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apomorphine (apomorphine, Chiesi / Apofin / Apofin Stylo)

✓ Approved

Chiesi Farmaceutici S.p.A. · DRD2 · Small Molecule

What is apomorphine?

apomorphine is a small molecule developed by Chiesi Farmaceutici S.p.A.. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

Brand Namesapomorphine, Chiesi, Apofin, Apofin Stylo
CompanyChiesi Farmaceutici S.p.A.
Drug ClassSmall Molecule
Molecular TargetDRD2
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Chiesi Farmaceutici S.p.A.

Mechanism of Action

Molecular Targets

apomorphine acts on 1 molecular target:

DRD2dopamine receptor D2 (D2DR, D2R)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

apomorphine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Nervous system disordersParkinson's disease✓ Approved

Related Research Articles

PubMedParkinsonism & related disorders2026-08-24

Comparative outcomes and healthcare costs of three device-aided pharmacotherapies for patients with advanced Parkinson's disease in Sweden: A nationwide registry-based cohort study.

Nyholm Dag D, Paonessa Davide D, Bergquist Filip F, Timmermann Jan Erik JE et al.

Patients with advanced Parkinson's disease often require treatment beyond conventional oral or transdermal therapy. However, real-world evidence across emerging advanced treatment strategies remains limited. To compare patient characteristics, treatment patterns, clinical outcomes, healthcare resource utilization (HCRU), and costs among Parkinson's disease patients treated with levodopa/carbidopa dispersible microtablets (LC-5), levodopa-carbidopa intestinal gel (LCIG)/levodopa-entacapone-carbidopa intestinal gel (LECIG), or continuous subcutaneous apomorphine infusion (CSAI). Patients initiating LC-5, LCIG/LECIG, or CSAI between 2014 and 2024 were identified in Swedish national register data. Treatment groups were balanced using inverse probability weighting. Descriptive analyses, cumulative incidence estimates, and Cox proportional hazards models were used to assess outcomes. 426 LC-5, 1112 LCIG/LECIG, and 490 CSAI users were included. 63.6% of LC-5 users were women, whereas men constituted the majority in the other treatment groups. 3.5% of LCIG/LECIG and 6.1% of CSAI users discontinued treatment, compared with 28.6% of LC-5 users. Compared with LCIG/LECIG users, the mortality hazard ratio estimates were lower for LC-5 (HR 0.71, 95% CI 0.45-1.11) and CSAI users (HR 0.80, 95% CI 0.63-1.02), but neither difference was statistically significant. In the 12 months following treatment initiation, weighted estimates of healthcare costs were higher among LCIG/LECIG (€37,613) and CSAI users (€29,214) than among LC-5 users (€17,290). In this nationwide Swedish cohort, no statistically significant mortality difference was detected. Weighted one-year HCRU and cost estimates were lower among LC-5 users than among infusion-therapy users; however, residual confounding by disease severity, treatment selection, and other unmeasured clinical factors limits causal interpretation.

PMID 42636761
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PubMedFrontiers in cellular neuroscience2026-08-21

Characterization of TRPV2-associated pathology in Parkinson's disease and therapeutic modulation using Tranilast.

Chunchuwar Apeksha A, Vaidya Bhupesh B, Sharma Shyam Sunder SS

Transient Receptor Potential (TRP) channels have gained worldwide attention for their expression and distribution in multiple human organs. Among these TRPs, Transient Receptor Potential Vanilloid (TRPV) channels play diverse physiological roles in the brain, and changes in their expression contribute to central nervous system (CNS) diseases. In a previous druggable-genome α-synuclein modifier screen, a member of the TRPV family, TRPV2, emerged as a Tier 3 ion-channel candidate, meeting directionality and conflict-score criteria, though with limited shRNA-level support. However, based on this preliminary data and the known role of TRPV2 in Ca2+ entry and cellular stress responses, we decided to investigate its role in detail using experimental PD models. In the present investigation, 6-hydroxydopamine (6-OHDA) was used in vivo (Sprague Dawley rats) and in vitro (SH-SY5Y cells) to induce Parkinson's disease (PD), and its effect on TRPV2 expression was investigated. The study further involved measuring behavioral parameters using the rotarod, open field, apomorphine, and cylinder tests. 6-OHDA administration induced excessive reactive oxygen species (ROS) production and increased expression of TRPV2 channels. This is also accompanied by increased intracellular calcium influx and reduces cell viability. However, Tranilast, a TRPV2 antagonist, exhibited promising neuroprotective effects in the 6-OHDA PD model by restoring tyrosine hydroxylase levels, reducing oxidative stress, and improving motor function. Also, it diminished the intracellular Ca2+ influx and reduced ROS levels in the 6-OHDA-treated SH-SY5Y cells. Overall, our results suggest that TRPV2 levels are elevated in PD, and targeting TRPV2 could be a potential therapeutic approach in the future.

