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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

PubMedInflammopharmacology2026-06-09

Anti-osteoporotic potential of Lawsonia inermis leaf extract: integration of network pharmacology, molecular docking, and experimental validation in ovariectomized rats.

Mandlik Deepa S DS, Lavhale Mitali P MP, Mandlik Satish K SK

With an emphasis on modulation of the oestrogen receptor (ER)/osteoprotegerin (OPG)/receptor activator of nuclear factor-κβ ligand (RANKL) signalling pathway, the current study sought to explore the anti-osteoporotic potential of Lawsonia inermis leaves ethanolic extract (LIEE) using a unified method linking network pharmacology, molecular docking, and experimental validation in an ovariectomised (OVX) rat model. LC-MS/MS and HPTLC were applied for the phytochemical profiling of LIEE. To find possible targets and pathways connected to osteoporosis, network pharmacology analysis was carried out using Cytoscape and public databases (PubChem, BindingDB, DisGeNET, and GeneCards). To confirm interactions between important phytoconstituents and target proteins, molecular docking was used. Six groups (n = 8) of female Wistar rats were randomly assigned for in vivo evaluation: OVX Control, Sham Control, OVX + LIEE (100, 200, and 400 mg/kg, p.o.), and OVX + 17β-estradiol (30 µg/kg/week, s.c.). Bone turnover markers (parathyroid hormone, calcitonin, osteocalcin, tartrate-resistant acid phosphatase, osteoprotegerin, receptor activator of nuclear factor), lipid profile, oxidative stress markers (superoxide dismutase, catalase, glutathione peroxidase, malondialdehyde), pro-inflammatory cytokines (Tumour necrosis factor-α, Interleukin-1β, Interleukin-6), and histopathology of the femur and reproductive tissues were assessed after ten weeks of treatment. RT-PCR was used to analyse the gene expression of epidermal growth factor receptor (EGFR), mammalian target of rapamycin (mTOR), and matrix metalloproteinase-9 (MMP-9). Fourteen bioactive phytoconstituents, including gallic acid, rutin, quercetin, apigenin, and many others, were found by LC-MS/MS analysis. With important hub genes including MMP-9, mTOR, B-cell lymphoma-2, Hypoxia-Inducible Factor 1-alpha, and EGFR, network pharmacology identified 61 common targets between LIEE and osteoporosis. Enrichment analysis highlighted the involvement of ER/OPG/RANKL signalling pathways. Molecular docking demonstrated strong binding affinity of major phytoconstituents with target proteins. In vivo studies showed that LIEE significantly attenuated OVX-induced body weight gain and restored uterine weight and serum estrogen levels, indicating phytoestrogenic activity. LIEE significantly improved bone physical parameters and increased BMD. Treatment normalised serum calcium, phosphorus, and alkaline phosphatase levels, and favourably modulated bone turnover markers by decreasing tartrate-resistant acid phosphatase, parathyroid hormone and osteocalcin levels while increasing calcitonin and osteoprotegerin levels and reducing receptor activator of nuclear factor kappa-B Ligand expression. LIEE also significantly enhanced lipid profile by reducing total cholesterol, triglyceride, and low-density lipoprotein while enhancing high-density lipoprotein levels. Furthermore, LIEE markedly reduced oxidative stress by increasing superoxide dismutase, catalase, and glutathione peroxidase levels and decreasing malondialdehyde. Pro-inflammatory cytokines (Tumour necrosis factor-α, Interleukin-1β, Interleukin-6) were considerably suppressed. Reestablishment of trabecular bone architecture and normalisation of uterine and vaginal morphology were verified by histopathological examination. Gene expression analysis demonstrated downregulation of MMP-9, mTOR, and EGFR in LIEE-treated groups. LIEE exhibits significant anti-osteoporotic effects through a multi-targeted mechanism involving modulation of ER/OPG/RANKL signalling, suppression of inflammation and oxidative stress, and regulation of key molecular targets. These outcomes propose that LIEE could help as a capable phytotherapeutic candidate for the management of postmenopausal osteoporosis and warrant more clinical exploration.

