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sumatriptan succinate (Zelrix / NP101 / Zecuity)

✓ Approved

Nupathe Inc. · HTR1D · Small Molecule

What is sumatriptan succinate?

sumatriptan succinate is a small molecule developed by Nupathe Inc.. It is approved for therapeutic indications via topical or transdermal.

Drug Profile

Brand NamesZelrix, NP101, Zecuity
CompanyNupathe Inc.
Drug ClassSmall Molecule
Molecular TargetHTR1D
RouteTopical, Transdermal
StatusApproved
Sources: ClinicalTrials.gov, Nupathe Inc.

Mechanism of Action

Molecular Targets

sumatriptan succinate acts on 1 molecular target:

HTR1D5-hydroxytryptamine receptor 1D (HTR1DA, HT1DA)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

sumatriptan succinate is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Nervous system disordersMigraine✓ Approved

Related Research Articles

PubMedPest management science2026-10-14

Design, synthesis, antifungal activity, and phloem mobility of novel aromatic amide phenylthiazole-4-carboxylic acid derivatives as potential succinate dehydrogenase inhibitors.

Mao Guoqing G, Cheng Zhi Z, Han Xin X, Zhao Yongtian Y et al.

Although succinate dehydrogenase inhibitors (SDHIs) display potent antifungal activity, the majority possess weak phloem mobility, limiting their efficacy against root and vascular diseases. To develop novel SDHI candidates with phloem mobility, 36 aromatic (heterocyclic) amide phenylthiazole-4-carboxylic acid derivatives were synthesized and subjected to antifungal evaluation. In vitro bioassays showed that compounds E11 and E21 exhibited high antifungal activities against Sclerotinia sclerotiorum, with median effective concentration (EC50) values of 0.34 and 0.19 μg mL-1, respectively, outperforming boscalid (EC50 = 0.65 μg mL-1). Further in vivo experiments and field trials indicated that E11 and E21 displayed stronger antifungal efficacy against sclerotinia stem rot in rapeseed compared with boscalid. Meanwhile, E11 and E21 showed no obvious effects on rapeseed germination and radicle growth at 200 μg mL-1. Phloem mobility studies revealed that compounds E1-E36 exhibited different degrees of phloem mobility in Ricinus communis L., with E21 achieving the greatest systemic accumulation in stems and leaves of rape seedlings within 24 h. Further antifungal mechanism studies indicated that compounds E11 and E21 had a similar mode of action to boscalid. These findings suggest that compounds E11 and E21 serve as promising phloem-mobile SDHI candidates for controlling sclerotinia stem rot in rapeseed. © 2026 Society of Chemical Industry.

PMID 42870719
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PubMedGenes & diseases2026-10-14

Molecular mechanisms and targeted therapeutic strategies for glycolytic reprogramming in osteosarcoma.

Ni Xuewen X, Xia Ping P, Liang Mengxue M, Zhang Li L et al.

Osteosarcoma, a highly invasive and metastatic malignant bone tumor, has a poor prognosis primarily because of early pulmonary metastasis and resistance to conventional treatments. The malignant progression of osteosarcoma cells significantly depends on glycometabolic reprogramming, a process characterized by enhanced aerobic glycolysis. This review begins by mapping the multi-dimensional networks driving sugar metabolism reprogramming, which revealed that functional abnormalities in core glycolytic enzymes, including hexokinase 2, pyruvate kinase M2, and lactate dehydrogenase A (LDHA), are driven by a multi-level regulatory network that includes altered transcription factor activity, epigenetic modifications, and interactions mediated by non-coding RNAs. Mitochondrial dysfunction leads to succinate and reactive oxygen species accumulation, synergistically promoting the remodeling of metabolic pathways. Furthermore, the synergistic interaction between the pentose phosphate pathway and glutamine metabolism accelerates the energy supply and biosynthesis, whereas lactate accumulation shapes the immunosuppressive microenvironment by inhibiting immune cell function. This review focuses on dissecting the core mechanisms of glucose metabolism reprogramming in osteosarcoma pathogenesis, including promoting proliferation, inhibiting apoptosis, enhancing invasion and metastasis, regulating immune metabolism, and mediating chemotherapy resistance. Additionally, it evaluates novel therapeutic strategies targeting key nodes of glucose metabolism in osteosarcoma, including advances in preclinical research on specific small-molecule inhibitors and gene regulatory approaches. Finally, it delves into the major challenges in translational research, such as metabolic heterogeneity, targeting selectivity, and compensatory resistance, as well as prospects for future research, including multi-omics analysis, smart delivery systems, organoid models, and combination immunotherapy. This study offers novel insights into overcoming the therapeutic bottlenecks in osteosarcoma treatment.

