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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

PubMedCurrent pain and headache reports2026-10-14

Current Evidence on the Use of Calcitonin Gene-Related Peptide-Targeting Therapies in Children and Adolescents.

Shin Lauren L, Moon Ryan R, Gelfand Amy A

This is a narrative review to summarize current evidence on use of therapies targeting calcitonin gene-related peptide (CGRP) for children and adolescents with headache disorders. The CGRP-targeting therapies have been used in adults for prevention of migraine since 2018. There is one randomized controlled trial (RCT) published on fremanezumab in children age 6-17 years old which showed favorable outcome as a preventive treatment for episodic migraine. Several real-world evidence (RWE) studies report on use of CGRP-targeting therapies in patients younger than 18 years old. Several clinical trials are pending for other CGRP-targeting therapies. There is a small number of RWE studies and one RCT study that shows that CGRP-targeting therapies have potential to be beneficial and safe to use in children and adolescents with headache disorders. Future clinical trials, once completed, will further shed light on efficacy and safety of CGRP-targeting therapies.

PMID 42873441
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PubMedEuropean journal of neurology2026-10-14

Migraine in Older Adults: Age-Related Clinical Features From the Italian RICe Registry.

Paparella Giulia G, Iannone Luigi Francesco LF, Paparella Giulia G, Sances Grazia G et al.

Primary headaches, particularly migraine, are prevalent disorders insufficiently characterized in older adults. This multicentre study evaluated headache diagnoses, focusing on migraine, across age groups in headache centers participating in the Italian Registry for Headache Disorders (RICe). Using a post hoc design, we evaluated 3477 patients enrolled at 30 headache centers (2019-2025). Patients were stratified into young adults (18-30 years), adults (31-45 years), middle-aged (46-59 years), and elderly individuals (≥ 60 years). Demographic and clinical migraine characteristics were collected. Group differences were assessed using χ2 tests and Kruskal-Wallis ANOVAs. Of 3477 patients, 644 (18.5%) were elderly, 1285 (36.9%) middle-aged, 990 (28.5%) adults, and 558 (16.1%) young adults. Among migraine patients (n = 3013, 86.7%), diagnoses differed across age groups (χ2(6) = 71.5, p < 0.001). Elderly individuals more frequently had chronic migraine (CM) (z = 4.18), whereas migraine with aura was more common in young and adult patients (z = 3.62 and 4.97, respectively). Medication-overuse headache was more frequent in the elderly (z = 3.56), who reported more monthly migraine days but lower pain intensity and fewer severe attacks (all p < 0.02). Stress and physical activity were common triggers. Among patients with available treatment data, some differences in prior preventive treatment patterns were observed, with more frequent use of beta-blockers and onabotulinumtoxinA in the elderly, whereas anti-calcitonin gene-related peptide (CGRP) monoclonal antibody prescriptions did not differ across groups. Older adults attending headache centers more frequently presented CM, with higher attack frequency, lower pain severity, greater medication overuse, and distinct triggers, supporting tailored diagnostic and therapeutic strategies.

PMID 42872890
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PubMedJAMA dermatology2026-10-14

Device-Free Auricular Acupressure for Rosacea: A Randomized Clinical Trial.

Xu Bingyang B, Chu Jiali J, Wang Ye Y, Wang Yuanqin Y et al.