PMID 42262669
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PubMedAnesthesiology2026-06-09

Dual Roles of Voltage-gated Calcium Channels and γ-Aminobutyric Acid-mediated Signaling in Modulating Neurotensin Receptor Type 2-induced Antinociception.

Martin Laurent François LF, Gomez Kimberly K, Park Joon J, Ismail Khaled K et al.

The potential to mitigate pain by targeting a single receptor while simultaneously modulating peripheral and spinal circuits, offers an exciting nonopioid therapeutic strategy. Neurotensin receptor type 2 (NTSR2) is a promising yet underexplored pathway for nonopioid analgesia. The authors investigated the antinociceptive effects of NTSR2 activation and its mechanisms in rodent models of perioperative and chronic pain. Using NT79, a selective NTSR2 agonist, the authors assessed pain behaviors in male and female rats and mice. Animals were randomly assigned to receive saline (control) or NT79 at multiple doses. Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9)-mediated NTSR2 knockdown and pharmacologic inhibition of γ-aminobutyric acid (GABA) receptors were used to dissect NTSR2-dependent mechanisms. Dorsal root ganglion (DRG) calcium imaging, whole cell patch clamp electrophysiology, and spinal neurotransmitter assays evaluated the modulation of voltage-gated calcium channels and γ-aminobutyric acid-mediated (GABAergic) signaling. Intrathecal NT79 produced robust, dose-dependent antinociception across pain models, species, and sexes, an effect abolished by NTSR2 knockdown. NT79 reduced high-voltage-activated calcium currents in DRG neurons, indicating a presynaptic inhibitory mechanism. In the spinal cord, NT79 enhanced GABA release and suppressed calcitonin gene-related peptide (CGRP) release. Pharmacologic blockade of GABA receptors partially reversed NT79's antinociceptive effects, as did NTSR2 knockdown in GABAergic neurons, supporting a central GABAergic mechanism in addition to the effect on central DRG terminals. Taken together, these results demonstrate that NTSR2 activation produces sustained antinociception via dual-site modulation: inhibition of peripheral voltage-gated calcium channels and enhancement of spinal GABAergic signaling. These findings identify a novel, nonopioid mechanism of analgesia and support NTSR2 as a therapeutic target for chronic pain.

PMID 42262386
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PubMedNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2026-06-09

Efficacy and safety of CGRP monoclonal antibodies in chronic migraine: a systematic review integrating randomized and real-world evidence.

Carta Diamante D, Lo Buono Viviana V, Grugno Rosario R, Lo Presti Riccardo R et al.

Chronic migraine (CM) is a highly disabling neurological disorder characterized by ≥ 15 headache days per month, of which at least 8 exhibit migrainous features. Despite the availability of preventive therapies, conventional treatments are often limited by suboptimal efficacy and poor tolerability. Monoclonal antibodies targeting calcitonin gene-related peptide (CGRP) or its receptor have emerged as mechanism-based preventive options. This systematic review aims to evaluate the efficacy, safety, and clinical relevance of CGRP-targeted monoclonal antibodies in the prevention of chronic migraine. A comprehensive literature search of PubMed, Scopus, and Web of Science was conducted from database inception to July 2025. Randomized controlled trials and observational real-world studies evaluating CGRP-targeted monoclonal antibodies in adult patients with chronic migraine were included. The review followed PRISMA 2020 guidelines (Page et al. 2021), was registered in the PROSPERO database (CRD420261284751), and included 11 studies out of 1,688 identified records. Across included studies, CGRP-targeted monoclonal antibodies consistently demonstrated reductions in migraine frequency, improvements in ≥ 50% responder rates, and favorable safety profiles. Randomized controlled trials showed robust efficacy compared with placebo, while real-world studies confirmed effectiveness in more heterogeneous and treatment-resistant populations. However, variability in outcome definitions, particularly between monthly migraine days and monthly headache days, and differences in study design contributed to heterogeneity across findings. CGRP-targeted monoclonal antibodies represent an effective and well-tolerated preventive option for chronic migraine, with clinically meaningful benefits across both controlled and real-world settings. While current evidence is strong, further research is needed to evaluate long-term outcomes, optimize treatment strategies, and improve standardization of outcome measures. This systematic review was registered in the PROSPERO database (CRD420261284751).

