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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

PubMedInternational journal of tryptophan research : IJTR2026-08-27

Tryptophan Supplementation Reduces Schizophrenia-Like Symptoms in Apomorphine Treated Rats: Role of D2, GABA, and Glutamate Receptor Expression.

Nawaz Shazia S, Ali Sadia Basharat SB, Afroz Rushda R, Ikram Huma H et al.

Schizophrenia is a multifaceted neuropsychiatric disorder characterized by disruptions in dopaminergic, GABAergic, and glutamatergic signaling pathways. While conventional antipsychotics primarily target dopamine D2 receptors, exhibit limited efficacy to alleviate cognitive deficits and negative symptoms and are associated with extrapyramidal side effects. Tryptophan (Trp), the essential amino acid precursor to serotonin, is critical modulator of these circuits. Serotonin acts as a brake on dopamine release and receptor activity. This study investigates the therapeutic potential of Trp supplementation in reducing schizophrenia-like symptoms in apomorphine-treated rats, focusing on the mRNA expression of D2, GABA, and glutamate receptors in nucleus accumbens and caudate. Apomorphine, a dopamine agonist, induces hyperdopaminergic activity, mimicking schizophrenia-like behaviors. In the present study, rats were divided into control, apomorphine-treated, Trp-supplemented and apomorphine plus Trp treated groups. Trp was administered at two different doses (25 and 50 mg/kg). Behavioral assessments were conducted in novel and familiar environments, Morris water maze and elevated plus maze to evaluate motor activity, learning and memory, and anxiety respectively. Results demonstrated that Trp supplementation significantly ameliorated the schizophrenia-like symptoms induced by apomorphine, exhibiting a distinct biphasic pattern: the 25 mg/kg dose was consistently more effective than the 50 mg/kg dose. Specifically, the low dose Trp reduced hyperactivity, improved cognitive performance and anxiolytic effects. In contrast, the 50 mg/kg dose showed a diminished therapeutic effect, likely due to competitive kynurenine pathway activation. Molecular analysis showed that optimal tryptophan treatment decreased the mRNA expression of D2 receptors, enhanced GABA receptor mRNA expression, and stabilized glutamate receptor mRNA levels in key brain regions. These findings suggest that low dose tryptophan supplementation may offer a promising adjunctive treatment for schizophrenia by restoring transcriptional balance of critical neurotransmitter systems.

PMID 42656638
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PubMedFrontiers in neurology2026-08-27

Parkinson's disease in the United Arab Emirates (UAE): Emirates Neurology Society consensus guidelines.

Mittal Shivam Om SO, Iantorno Vittorio V, Hassan Ali A, Krystkowiak Pierre P et al.

Parkinson's disease (PD) incidence has risen by more than eightfold in the United Arab Emirates (UAE) between 1990 and 2019, representing one of the highest increases globally and creating substantial pressure on a fragmented, multi-payer health system. Region-specific guidance has been lacking, leading clinicians to extrapolate from international guidelines that do not fully address formulary heterogeneity, advanced therapy centralization, and cultural factors. Under the auspices of the Emirates Neurology Society, a national taskforce of 10 specialists representing major PD centers across the UAE used a three-round modified Delphi process informed by systematic literature review and key randomized controlled trials. Recommendations were graded using a GRADE-aligned system (A-C, Good Practice Points) and adapted to UAE formulary, service configuration, and cultural context. Consensus was achieved on 146 recommendations across eight domains: (1) mandatory adoption of MDS-2015 diagnostic criteria; (2) age-stratified pharmacologic algorithms with levodopa as first-line for older or cognitively vulnerable patients; (3) structured non-motor symptom management; (4) rehabilitation and UAE cultural lifestyle adaptations including Ramadan fasting management, DBS considerations in women, family-centered care, and multilingual practice; (5) advanced therapy referral using the 5-2-1 rule integrated with the Making Informed Decisions to Aid Timely Management of Parkinson's Disease (MANAGE-PD) tool, with five device-aided options (subcutaneous foslevodopa/foscarbidopa, apomorphine SC- subcutanous, LCIG- Levodopa Carbidopa Intestinal Gel, DBS- Deep Brain Stimulation, MRgFUS- MRI guided focussed ultrasound) presented through shared decision-making; (6) a three-tier service model; (7) UAE formulary mapping; and (8) center accreditation and registry metrics. Advanced therapies are centralized in accredited centers with clear minimum volume and multidisciplinary staffing criteria. These UAE consensus recommendations provide a pragmatic, context-adapted framework for PD management, emphasizing structured diagnosis, age-appropriate pharmacotherapy, systematic use of MANAGE-PD and 5-2-1 for advanced therapy referral, culturally sensitive practice adaptations, and a three-tier network model integrated through the Malaffi health information exchange and a planned national PD registry.

PMID 42656222
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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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