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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

PubMedThe European journal of neuroscience2026-10-13

Freezing of Gait: A Therapeutic Perspective.

LeWitt Peter A PA

Despite improved definition of the problem and better understanding of its phenomenology, freezing of gait (FoG) remains a therapeutic enigma for clinicians and neuroscientists alike. Patients with Parkinson disease (PD) or other neurological disorders experiencing FoG are similarly frustrated, despite the benefits that levodopa and other medications provide for control of PD's primary motor features. For those burdened by episodes of FoG, current therapeutic options are quite limited. Some patients achieve improvements from pharmacotherapy-for example, by adjunctive use of an oral dopaminergic agonist or by subcutaneous infusion of apomorphine. If needed, deep brain stimulation sometimes offers symptomatic improvements. Certain interventions devised by physical therapists (or discovered by patients themselves) can improve FoG. However, successful pharmacotherapy for FoG has lagged behind, though the future holds some promising leads for therapies acting on dopaminergic, adenosinergic, noradrenergic, glutamatergic, and cholinergic circuitry.

PMID 42865107
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PubMedCerebral cortex (New York, N.Y. : 1991)2026-10-12

Dopamine synchronizes hippocampal-prefrontal networks.

de Oliveira-Junior Benedito A BA, Padovan-Neto Fernando E FE, Narayanan Nandakumar S NS, Leite João P JP et al.

Interactions among brain networks support cognition and behavior. Oscillatory activity may contribute by coordinating distant neuronal populations, and identifying mechanisms that dynamically modulate this connectivity is crucial for understanding brain function. Dopamine (DA) is a well-positioned candidate, given its role in altering neuronal excitability and regulating oscillatory cognitive networks connecting the hippocampus (HPC) and prefrontal cortex (PFC). However, how DA modulates HPC-PFC synchrony remains mostly unknown. Here, we recorded HPC and PFC activity in urethane-anesthetized rats while manipulating DA levels. Our results show that DA dose-dependently induces HPC-PFC theta coupling, including non-zero-lag phase synchrony. In PFC single units, DA reduced firing rates while strengthening spike-theta phase locking and shifting the preferred firing phase. Preferential stimulation of D1-like receptors with SKF-38393 or D2-like receptors with quinpirole did not reproduce the complete DA-induced oscillatory pattern, whereas systemic apomorphine, a non-selective DA receptor agonist, produced a distinct dose-dependent modulation of theta phase synchrony. Together, these findings demonstrate that DA rapidly reorganizes HPC-PFC network dynamics, enhancing interareal theta phase coordination and the temporal organization of prefrontal neuronal activity. This network response was not fully reproduced by preferential activation of either D1-like or D2-like receptors alone, pointing to a more complex dopaminergic modulation of HPC-PFC network dynamics.

PMID 42862860
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PubMedJournal of inflammation research2026-10-11

HMGCS2 Palmitoylation Promotes Diabetes-Induced Erectile Dysfunction Through PPARα-Mediated Macrophage Extracellular Trap Formation.

Zhang Chaohong C, Li Guangjie G, Jiang Lixing L, Fang Huilong H et al.

Diabetes mellitus-induced erectile dysfunction (DMED) is a prevalent complication with limited therapeutic options for non-responders to conventional treatments. Macrophage extracellular traps (METs) are implicated in various pathologies, but their role and regulatory mechanisms in DMED remain unclear. This study investigates the role of HMGCS2 palmitoylation in promoting MET formation and DMED pathogenesis through PPARα interaction. In vitro models were established using RAW264.7 macrophages treated with high glucose (HG) and palmitic acid (PA). A DMED rat model was induced by high-fat diet and streptozotocin injection, followed by administration of the palmitoylation inhibitor CMA (cyano-myracrylamide). HMGCS2 palmitoylation, protein expression, and its interaction with PPARα were assessed using acyl-biotin exchange (ABE) and co-immunoprecipitation (Co-IP) assays. MET formation, reactive oxygen species (ROS) production, oxidative stress markers (MDA, GSH), mitochondrial function (MMP, ATP, morphology), macrophage infiltration, and cell apoptosis were evaluated via Western blot, immunofluorescence, ELISA, transmission electron microscopy, flow cytometry, and TUNEL staining. Erectile function was assessed in vivo by apomorphine-induced penile erection tests. HMGCS2 expression and palmitoylation were significantly upregulated in both HG/PA-treated macrophages and corpus cavernosum of DMED rats. CMA treatment effectively reduced HMGCS2 palmitoylation, attenuated its interaction with PPARα, and downregulated HMGCS2 expression. Consequently, pharmacological inhibition of palmitoylation suppressed HG/PA-induced MET formation, ROS overproduction, oxidative stress, and mitochondrial dysfunction in vitro. In DMED rats, CMA administration significantly improved penile erectile function, which recovered to 78% of the number of erections of the control group per unit time, as well as reduced peripheral blood PA levels, and alleviated pathological changes in corpus cavernosum. Furthermore, CMA inhibited MET formation, reduced macrophage infiltration, suppressed ROS and oxidative stress, and decreased cell apoptosis in vivo. Our findings demonstrate that HMGCS2 palmitoylation drives DMED pathogenesis by promoting MET formation through enhanced PPARα interaction. Targeting HMGCS2 palmitoylation represents a promising therapeutic strategy for DMED.