PMID 42262668
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PubMedHeadache2026-06-09

Inhibiting astrocyte activation is effective in triptan-induced medication-overuse headache model and prolonged hyperalgesia.

Wang Yanyun Y, Zhang Xiaoyan X, Zhang Yun Y, Zhang Shuhua S et al.

We hypothesized that sustained astrocyte activation in the trigeminal nucleus caudalis (TNC) drives prolonged hyperalgesia in triptan-induced medication-overuse headache (MOH). This study aimed to investigate the role of astrocyte activation and evaluate the therapeutic potential of targeted astrocyte inhibition. Chronic triptan use for migraine can lead to MOH, characterized by persistent hyperalgesia and high relapse rates. The mechanisms underlying this transition remain poorly understood. Although central sensitization and neuroinflammation are implicated, the specific contribution of astrocytes in TNC has not been investigated. A rat MOH model was established by repeated intraperitoneal administration of sumatriptan for 9 days. Cutaneous allodynia was assessed using von Frey filaments, and latent sensitization was evaluated under the 0.5 mg/kg nitroglycerin challenge. To selectively inhibit astrocyte activation, an adeno-associated virus vector was injected into bilateral TNC, followed by the administration of its ligand, deschloroclozapine. Neuronal (cellular proto-oncogene Fos, calcitonin gene-related peptide, postsynaptic density protein 95, and synaptophysin), microglial (ionized calcium-binding adapter molecule 1), and astrocytic (glial fibrillary acidic protein) markers, along with proinflammatory mediators (inducible nitric oxide synthase, tumor necrosis factor-alpha, etc.), were analyzed via immunofluorescence and Western blot. Repeated sumatriptan induced long-term cutaneous allodynia and latent sensitization. This process was accompanied by transient activation of neurons and microglia, and a short-term increase in synaptic proteins and proinflammatory cytokines in TNC. However, astrocyte activation sustained after the behavioral hypersensitivity had apparently resolved. Chemogenetic inhibition of astrocytes in TNC prevented the development of long-term cutaneous allodynia and latent sensitization. This intervention also ameliorated the overexpression of synaptic proteins and proinflammatory cytokines. Our findings demonstrate that sustained astrocyte activation in TNC is a potential driver of prolonged hyperalgesia in triptan-induced MOH. Inhibiting astrocyte activity effectively reverses behavioral and molecular markers of MOH, highlighting astrocyte inhibition as a promising therapeutic strategy for MOH.

PMID 42260315
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PubMedNeurology and therapy2026-06-09

Real-World Response and Super-Response to Eptinezumab over 48 Weeks in Migraine: The Prospective Multicenter EMBRACE III Study.

Barbanti Piero P, Aurilia Cinzia C, Filippi Massimo M, Doretti Alberto A et al.