Transcutaneous auricular vagus nerve stimulation is effective for rosacea. However, its neuroimmunomodulatory effects lack sham-controlled serum biochemical evidence, and specialized device reliance limits its clinical popularization. To evaluate the clinical efficacy of device-free auricular acupressure for rosacea and verify its neuroimmunomodulatory effects using serum biomarkers and immediate vascular imaging in a sham-controlled trial. This single-center, randomized, sham-controlled, assessor-masked trial was conducted in the Dermatology Outpatient Department of the Second Affiliated Hospital of Xi'an Jiaotong University from October 2025 to May 2026 and included 204 patients with rosacea who were receiving standard first-line treatment. Participants were assigned in a 1:1 ratio using block randomization. Data analysis was initiated in May 2026. The active acupressure group received a Vaccaria segetalis seed on the bilateral cavum conchae (innervated by the auricular vagus branch), while the sham group received a seed on the auricular tubercle superior margin (pure somatosensory innervation). Participants performed acupressure 3 times daily for 30 seconds, with extra pressing allowed during acute flare-ups. The intervention lasted 8 weeks. Serum levels of cathelicidin antimicrobial peptide (LL-37), calcitonin gene-related peptide (CGRP), tumor necrosis factor α (TNF-α), and interleukin (IL) 6 were measured at baseline and week 8. Multispectral imaging was performed at baseline and week 4 to assess immediate vascular responses. The primary outcome was treatment success, defined as an Investigator Global Assessment (IGA) score of 0 or 1 at week 8. The number needed to treat was calculated from absolute risk difference. The 204 participants were equally divided into 2 groups (102 each; active acupressure: mean [SD] age, 32.51 [10.60] years, 86 female individuals [84.3%]; sham acupressure: mean [SD] age, 30.82 [9.32] years, 86 female individuals [84.3%]). At week 8, the active acupressure group had a higher IGA success rate (58 [56.9%] vs 36 [35.3%]; relative risk, 1.61; 95% CI, 1.18-2.20; P = .003; number needed to treat, 5). Serum LL-37, CGRP, TNF-α, and IL-6 levels decreased more significantly in the active acupressure group. The immediate vascular improvement rate was 59.3% vs 7.4% (P < .001). At week 20, the active acupressure group maintained significantly lower IGA and Clinical Erythema Assessment scores. No serious adverse events occurred. This randomized clinical trial found that device-free, on-demand intervention yielded substantial additional clinical benefits when combined with standard first-line therapy and established early sham-controlled, serum-based evidence for its neuroimmunomodulatory mechanism, potentially offering a strategy for self-management of rosacea. Chinese Clinical Trial Registry Identifier: ChiCTR2500110787.

PMID 42873508
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PubMedMenopause (New York, N.Y.)2026-10-13

Menopausal hormone therapy combined with antiresorptive therapy for skeletal outcomes in postmenopausal women: a systematic review and network meta-analysis of randomized controlled trials.

Wang Xiaochun X, Hu Xiaorong X, Chen Jianhong J

Postmenopausal bone loss is a major contributor to osteoporosis, fracture-related morbidity, loss of independence, and mortality. Although systemic menopausal hormone therapy (MHT), antiresorptive therapy, and combination regimens improve bone mineral density (BMD), their comparative skeletal benefits and safety profiles remain incompletely defined. The study aims to compare the therapeutic and preventive skeletal effects of systemic MHT, antiresorptive therapy, and combined MHT plus antiresorptive therapy on site-specific BMD, fracture outcomes, and selected safety outcomes in postmenopausal women. PubMed, Embase, Scopus, and the Cochrane Library were searched from database inception until April 14, 2026, for randomized controlled trials evaluating systemic MHT, bisphosphonate therapy, calcitonin therapy, or MHT combined with antiresorptive therapy in postmenopausal women. Eligible comparators included placebo, no active bone-specific therapy, or another eligible randomized treatment arm. Study selection and data extraction were performed using predefined eligibility criteria and standardized extraction forms. Treatment effects were synthesized using frequentist random-effects network meta-analysis. Sixteen randomized controlled trials, including 2,861 postmenopausal women, were included. Compared with control, all active treatment nodes were associated with greater increases in lumbar spine BMD. The largest estimates were observed for MHT plus calcitonin therapy (mean difference [MD], 12.24%; 95% CI, 7.46-17.01) and MHT plus bisphosphonate therapy (MD, 9.71%; 95% CI, 6.99-12.42), although calcitonin-based estimates were informed by limited evidence. Across hip-region outcomes, MHT plus bisphosphonate therapy showed the most favorable BMD profile, including at the femoral neck (MD, 4.87%; 95% CI, 2.66-7.07) and femoral trochanter (MD, 6.65%; 95% CI, 5.12-8.17). MHT alone and MHT plus bisphosphonate therapy were associated with higher risks of mastalgia and vaginal spotting or bleeding. MHT plus bisphosphonate therapy was associated with a lower risk of any fracture compared with control (risk ratio, 0.51; 95% CI, 0.28-0.93), but fracture events were sparse and were often not prespecified efficacy outcomes. In postmenopausal women, systemic MHT, bisphosphonate therapy, and their combination improved BMD compared with control. Combination MHT plus bisphosphonate therapy showed the most favorable hip-region BMD profile; however, current evidence is insufficient to establish superior fracture prevention or long-term safety.

PMID 42868070
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PubMedExperimental dermatology2026-10-13

Vitamin D3 Inhibits Expression of Interleukin-6 and Calcitonin Gene-Related Peptide by Transformed Dorsal Root Ganglion Neurons.

Zhou Jiong J, Ding Wanhong W, Stohl Lori L LL, Alerte Katherine K et al.

