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pasireotide (Signifor LAR / pasireotide, LAR / pasireotide LAR)

✓ Approved

Novartis AG · SSTR1 · Small Molecule

What is pasireotide?

pasireotide is a small molecule developed by Novartis AG. It is approved for therapeutic indications via injectable (others) or intramuscular (im) injection or subcutaneous injection.

Drug Profile

Brand NamesSignifor LAR, pasireotide, LAR, pasireotide LAR
CompanyNovartis AG
Drug ClassSmall Molecule, Polypeptide
Molecular TargetSSTR1, SSTR2, SSTR3, SSTR5
RouteInjectable (Others), Intramuscular (IM) Injection, Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Novartis AG

Mechanism of Action

Molecular Targets

pasireotide acts on 4 molecular targets:

SSTR1somatostatin receptor 1 (SS-1-R, SS1-R)
SSTR2somatostatin receptor 2 (SST2)
SSTR3somatostatin receptor 3 (SST3, SS3R)
SSTR5somatostatin receptor 5 (SST5, SS-5-R)
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Therapeutic Indications

pasireotide is developed for 11 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Endocrine disordersAcromegaly✓ Approved
Endocrine disordersPituitary-dependent Cushing's syndrome✓ Approved
Endocrine disordersCarcinoid syndromePhase III
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Colon cancer recurrentPhase III
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Pituitary tumour benignPhase II

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Related Research Articles

PubMedEuropean journal of pharmacology2026-11-09

Prostaglandin-Endoperoxide Synthase 1 Regulatory Variants Link Aspirin-Treated Cardiovascular Outcomes to Multicellular Cyclooxygenase-1 Expression and Activity Beyond Platelet-Derived Cyclooxygenase-1 Inhibition.

Li Xiao-Li XL, Wang Yu-Zhe YZ, Wang Qiang Q, Hu Xiao-Xiang XX et al.

Prostaglandin-endoperoxide synthase 1 (PTGS1) encodes cyclooxygenase-1 (COX-1). Aspirin inhibits platelet COX-1/thromboxane A2 (TXA2)-dependent aggregation to prevent major adverse cardiovascular events (MACE). However, relationships of low aspirin response, namely laboratory aspirin resistance (LAR) and MACE, with PTGS1 variants remain uncertain. In total, 486 cardiovascular patients, 454 on mono-antiplatelet therapy (MAPT), 32 on dual antiplatelet therapy (DAPT, aspirin plus clopidogrel), had complete data including COX-1-specific platelet function and median 4.75-year follow-up. MACE comprised acute myocardial infarction, acute stroke, and ischemia-driven revascularization. Eighteen bioinformatically annotated PTGS1 regulatory variants were genotyped. Smoking and clopidogrel exposure significantly modified LAR. Kaplan-Meier analysis linked LAR to higher crude MACE odds in MAPT and MAPT+DAPT groups (log-rank P < 0.05). Genetic analyses clarified gene-LAR, gene-MACE, gene-LAR-MACE interrelationships. Promoter rs1330344 showed lower LAR odds, with unchanged MACE odds, consistent with mild COX-1 modulation. Intronic rs7866582 conferred higher MACE odds alone, consistent with leukocyte COX-1/proinflammatory prostaglandin elevation. 3'-untranslated region (3'-UTR) rs10306190 exhibited marginally higher LAR odds yet lower MACE odds, consistent with variant-mediated COX-1 upregulation and marked vascular COX-1/PGI2 elevation counteracting residual TXA2 under aspirin. 3'-UTR rs10306196 displayed higher MACE odds alone, consistent with marked vascular COX-1/PGI2 reduction (nominal Firth P < 0.05, except for rs10306190-LAR). However, after multiple testing correction, no significant associations were observed (all BH-FDR Q > 0.05). LAR and PTGS1 variants lack population-level value for MACE prediction. This study links aspirin-treated MACE to multicellular COX-1 actions beyond platelets.

PMID 43003331
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PubMedJournal of thoracic disease2026-11-08

Lactate dehydrogenase to albumin ratio as a potential indicator of pathological response and prognosis in non-small cell lung cancer patients undergoing neoadjuvant chemoimmunotherapy followed by surgery.

Wei Bohua B, Shi Kejian K, Qian Kun K, Li Yuanbo Y et al.

