normal C-reactive protein and no identifiable infectious focus. Computed tomography identified an incidental thyroid nodule, and a dedicated thyroid ultrasound demonstrated a Thyroid Imaging Reporting and Data System (TI-RADS) 4 lesion measuring approximately 1.6 cm. Fine needle aspiration cytology was Bethesda category V, suspicious for MTC. Serum calcitonin was markedly elevated at 899 pg/mL. The patient underwent total thyroidectomy with bilateral central neck dissection and histopathological examination confirmed a 1.8 cm unifocal MTC (pT1bN0) with lymphatic invasion and minimal extrathyroidal extension. Postoperatively, calcitonin decreased to 71.4 pg/mL. This case highlights that persistent elevation of PCT following apparent resolution of infection served as the clinical trigger for further diagnostic evaluation, ultimately revealing occult MTC. Clinicians should investigate persistent biomarker abnormalities when clinical and biochemical trajectories diverge, as this may facilitate early diagnosis of an underlying malignancy.

PMID 42750968
Read full article →
PubMedFrontiers in immunology2026-09-17

Calcitonin gene-related peptide promotes mast cell-mediated neuroimmune inflammation through the CALCRL/RAMP1-JAK3-STAT1 axis in rosacea.

Li Xiaojin X, Fan Huiping H, Sun Rui R, Ma Qingsong Q et al.

Rosacea is a chronic inflammatory skin disorder characterized by neurovascular instability and dysregulated innate immunity. Although mast-cell activation is increasingly recognized as a central pathogenic feature, the neuroimmune mechanisms linking neuropeptide signaling to mast cell-mediated inflammation remain incompletely defined. This study investigated whether calcitonin gene-related peptide (CGRP) promotes mast cell-mediated inflammation in rosacea and explored the underlying signaling mechanism. Bioinformatic analyses of the GSE65914 dataset were performed to characterize rosacea-associated molecular pathways and mast-cell signatures. Serum and skin samples from patients with rosacea and healthy controls were analyzed by ELISA, histological staining, and immunofluorescence. In vitro, CGRP-induced mast-cell activation and CALCRL/RAMP1-JAK3-STAT1 signaling were investigated in LUVA cells using RT-qPCR, western blotting, immunofluorescence, degranulation assays, ELISA, and pharmacological approaches, while the potential CALCRL-JAK3 association was assessed by molecular docking and reciprocal co-immunoprecipitation. In vivo, ACK2-mediated mast-cell depletion and pharmacological blockade of the CGRP receptor or JAK3 were evaluated in CGRP-aggravated LL37-induced rosacea-like mouse models. Rosacea lesions showed enrichment of immune-inflammatory pathways, JAK-STAT signaling, and mast cell-associated signatures. Serum CGRP levels were elevated in patients with rosacea and positively correlated with flushing and erythema severity. Lesional skin showed increased CGRP expression and enhanced localization of CALCRL, RAMP1, phosphorylated JAK3, and phosphorylated STAT1 in dermal CD117+ mast cells. In LUVA mast cells, CGRP upregulated CALCRL/RAMP1 expression, activated JAK3-STAT1 signaling, and promoted degranulation, histamine release, and inflammatory mediator production. Molecular docking and reciprocal co-immunoprecipitation supported a potential association between CALCRL and JAK3. Rimegepant or ritlecitinib attenuated CGRP-induced JAK3-STAT1 activation and mast-cell responses. Modulation of the canonical Gαs-cAMP-PKA pathway did not abolish CGRP-induced JAK3-STAT1 phosphorylation, indicating that this response is not primarily mediated by the cAMP-PKA cascade. In vivo, mast-cell lineage depletion attenuated CGRP-driven exacerbation of LL37-induced rosacea-like inflammation, while rimegepant or ritlecitinib alleviated inflammatory changes and reduced JAK3-STAT1 activation and mast-cell responses. These findings identify a CGRP-associated neuroimmune pathway in rosacea in which CALCRL/RAMP1-linked JAK3-STAT1 signaling promotes mast cell-mediated inflammatory amplification. Targeting the CGRP-CALCRL/RAMP1-JAK3-STAT1 axis may provide a mechanism-based therapeutic strategy for neurovascular-dominant or treatment-refractory rosacea.

PMID 42751103
Read full article →
PubMedThe journal of headache and pain2026-09-17

Acupuncture modulates migraine-related neural and neuroendocrine regulatory pathways.

Huang Hao H, Tao Yu Y, Zhang Yuan Y, Luo Fangting F et al.

Migraine is a common, disabling neurological disorder driven by neurovascular and neuroinflammatory mechanisms. Although calcitonin gene-related peptide (CGRP)-targeted and serotonergic drugs have improved treatment, many patients still respond inadequately or experience side effects. Acupuncture is widely used as a non-pharmacological alternative, yet its mechanistic basis lacks systematic integration. Accumulating clinical and experimental evidence suggest that acupuncture effectively reduces migraine frequency, pain intensity, and disability, with sustained preventive benefits. Neuroimaging studies reveal that acupuncture modulates key brain regions and networks involved in pain perception, emotional regulation, and descending pain control, including the default mode, salience, and sensorimotor networks. At the molecular level, preclinical evidence indicates that acupuncture may modulate CGRP signaling, serotonergic neurotransmission, neuronal excitability, and inflammatory pathways, thereby attenuating central sensitization and neuroimmune activation. Emerging evidence further suggests that acupuncture affects hypothalamic metabolic pathways involving glucagon-like peptide-1 (GLP-1) and orexin. Given that these neuropeptides are also implicated in the pathogenesis of migraines, this finding may offer a potential mechanistic perspective on how acupuncture alleviates this condition. These findings support a multi-level regulatory role of acupuncture that extends beyond symptomatic analgesia. Acupuncture is supported as a preventive therapy for select migraine patients, but mechanistic evidence remains heterogeneous and mostly associative or preclinical. While a multilevel framework might link acupuncture-evoked brain, molecular, and homeostatic changes, direct validation in migraine is needed. Future work should prioritize standardized interventions, credible sham controls, longitudinal neuroimaging, and integrated molecular readouts to elucidate response mechanisms and predictive biomarkers. Not applicable.

PMID 42750006
Read full article →

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about calcitonin