PMID 42859802
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PubMedMovement disorders clinical practice2026-10-08

Continuous Subcutaneous Apomorphine as a Temporary Bridging Therapy for Dopamine Dysregulation Syndrome in Patients with Deep Brain Stimulation.

Binder Tobias T, Hartig Johannes J, Sitzmann Lennart L, Ip Chi Wang CW et al.

Dopamine dysregulation syndrome (DDS) is a challenging complication of dopaminergic therapy in Parkinson's disease and can persist despite subthalamic deep brain stimulation (STN-DBS). We evaluated a temporary bridging concept in which oral dopaminergic medication was replaced by continuous subcutaneous apomorphine infusion while maintaining DBS. Six patients with STN-DBS and DDS were temporarily transitioned from oral dopaminergic medication to continuous subcutaneous apomorphine infusion. Treatment success was defined as reduction of DDS below a predefined threshold (<3 characteristic DDS features). Four of six patients (66.7%) no longer fulfilled the operational DDS criteria. Typical apomorphine-related adverse effects occurred in all patients; however, nausea and malaise limited the treatment in two non-responders. In this uncontrolled case series, continuous subcutaneous apomorphine may represent a useful temporary adjunct to STN-DBS for managing DDS in selected patients. Treatment tolerability appears to be a major determinant of success and requires careful patient selection and monitoring.

PMID 42845107
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PubMedBMC neuroscience2026-10-08

Oral sodium butyrate alleviates motor deficits and dopaminergic neuronal loss in 6-hydroxydopamine-induced Parkinson's disease rat model.

Yang Shun-Tai ST, Chen Yang-Ching YC, Kao Tzu-Jen TJ, Kuo Chi-Wei CW et al.

Short-chain fatty acids regulate intestinal homeostasis and modulate the gut-brain axis, suggesting they may be applicable in adjunctive treatments for Parkinson's disease (PD). However, the therapeutic efficacy of sodium butyrate (NaB) in PD remains unclear. Using appropriate PD animal models may aid in clarifying the therapeutic effects of NaB and facilitate the development of NaB-based PD treatment strategies. We comprehensively evaluated the therapeutic effects of oral NaB in rats with 6-hydroxydopamine (6-OHDA)-induced PD. We induced hemiparkinsonism in rats by administering unilateral 6-OHDA in the medial forebrain bundle. At 24 h after confirming lesion development, some rats were randomized to receive oral NaB (administered daily) over 4 weeks. Behavioral assessments-comprising gait analysis, open-field activity, and apomorphine-induced rotations-were performed longitudinally in weeks 1 and 4. Finally, dopaminergic neuronal degeneration was evaluated to correlate functional recovery with structural neuroprotection. The 4-week oral NaB intervention significantly alleviated 6-OHDA-induced motor deficits (i.e., locomotor activity, akinesia, and gait) and anxiety-like behavior; however, it did not alleviate apomorphine-induced rotations. Tyrosine hydroxylase immunohistochemical staining confirmed these findings, indicating that the dopaminergic neuron survival rate was significantly higher in the NaB-treated groups than in the sham control group. Early long-term oral NaB treatment afforded neuroprotection and alleviated motor and non-motor deficits (such as gait and central time in the open field) in rats with 6-OHDA-induced PD. Our model indicates the therapeutic potential of oral NaB and provides a translational framework for investigating the mechanisms of NaB therapy in PD and associated neurological disorders.

PMID 42844586
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PubMedJournal of neural transmission (Vienna, Austria : 1996)2026-09-29

Continuous infusion therapy after deep brain stimulation in Parkinson's disease: indications, outcomes, and patient selection.

Hero Mario M, Papić Eliša E, Grozdanić Nadja N, Vuletić Vladimira V

Patients with Parkinson's disease now live for decades after deep brain stimulation, and many develop recurrent symptoms while the stimulator still functions. A continuous infusion is sometimes added, but the circumstances justifying it are undefined, and the two modalities are still viewed as competing rather than complementary. This review examines the addition of the four infusion therapies after stimulation. A search of three databases identified fifteen reports, almost all small and retrospective. They report 118 patients and 119 infusion courses: 68 with intestinal levodopa gel, 23 with apomorphine, 28 with foslevodopa/foscarbidopa, and none with entacapone. Off time fell in every study that measured it, though fewer than half did. The on-state motor examination improved significantly only in the largest series to test it. In a post hoc trial subgroup, off time improved similarly with and without previous stimulation, while activities of daily living and speech improved significantly less in those with prior stimulation. Severe adverse events were more frequent after prior stimulation. The combination is uncommon: 1% to 2% of patients in larger cohorts, under 0.1% in a national apomorphine cohort. Stimulation parameters are reported or unchanged in only 10 of the 118 patients, and primary failure cannot be separated from secondary failure in 29. We propose a structured assessment separating correctable device problems, recurrent dopaminergic symptoms, stimulation-induced effects and levodopa-resistant progression. Infusion therapy may help recurrent levodopa-responsive complications after stimulation has been re-evaluated and optimized. Its use in late axial or cognitive decline is untested rather than disproven.

PMID 42806146
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