In recent years, neoadjuvant chemoimmunotherapy followed by radical resection has become a new treatment option for non-small cell lung cancer (NSCLC). However, there remains a paucity of simple yet effective biomarkers for assessing pathological response and long-term prognosis. This study aimed to investigate the potential value of serum lactate dehydrogenase to albumin ratio (LAR) in this clinical setting. The clinicopathological data of 81 consecutive patients with NSCLC who received neoadjuvant chemoimmunotherapy and radical surgery at Xuanwu Hospital, Capital Medical University between January 2019 and December 2024 were retrospectively analyzed. Baseline LAR, post-treatment LAR, and the ratio of baseline to post-treatment LAR were calculated and evaluated for their associations with pathologic response and event-free survival (EFS). Of the 81 patients, 48 (59.3%) achieved major pathological response (MPR). MPR patients had significantly lower post-treatment LAR and a higher baseline to post-treatment LAR ratio than non-MPR patients, whereas baseline LAR showed no significant difference. Post-treatment LAR and baseline to post-treatment LAR ratio discriminatedMPR with an area under the curve (AUC) of 0.747 and 0.719, respectively. Multivariate logistic regression identified post-treatment LAR [odds ratio (OR) =0.498, P=0.02] and radiological response (OR =6.297, P=0.008) as independent factors associated with MPR. Multivariate Cox regression demonstrated that higher post-treatment LAR [hazard ratio (HR) =1.664, P=0.003] and non-MPR status (HR =3.498, P=0.004) were independent prognostic factors for poor EFS. Restricted cubic spline (RCS) analysis further revealed a positive association between post-treatment LAR and EFS risk, with higher LAR corresponding to increased HRs. A nomogram based on these two EFS prognostic factors demonstrated good calibration at 24 months with internal bootstrap validation (C-index =0.769). Post-treatment LAR could serve as a potential indicator for response assessment and long-term prognostication in NSCLC patients undergoing neoadjuvant chemoimmunotherapy. Its simplicity, cost-effectiveness, and accessibility through routine laboratory testing render it a promising candidate for integration into clinical practice.

PMID 42996685
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PubMedJCEM case reports2026-11-08

Pediatric gigantism due to ectopic growth hormone releasing hormone secretion from a metastatic bronchial neuroendocrine tumor.

Vidal-Ostos De Lara Fernando F, Sanchis-Pascual David D, Hernández-Rienda Lorena L, Del Olmo-García María Isabel MI

Pediatric gigantism due to ectopic secretion of growth hormone-releasing hormone (GHRH) is exceptionally rare. Most pediatric reports have involved pancreatic neuroendocrine tumors in the context of multiple endocrine neoplasia 1 (MEN1). We describe a female patient diagnosed at 9 years of age with a typical bronchial neuroendocrine tumor and subsequently found to have diffuse hepatic and skeletal metastases, accelerated linear growth, and acromegalic features. Evaluation demonstrated markedly elevated plasma GHRH, growth hormone, and insulin-like growth factor 1, with diffuse pituitary hyperplasia on magnetic resonance imaging and no discrete pituitary adenoma. Genetic testing for MEN1 was negative. Management required repeated surgery, first-generation somatostatin analogs, dopamine agonist therapy, pegvisomant, pasireotide, and peptide receptor radionuclide therapy with lutetium-177 DOTA-Tyr3-octreotate. Pasireotide achieved improved biochemical control, while peptide receptor radionuclide therapy contributed to long-term structural stability. After 23 years of follow-up, the patient remains clinically well with stable tumor burden and controlled somatotropic axis. This case highlights the natural history of a pediatric-onset GHRH-secreting neuroendocrine tumor and highlights the efficacy of aggressive, multidisciplinary management in achieving long-term survival.

PMID 42996503
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PubMedIndian journal of surgical oncology2026-11-08

Lighting the Anastomosis: Role of Intraoperative ICG Fluorescence in Reducing Leak Rates in Minimally Invasive Rectal Cancer Surgery.

Nishtha, Daima Mahesh M, Sugoor Pavan P

Anastomotic leakage (AL) remains a major complication following sphincter-preserving rectal cancer surgery. This study evaluates the association between intraoperative indocyanine green (ICG) fluorescence angiography and AL reduction. A retrospective propensity score-matched cohort study including 318 consecutive patients undergoing minimally invasive anterior resection (AR), low anterior resection (LAR), or ultra-low anterior resection (ULAR). The Conventional Assessment Group (CAG) utilized white-light visualization including bowel color, mesenteric pulsation, and marginal bleeding. The ICG group underwent standardized intravenous ICG angiography (0.1-0.2 mg/kg) with near-infrared imaging prior to anastomosis. AL was defined according to ISREC criteria and confirmed clinically and/or radiologically. AL occurred in 1/92 (1.1%) in the ICG group versus 9/92 (9.8%) in CAG (p = 0.018). ICG prompted intraoperative revision in 9 (9.7%) patients, none of whom developed AL. On multivariate analysis, non-use of ICG (OR 8.9; p = 0.011), hypertension (OR 3.2; p = 0.015), and Left colic artery non-preservation (OR 2.5; p = 0.032) were independently associated with AL. ICG perfusion assessment should be considered in minimally invasive rectal cancer surgery, particularly in high-risk anastomoses.