PMID 42625634
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PubMedBrain and behavior2026-08-18

Integrative Network Pharmacology and Transcriptomics Reveal the Mechanism of XuanShi Choudong Recipe in the Treatment of Tic Disorder.

Jue Hu H, Jingying Ma M, Yaqin Chen C, Yulu Pan P et al.

The Xuanshi Choudong Recipe (CDR), a classic traditional Chinese medicine (TCM) formula, has long been clinically prescribed to relieve tic disorder (TD). However, its underlying in-depth mechanism remains largely unknown. To elucidate the mechanism by which CDR exerts therapeutic effects in the treatment of TD. Four-week-old SD rats were injected intraperitoneally with apomorphine at 2 mg/kg per day to establish the model. After successful modeling, the rats were randomly divided into the model, CDR low-dose (CDRL, 6.84 g/kg), CDR medium-dose (CDRM, 13.67 g/kg), CDR high-dose (CDRH, 27.34 g/kg), and haloperidol (1 mg/kg) groups. Age-matched SD rats served as the control group. Therapeutic efficacy was evaluated using the open field test, hematoxylin and eosin (H&E) staining, and biochemical analysis. The potential mechanisms of CDR were explored using network pharmacology and transcriptomic analyses and validated by western blotting, immunofluorescence, biochemical analysis, and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. In this study, a total of 126 compounds were identified in CDR using liquid chromatography-mass spectrometry, with phenylpropanoids, polyketides, benzenoids, and lipids being the main components. Network pharmacology prediction revealed 265 overlapping targets between CDR and TD, with core targets including AKT1, BCL2, and IL6, and the phosphoinositide 3-kinase/protein kinase B (PI3K-AKT) signaling pathway being significantly enriched. Transcriptomic analysis showed that CDR reversed the expression of 111 genes in the striatum of TD rats, and these genes were significantly enriched in pathways related to apoptosis and the PI3K-Akt signaling pathway. Behavioral assessment demonstrated that CDR dose-dependently reduced apo-induced stereotypic behavior scores and spontaneous locomotor activity in TD rats. H&E staining indicated that CDR attenuated striatal neuronal damage. High dose CDR treatment significantly decreased the elevated levels of dopamine, 5-HT, norepinephrine, glutamate, and gamma-aminobutyric acid in the striatum (p < 0.01 or p < 0.001). Furthermore, High-dose CDR alleviated oxidative stress-induced injury by reducing reactive oxygen species and oxidized glutathione (GSSG) levels and increasing superoxide dismutase (SOD) activity, reduced glutathione (GSH) levels, and the GSH/GSSG ratio (p < 0.01 or p < 0.001). TUNEL staining and immunofluorescence results showed that CDR inhibited neuronal apoptosis in the striatum. Western blotting confirmed that CDR upregulated the phosphorylation levels of PI3K and AKT, increased the Bcl-2/Bax ratio, and downregulated caspase-3 expression, with high-dose CDR exerting the most significant effect.

PMID 42608906
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PubMedNeuroscience bulletin2026-08-17

Species Divergence in Oxytocin-Dependent Yawning on a Conserved Glutamatergic Erection Circuit.

Zhang Yan-Chu-Fei YC, Zheng Qing-Wu QW, Lu Yang Y, Wang Hao-Yuan HY et al.

Yawning coupled with penile erection is a conserved neurobehavioral syndrome mediated by the paraventricular hypothalamus (PVH). However, the distinct roles of oxytocin and its co-transmitters remain unresolved. Using chemogenetics, we showed that activation of PVH oxytocin neurons was sufficient to elicit both responses, whereas silencing these neurons abolished them. Viral tracing revealed that these neurons project collaterally to the brainstem reticular nucleus and spinal cord to spatially coordinate autonomic and somatic motor outputs. By dissecting the molecular mechanisms using CRISPR-Cas9, we found that vesicular glutamate transporter 2 (VGLUT2)-dependent glutamatergic transmission provides the primary drive for both behaviors, whereas the oxytocin peptide is selectively required for yawning but dispensable for erection. Comparative analyses across rats, hamsters, and mice demonstrated that while the glutamatergic erectile circuit was conserved, mice lacked spontaneous yawning and were resistant to apomorphine-induced yawning. These findings suggest a hierarchical co-transmission framework in which fast glutamatergic signaling provides the core drive, while oxytocin confers behavioral specificity.