Long-term (> 24 weeks) real-world evidence of eptinezumab's effectiveness is limited. We evaluated ≥ 50% and ≥ 75% response rates over 48 weeks in patients with high-frequency episodic migraine (HFEM) or chronic migraine (CM). EMBRACEIII (NCT05570149) is a prospective, multicenter, observational study. Adults with HFEM or CM who experienced ≥ 3 preventive treatment failures received eptinezumab 100 mg intravenously every 12 weeks, with optional 300 mg escalation after week 12 for inadequate response. Co-primary endpoints were ≥ 50% and ≥ 75% reductions in monthly migraine/headache days (MMD/MHD) at weeks 45-48 versus baseline. Secondary endpoints were changes in MMD/MHD, monthly analgesic intake (MAI), pain intensity (assessed using the numeric rating scale [NRS]), migraine-related disability and impact (assessed using the Headache Impact Test-6 [HIT-6], Migraine Disability Assessment [MIDAS], the Migraine Interictal Burden Scale-4 [MIBS-4]), patient-reported global treatment response (assessed using the Patient Global Impression of Change [PGI-C] questionnaire), and 100% response. Exploratory analyses assessed dose escalation, prior anti-calcitonin gene-related peptide monoclonal antibodies (CGRP mAbs) treatment failures, responders without adverse events, ≥ 30% reduction in the NRS during residual attacks, and clinically complex subgroups. Among the 261 patients (safety population) included in the study, 124 completed ≥ 48 weeks of treatment with eptinezumab. At week 48, the response rates for ≥ 50%, ≥ 75%, and 100% were 82.3%, 51.6%, and 9.7%, respectively. All secondary endpoints improved significantly (p < 0.001), with significant reductions from baseline: MMD/MHD, - 15.5; MAI, - 14.9; NRS, - 3.3; HIT-6, -  20.6; MIDAS, - 74; and MIBS-4, - 4.3. Also, 94.8% of patients reported PGI-C improvement. Dose escalation occurred in 69.4% of patients. Patients receiving ≥ 3 doses of 300 mg eptinezumab achieved outcomes comparable to responders receiving 100 mg. Among patients with prior anti-CGRP mAb treatment failures (51.6%), ≥ 50% and 100% responders were similar to mAb-naïve patients, whereas ≥ 75% response was lower (37.5%; p = 0.002). Response rates of ≥ 50%,  ≥ 75% and 100% were achieved by 81.2%, 50.4%, and 8.5%, respectively, in patients without adverse events; 85.7%, 51.4%, and 8.6% in patients with psychiatric comorbidities; 87.8%, 54.9%, and 7.3% in patients with CM with medication overuse; and 89.2%, 50.0%, and 7.1% in patients with CM with both conditions. Eptinezumab demonstrated sustained 48-week effectiveness, with high response rates of ≥ 75% and 100% in a difficult-to-treat population. Effectiveness was preserved in patients with prior anti-CGRP mAb failures after 300 mg escalation and in clinically complex subgroups. Many patients achieved ≥ 30% reduction in NRS during residual migraine attacks. ClinicalTrials.gov: NCT05570149.

PMID 42262724
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PubMedHealth care science2026-06-08

Combined Detection of Preoperative Serum Calcitonin and Carcinoembryonic Antigen in Medullary Thyroid Carcinoma: A Retrospective Multicenter Cohort Study.

Yang Yu Y, He Yufei Y, Lin Bo B, Zheng Yuanyuan Y et al.

The aim of this study was to investigate the clinical value of combined detection of preoperative serum calcitonin (Ctn) and carcinoembryonic antigen (CEA) for diagnosing medullary thyroid carcinoma (MTC), as well as predicting lymph node metastases and prognosis, compared with the value of detection of either marker alone. This retrospective multicenter cohort study included patients with thyroid nodules who underwent preoperative measurements of serum Ctn and CEA at six medical centers between 2012 and 2024. Receiver operating characteristic (ROC) curves were analyzed to compare the diagnostic performances of Ctn, CEA, and their combination. A total of 13,272 patients were included in the study, comprising 115 with MTC, 10,845 with papillary thyroid carcinoma, and 2312 with benign nodules. For diagnosing MTC, the area under the ROC curve (AUC) values for Ctn and CEA alone were 0.992 and 0.983, respectively, while the combination of the two markers achieved the highest AUC of 0.999. Ctn had a higher positive predictive value (PPV) for MTC diagnosis than CEA (51% vs. 31%), and the combination did not improve the PPV (46%) compared with Ctn alone. For predicting cervical and lateral neck lymph node metastases in MTC, the combination had a higher AUC than Ctn or CEA alone (0.735 vs. 0.708 vs. 0.655 and 0.769 vs. 0.707 vs. 0.675). The combination also had a higher AUC for predicting recurrence than Ctn or CEA alone (0.734 vs. 0.642 vs. 0.611). Compared with the detection of either marker alone, the combined detection of Ctn and CEA improved the diagnostic accuracy for MTC but did not enhance the PPV. The combined detection also improved the predictive accuracy for cervical and lateral lymph node metastases and disease recurrence.

PMID 42255039
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