PMID 42996513
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PubMedbioRxiv : the preprint server for biology2026-11-08

Nanoarchitecture of the presynaptic cell adhesion molecule PTPσ in relation to prospective vesicle fusion sites and postsynaptic NMDA receptors.

DeMarco Hibbs Emily M EM, Mitias Samira S, Aitken Rebecca R, Levy Aaron D AD et al.

Protein organization at individual synapses tunes synaptic function. Presynaptic release-regulating proteins and postsynaptic receptors each concentrate into subsynaptic nanoclusters, and their precise alignment across the cleft into nanocolumns can maximize receptor activation following vesicle fusion. However, both the molecular organization defining presynaptic fusion sites and the mechanisms by which they are spatially coordinated with postsynaptic complexes remains unclear. Presynaptic transmembrane cell adhesion molecules may mediate both processes as they could simultaneously anchor cytosolic fusion machinery to the presynaptic membrane and bridge the cleft to coordinate PSD organization. The LAR-RPTP family member PTPσ is an important possibility, as its trans-synaptic interactors that bind PSD-95 are associated with NMDAR dysfunction, suggesting PTPσ may coordinate NMDAR positioning. However, PTPσ subsynaptic organization has not been determined. Here, we investigate the cellular expression and subsynaptic nano-organization of endogenous PTPσ in cultured rat hippocampal neurons. We find that PTPσ is enriched at most excitatory synapses, but unexpectedly, PTPσ nanoclusters do not colocalize with the vesicle priming protein Munc13-1. Instead, they adopt a stereotyped position adjacent to this machinery, without preferential association with sites in nanocolumns. PTPσ nanoclusters also lie offset from postsynaptic NMDA receptors, mirroring their relationship to vesicle fusion sites, yet the presence of PTPσ at a nanocolumn does not predict NMDAR abundance. Together, these findings suggest that PTPσ does not directly coordinate release site- NMDAR alignment but instead occupies defined nanoscale positions adjacent to vesicle fusion sites, potentially helping to shape or stabilize the vesicle priming landscape of the active zone. Synaptic vesicles fuse at specific presynaptic locations, called release sites, whose precise position-and alignment with postsynaptic receptor density-critically regulates synaptic strength. NMDA receptors, which flux calcium to gate diverse forms of brain plasticity, are especially sensitive to glutamate release location. Here, we test whether the cell adhesion molecule PTPσ helps establish the relationship between release sites and NMDARs. We find that PTPσ occupies defined nanoscale positions adjacent to release sites, offering new insight into the molecular machinery organizing these sites and suggesting that PTPσ helps shape the probability distribution of vesicle fusion within the synapse.

PMID 42995974
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PubMedArchives of endocrinology and metabolism2026-11-06

Effectiveness and safety of pharmacological treatments for Cushing's disease: An updated systematic review and meta-analysis.

Zimmermann Amanda Cristina AC, Cardoso Ana Beatriz Ribeiro ABR, Galendi Julia Simões Corrêa JSC, Glezer Andrea A et al.

To provide an updated assessment of the efficacy, safety, and clinical outcomes of pharmacological treatments for Cushing's disease, focusing on cabergoline, ketoconazole, pasireotide, and osilodrostat. This systematic review update was conducted using the Joanna Briggs Institute methodology. Outcomes included disease control rates, adverse events, and improvements in comorbidities and quality of life. Eleven new studies were included. In the updated analysis, disease control rates were 35.5% for cabergoline (95% confidence interval [CI]: 28-43%; 7 studies, 155 patients), 42% for ketoconazole (95% CI: 38-47%; 7 studies, 488 patients), 42% for pasireotide (95% CI: 28-58%; 10 studies, 580 patients), and 67% for osilodrostat (95% CI: 61-73%; 4 studies, 263 participants). According to GRADE, certainty of evidence was very low for pasireotide and low for the other agents. Osilodrostat increased cortisol normalization 4.56-fold versus placebo (95% CI: 1.53-13.56; 2 studies, 144 patients; moderate certainty). Osilodrostat and pasireotide improved CushingQoL scores by 13.23 points (95% CI: 10.78-15.68) and 8.96 points (95% CI: 4.37-13.55), respectively. Pasireotide was predominantly associated with dysglycemia. Cabergoline most often caused mild adverse events, with treatment escape in 11%. Ketoconazole was linked to mildly elevated transaminases and gastrointestinal symptoms. Osilodrostat most commonly resulted in fatigue and adrenal insufficiency, often reflecting therapeutic response. Pharmacological disease control rates in Cushing's disease range from 35.5% to 67%, with osilodrostat achieving the highest rates and being the only agent supported by placebo-controlled evidence demonstrating a statistically significant effect. In the absence of head-to-head comparisons, treatment decisions remain individualized.

PMID 42992517
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