PMID 42606661
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PubMedDrug development research2026-08-17

TEAD1 Knockdown Ameliorates Diabetic Erectile Dysfunction in Rats and Is Associated With Modulation of Calcium Signaling-Mediated Contractile Machinery.

Zhang Tao T, Wu Chenxiao C, Lu Youlong Y, Li Weili W et al.

Diabetes mellitus (DM) related erectile dysfunction (ED) is a common complication in males. We aim to explore the specific regulatory mechanisms of TEA domain family member 1 (TEAD1) in DMED rats. Diabetic ED in rats was induced by streptozotocin and evaluated by the intracavernosal pressure response to electrical stimulation and the apomorphine test. Corpus cavernosum smooth muscle cells (CCSMCs) were isolated to explore the role of TEAD1 in phenotypic transformation. TEAD1 knockdown was performed in DMED rats and CCSMCs using the CRISPR/Cas9 technology. Hematoxylin-Eosin and Masson staining were applied to observe the penile tissue pathology. The CCSMC function was evaluated by detecting viability and apoptosis. Protein and gene expression levels were examined by Western blot and real-time quantitative polymerase chain reaction. The TEAD1 gene knockdown ameliorated erectile function in DMED rats. Knockdown of TEAD1 in CCSMCs of DMED rats enhanced their viability and inhibited their apoptosis, promoting the transformation of CCSMCs from a synthetic to a contractile phenotype. Furthermore, bioinformatics analysis identified the calcium signaling pathway as a candidate pathway warranting further experimental investigation. TEAD1 knockdown was associated with altered expression of calcium-related proteins and elevated intracellular Ca2+ levels. The calcium channel blocker Nimodipine could reverse the improvement of erectile function in DMED rats and the transformation of CCSMC phenotype caused by TEAD1 knockdown. TEAD1 knockdown promotes the transformation of CCSMCs from a synthetic to a contractile phenotype and is associated with modulation of calcium signaling-mediated contractile machinery, contributing to the relief of DMED.

PMID 42606539
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PubMedACS omega2026-08-14

Structure-Affinity Relationship Optimization of SYA16263 Yields New Ligands with Improved Receptor Affinity and Antipsychotic-Like Properties.

Gonela Uma M UM, Bricker Barbara A BA, Voshavar Chandrashekhar C, Onyameh Edem K EK et al.

Central nervous system (CNS) disorders are multifactorial in nature. Dopamine (DA) and serotonin (5-HT) receptors are the prime targets for antipsychotic drug development. In particular, D2-like (D2, D3 and D4), 5-HT1A and 5-HT2A receptors are strongly implicated in the pathophysiology of many neuropsychiatric conditions such as anxiety, schizophrenia, mood and hyperactivity disorders. However, selectivity of the ligands at different receptor subtypes and crosstalk between them complicates the scenario. Development of new ligands that exhibit selectivity toward specific receptor subtypes may aid in understanding their interplay in various CNS disease pathologies. Previously, we reported SYA16263 (6) with high binding affinities toward the D4 and 5-HT1A receptors and moderate binding affinities at the D2, D3, 5-HT2A and 5-HT7A receptors. Further, we have shown that compound 6 exhibits functional selectivity, producing antipsychotic-like effects in rodents without inducing the side effect of catalepsy. In this work, an extended structure-affinity relationship (SAfiR) investigation was carried out with structural modifications at the p-fluorophenyl moiety of 6 by varying the aryl/heteroaryl groups, tweaking the linkage connectivity, and the connecting chain length at the nonpiperazinyl aryl region to improve receptor affinity at D2R, and 5-HT1AR. Our SAfiR studies resulted in compounds 35 and 36, with enhanced affinities at D2R, D3R, and 5-HT1AR compared to 6. In addition, compound 35 exhibited improved binding affinity at 5-HT2AR while compound 36 showed enhancement at 5-HT7AR. Docking studies were performed with compounds 6, 36 and reference drug, lurasidone to gain structural insight into the ligand-receptor interactions at both the D2 and 5-HT2A receptors. Subsequently, pharmacological evaluation of 35 and 36 in the mouse model of schizophrenia using the apomorphine-induced climbing behavior study produced a dose-dependent reduction in climbing behavior and its effects were compared against lurasidone, a standard antipsychotic drug. Further, 35 and 36 did not induce catalepsy in rats even at their respective 3 x 3ED50 doses. Thus, 35 and 36 have the potential to produce antipsychotic-like results in humans in a manner similar to lurasidone. Our future studies are planned to include preclinically evaluating pharmacological responses in specific genetic models to strengthen findings on antipsychotic effects.

PMID 42598466
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