Interleukin-6 (IL-6) and the neuropeptide calcitonin gene-related peptide (CGRP) promote the generation of T helper 17 (Th17) cells. Th17-type immunity is involved in several autoimmune disorders, including psoriasis. Also, there is evidence that sensory nerves play a role in Th17-type immunity, including in psoriasis. Vitamin D (VD) blood levels vary inversely with the severity of psoriasis, and topical VD analogs are effective treatments for this disease. We have now asked whether 25-dihydroxyvitamin D3 [25(OH)D3] and the more potent, active analog 1α,25-dihydroxyvitamin D3 [1α,25(OH)2D3] inhibit IL-6 and/or α-CGRP production by transformed mouse embryonic dorsal root ganglion (DRG) neurons (MED17.11 cells), which serve as a surrogate for primary DRG neurons. After culture in differentiation medium, MED17.11 cells express markers of mature DRG neurons. Lymph nodes are innervated, so IL-6 and CGRP released from nerves are anatomically situated to influence Th17 cell generation. MED17.11 cells were cultured in differentiation medium for 48-h to induce differentiation; then, medium in each well was replaced with fresh differentiation medium containing a range of concentrations of 25(OH)D3 or 1α,25(OH)2D3. Twenty-four and 48-h later, supernatants were collected, and cells were harvested and lysed. IL-6 and α-CGRP content of supernatants and lysates were assessed by ELISA. Both 25(OH)D3 and 1α,25(OH)2D3 significantly inhibited IL-6 content of supernatants and α-CGRP content of cell lysates in a dose-dependent manner with 1α,25(OH)2D3 being more potent. 25(OH)D3 and 1α,25(OH)2D3 also inhibited expression of IL-6 mRNA. VD may beneficially affect disorders involving Th17-type immunity by decreasing expression of IL-6 and α-CGRP by DRG nerves.

PMID 42865303
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PubMedHeadache2026-10-13

Plasma amylin levels in migraine and after erenumab treatment: A REFORM study.

Domínguez-Moreno Rogelio R, Alexander Tyla I TI, Karlsson William K WK, Al-Khazali Haidar M HM et al.

To investigate whether plasma amylin concentrations differ between adults with migraine and healthy controls (HCs) and whether baseline or longitudinal amylin levels are associated with treatment response to erenumab. Amylin is a calcitonin family peptide closely related to calcitonin gene-related peptide, with overlapping receptor pharmacology, and has been implicated in migraine. Human provocation studies have shown that pramlintide, an amylin analogue, triggers migraine attacks, but it remains unclear whether plasma amylin distinguishes people with migraine from HCs, varies across migraine subtypes, predicts response to erenumab, or changes during treatment. This prospective longitudinal analysis was conducted within the Registry for Migraine study at the Danish Headache Center (Copenhagen, Denmark). Adults with migraine (≥4 monthly migraine days) and age- and sex-similar HCs were enrolled between September 2020 and June 2022. Plasma samples were collected under standardized conditions at baseline and after 24 weeks of erenumab treatment (140 mg every 4 weeks). Treatment response was defined as a ≥50% reduction in monthly migraine days during weeks 13 to 24 compared with baseline. Plasma amylin was quantified from November 2023 to March 2024 using a competitive immunoassay that was selected after head-to-head kit validation, which included assessment of parallelism and spike recovery with human plasma. A total of 121 adults with migraine and 63 HCs were enrolled; 100 participants with migraine completed 24 weeks of erenumab treatment and provided evaluable efficacy data. At baseline, plasma amylin concentrations were not significantly different between erenumab responders (n = 55) and nonresponders (n = 45) (9.0 ± 2.3 vs. 8.6 ± 1.7 ng/mL; p > 0.999), and concentrations of both groups were not statistically significantly different from HCs (9.2 ± 1.7 ng/mL; p > 0.999 and p = 0.220, respectively). At 24 weeks, plasma amylin concentrations did not differ significantly between responders and nonresponders (8.8 ± 2.2 vs. 8.3 ± 2.1 ng/mL; p = 0.676). In paired analyses (n = 100), plasma amylin levels did not change from baseline to week 24 (p = 0.208). Baseline plasma amylin concentrations did not differ across migraine subgroups (episodic vs. chronic, with aura vs. without aura, ictal vs. interictal) and were not associated with key clinical variables. Plasma amylin levels did not differ between adults with migraine and HCs, across clinically relevant migraine subgroups, or by response to erenumab. These findings do not support plasma amylin as a clinically useful disease or treatment-response biomarker and are consistent with the broader concept that migraine-relevant peptidergic signaling may be compartmentalized and not captured by peripheral venous blood sampling.

PMID 42867283
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