PMID 42871472
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PubMedRedox biology2026-10-14

HDAC1-mediated SUCLA2 lysine β-hydroxybutyrylation modulates myocardial mitochondrial function in sepsis-induced heart dysfunction.

Wen Ri R, Ning Wanshan W, Huang Xin-Mei XM, Hao Peng-Hui PH et al.

Lysine β-hydroxybutyrylation (Kbhb) is associated with energy regulation and mitochondrial function, and its role in sepsis-induced heart dysfunction has not been elucidated. Reveals the extensive effects of Kbhb in sepsis-induced heart dysfunction and identifies the potential targets. A septic heart dysfunction rat model was induced by lipopolysaccharide intraperitoneal injection. Proteomic and β-hydroxybutyrylomic analyses were conducted to assess alterations in Kbhb between cardiac tissues from the control and lipopolysaccharide rats. Putative regulatory proteins were identified by leveraging a multifaceted hybrid learning framework combined with protein language models. Lysine to arginine (R) mutation was made to mimic decreased Kbhb levels. Transcriptomic analysis was further performed to predict the potential downstream mechanisms. Succinate-CoA Ligase ADP-Forming Subunit Beta (SUCLA2) was selected because of its role in mitochondrial function, and the Kbhb level at the K444 site was significantly different. Decreased Kbhb level at K444 of SUCLA2 was confirmed in septic cardiac tissues and lipopolysaccharide-treated H9c2 cardiomyocytes using specific antibody. SUCLA2K444R mutant reversed the protective effects of SUCLA2WT on mitochondrial function in lipopolysaccharide-treated H9c2 cardiomyocytes, accompanied by decreased succinyl-CoA synthetase activity, reduced mitochondrial membrane potential, suppressed adenosine triphosphate production, and increased reactive oxygen species accumulation. The aggravating effects of the SUCLA2K444R mutant on septic heart dysfunction were confirmed in vivo using the specific promoter. Mechanistically, histone deacetylase 1 inhibited SUCLA2 Kbhb at K444 residue. Reduced SUCLA2 Kbhb level at K444 site aggravates myocardial mitochondrial dysfunction, leading to sepsis-induced heart dysfunction. This study reveals a novel function of Kbhb in sepsis-induced heart dysfunction and elucidates the mechanism of SUCLA2 K444 Kbhb.

PMID 42874129
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PubMedComparative biochemistry and physiology. Part B, Biochemistry & molecular biology2026-10-13

Tissue specific metabolite responses of the liver, muscle and heart of the Pacific hagfish, (Eptatretus stoutii) to prolonged anoxia exposure.

Yutsyschyna Maria A MA, Al-Abdul-Wahid M Sameer MS, Cox Georgina K GK, Gillis Todd E TE

Pacific hagfish (Eptatretus stoutii) can tolerate up to 36 h of anoxia. Characteristics that enable this include a low constitutive metabolism as well as moderate hypometabolism during anoxia exposure. However, additional stressors manifest during anoxia and reoxygenation including the accumulation of metabolic products and mitochondrial dysfunction upon reoxygenation. We investigated these by examining the metabolite responses of hagfish exposed to 6 h and 24 h of anoxia. Metabolites of interest were lactate, an anaerobic product, and succinate, a driver of mitochondrial dysfunction in reoxygenation. We quantified metabolites in three tissues; the systemic heart, white muscle, and liver. We found that six hours of anoxia caused minimal change to the metabolites with no significant accumulation of lactate or succinate compared to control fish. Twenty-four hours of anoxia did have a larger impact on metabolite balance. Lactate concentrations increased by 36.3-fold, 2.1-fold, and 17.1-fold in the systemic heart, white muscle, and liver respectively. Succinate was 9.0-fold higher in the systemic heart and 3.5-fold higher in the white muscle. This accumulation is comparable to other anoxia-tolerant species that may reduce the potential for mitochondrial dysfunction upon reoxygenation. Additional metabolite changes were related to amino acid balance and energy availability, and the heart was the most affected organ. Finally, we identified three novel metabolites more common to invertebrates, N-methyl taurine, homarine, and zooanemonin. In conclusion, Pacific hagfish demonstrated high lactate and low succinate accumulation following 24 h of anoxia. This anoxia response resembles that of the anoxia-tolerant freshwater turtles more than that of the crucian carp.

PMID 42863809
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PubMedComparative biochemistry and physiology. Part B, Biochemistry & molecular biology2026-10-13

Succinate-driven methyl thiazolyl tetrazolium (MTT) reduction is coupled to mitochondrial electron transport chain (ETC) activity: comparative evidence from subcellular fractionation in the lobster cockroach (Nauphoeta cinerea) and zebrafish (Danio rerio).

Nwawuba Stanley U SU, Ferreira Sabrina A SA, Barbosa Nilda V NV, Adedara Isaac A IA et al.

The tetrazolium-based MTT assay is widely used to assess cellular metabolic activity, yet the subcellular origin and mechanistic basis of MTT reduction remain incompletely defined. Here, we investigated the localization and biochemical determinants of MTT reductive activity using subcellular fractionation of lobster cockroach Nauphoeta cinerea head tissue and zebrafish Danio rerio brain, combined with substrate specificity, protein-dependence analysis, and mitochondrial electron transport chain (ETC) inhibition. Succinate-driven MTT reduction was predominantly localized to mitochondrial fractions (P2 and P3), accounting for ~60-65% of total activity in both species, while post-mitochondrial supernatants exhibited minimal activity. MTT reduction increased linearly with protein concentration across all fractions (R2 = 0.95-0.99), with mitochondrial fractions displaying the highest protein-normalized reductive capacity. MTT reduction was highly sensitive to malonate and significantly inhibited by antimycin A and sodium azide, confirming dependence on Complex II-mediated electron entry and downstream ETC activity, whereas rotenone produced only partial inhibition, consistent with bypass of Complex I under succinate-driven conditions. Collectively, these findings demonstrate that MTT reduction is strongly dependent on substrate selection and experimental conditions. Under succinate-driven conditions, MTT reduction reflects mitochondrial ETC activity, with minimal non-mitochondrial contribution. This work provides a mechanistic framework that clarifies the intracellular origin of MTT reduction and supports its use as a substrate-dependent indicator of mitochondrial function in bioenergetic and toxicological studies. The consistent findings obtained in insect and fish tissues further support the conservation of the underlying mechanisms across phylogenetically distinct species and reinforce the value of alternative experimental models for investigating mitochondrial bioenergetics.

PMID 42863808
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PubMedBiochemical pharmacology2026-10-13

Heteronemin induces ROS-dependent apoptosis and mitophagy-associated responses through SDHB-associated mitochondrial Complex II dysfunction in oral squamous cell carcinoma.

Chin Hsien-Kuo HK, Chang Chun-Feng CF, Yu Chung-I CI, Chen Ya-Hsin YH et al.

Oral squamous cell carcinoma (OSCC) is difficult to treat because of its aggressive growth and limited therapeutic response. Heteronemin (HET), a marine sesterterpenoid, has anticancer activity, but its mitochondrial effects in OSCC remain incompletely defined. In this study, we investigated the relationship between HET-induced cytotoxicity, succinate dehydrogenase complex iron-sulfur subunit B (SDHB)-related Complex II dysfunction, and reactive oxygen species (ROS)-dependent mitochondrial injury using OSCC cells (HSC-3 and Ca9-22), normal oral cells (HGF-1), and zebrafish xenografts. HET selectively suppressed OSCC cell viability and colony formation while inhibiting cell-cycle progression. HET increased intracellular ROS and mitochondrial superoxide, impaired mitochondrial respiration, reduced SDHB abundance, and decreased succinate dehydrogenase activity. SDHB knockdown altered HET-induced ROS accumulation and limited the additional cytotoxic effect of HET, supporting the functional involvement of SDHB-associated mitochondrial dysfunction. N-acetyl-L-cysteine and MitoTEMPO attenuated oxidative stress, mitochondrial depolarization, apoptosis, and cell death. HET also increased mitophagy-associated proteins, including LC3B, PINK1, Parkin, BNIP3, and Nix, and promoted autophagosome/autolysosome formation. Transmission electron microscopy showed damaged mitochondria enclosed within autophagic vacuoles. Furthermore, NAC reduced these mitophagy-related changes, In zebrafish xenografts, HET reduced OSCC tumor without overt toxicity and increased mitophagy-associated markers. Together, these findings indicate that HET-induced OSCC cytotoxicity is associated with SDHB-related Complex II dysfunction, ROS accumulation, mitochondrial injury, intrinsic apoptosis, and mitophagy-associated responses.

PMID 42863582
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