Fig. 1 · Structure

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Sumatriptan succinate

5-HT1 Receptor Agonist

Sumatriptan succinate is a selective agonist for the 5-HT1 receptor subtype, notably demonstrating IC50 values of 7.3 nM, 9.3 nM, and 17.8 nM for the 5-HT1D, 5-HT1B, and 5-HT1F receptors, respectively. This compound is primarily utilized in the study of migraine pathophysiology and therapeutics, providing insights into serotonin modulation during migraine attacks. Its pharmacological profile makes it an essential reagent for research investigating the efficacy of triptans in headache relief.

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In Vitro Studies

Sumatriptan succinate pretreatment attenuated KCl-evoked calcium responses in a subset of CGRP+ DRG neurons compared with vehicle-treated controls. Attenuation of CGRP+ neuron excitability was absent in the reported conditional knockout mice. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Sumatriptan attenuates evoked calcium responses in CGRP+ sensory neurons

Cell-based study · CGRP+ DRG neurons [1]

Approximately 40% of CGRP+ DRG neurons exhibited an attenuated calcium response when pretreated with sumatriptan (10 μM). In Htr1b cKOCalca mice, sumatriptan failed to attenuate excitability of CGRP+ neurons.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
KCl-evoked calcium responsecalcium response 10 μM: Approximately 40%[1]

Literature-Reported Treatment Conditions

Treatment concentration
10 μM
Exposure duration
pretreated with sumatriptan
Method
applied directly to CGRP+ DRG neurons
Co-treatment
Other interventions in this design: KCl 25 mM; tamoxifen 1 mg. Compound effect isolated by the comparison: compared to vehicle-treated control neurons.
Reported limits
Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Sumatriptan succinate; Compound label in the paper: Sumatriptan

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > Activation of Gi/o-coupled GPCRs reduces CGRP+ DRG neuronal excitability in vitro (S22, S23, S24, S25); Results > Sumatriptan acting through Htr1b reduces both CGRP+ neuron excitability and synaptic transmission in the spinal cord (S68, S69); STAR★Methods > Method details > Drug treatments (S168); STAR★Methods > Method details > In vitro calcium imaging (S205)

KCl-evoked calcium response: KCl-evoked calcium response; comparator: vehicle-treated control neurons — Results > Activation of Gi/o-coupled GPCRs reduces CGRP+ DRG neuronal excitability in vitro (S23, S24); Results > Sumatriptan acting through Htr1b reduces both CGRP+ neuron excitability and synaptic transmission in the spinal cord (S68)

In Vivo Studies

In mice of mixed genetic backgrounds, intraperitoneal Sumatriptan succinate dose-dependently reduced cold-evoked nocifensive behaviors compared with vehicle. Repeated daily Sumatriptan succinate administration in wild-type mice produced facial mechanical hypersensitivity that persisted during subsequent administration and resolved after cessation. Following optogenetic CSD induction, hind-paw and periorbital allodynia were alleviated to varying degrees in mice receiving Sumatriptan in the CSD + Suma group relative to the CSD + NS group. [1,2,3]

Sumatriptan reduced nocifensive behaviors in control mice

Animal study · Male and female mice of mixed genetic backgrounds [1]

In the noxious cold plate assay, sumatriptan reduced nocifensive behaviors in control animals. Sumatriptan (30–300 μg/kg, i.p.) dose-dependently reduced nocifensive behaviors in the cold plate (0°C) assay.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
nocifensive behaviorsReported result In the noxious cold plate assay, sumatriptan reduced nocifensive behaviors in control animals. Sumatriptan (30–300 μg/kg, i.p.) dose-dependently reduced nocifensive behaviors in the cold plate (0°C) assay.[1]

Conditions shared by the study groups

Route
intraperitoneal injection
Treatment course
30 min before behavior assays
Vehicle
saline
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Sumatriptan succinate 30–300 μg/kgvehicleIn the noxious cold plate assay, sumatriptan reduced nocifensive behaviors in control animals. Sumatriptan (30–300 μg/kg, i.p.) dose-dependently reduced nocifensive behaviors in the cold plate (0°C) assay.[1]
Sumatriptan succinate 30–300 μg/kg
Model: Male and female mice of mixed genetic backgrounds
Methods and source locations

Compound reported in the paper: Sumatriptan succinate; Compound label in the paper: Sumatriptan

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Results > Analgesic actions of sumatriptan are mediated through Htr1b expressed in somatosensory neurons (S87); STAR★Methods > Experimental model and study participant details (S149); STAR★Methods > Method details > Drug treatments (S169); STAR★Methods > Method details > Cold and hot plate (S254); Figure 2 legend (S382)

nocifensive behaviors: nocifensive behaviors; comparator: vehicle — Results > Analgesic actions of sumatriptan are mediated through Htr1b expressed in somatosensory neurons (S87); Figure 2 legend (S382)

Sumatriptan succinate 30–300 μg/kg · Results > Analgesic actions of sumatriptan are mediated through Htr1b expressed in somatosensory neurons (S87); STAR★Methods > Method details > Drug treatments (S169); STAR★Methods > Method details > Cold and hot plate (S254); Figure 2 legend (S382)

Sumatriptan induces facial mechanical hypersensitivity in mice

Animal study · male and female wild-type mice; wild-type (C57BL/6J) [2]

In male and female wild-type mice, daily intraperitoneal Sumatriptan succinate produced robust facial mechanical hypersensitivity. Hypersensitivity was maintained by subsequent administration and resolved after treatment cessation.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
withdrawal thresholds to mechanical stimuli on facial skinReported result 2 daily injections of sumatriptan (0.6 mg/kg, i.p.) resulted in robust facial mechanical hypersensitivity; This was maintained by subsequent sumatriptan administration and was resolved one week after the cessation of sumatriptan[2]

Conditions shared by the study groups

Route
intraperitoneal (i.p.) injections
Treatment course
once every day for 12 days
Vehicle
saline
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Sumatriptan succinate 0.6 mg/kgday 1 baseline threshold within individual groups2 daily injections of sumatriptan (0.6 mg/kg, i.p.) resulted in robust facial mechanical hypersensitivity; This was maintained by subsequent sumatriptan administration and was resolved one week after the cessation of sumatriptan[2]
Sumatriptan succinate 0.6 mg/kg
Model: male and female wild-type mice; wild-type (C57BL/6J)
Methods and source locations

Compound reported in the paper: Sumatriptan succinate; Compound label in the paper: Sumatriptan

Literature evidence for the named compound in the stated model; no Adooq product-use or lot-performance claim.

Materials and methods > Mouse model of medication overuse headache (S19, S20); Materials and methods > Drug treatments (S29); Results > The endogenous CCL2-CCR2 signaling pathway is not required for repeated sumatriptan-induced behavioral sensitization (S104, S105, S106); Fig. 2 legend (S178)

withdrawal thresholds to mechanical stimuli on facial skin: withdrawal thresholds to mechanical stimuli on facial skin; comparator: day 1 baseline threshold within individual groups — Materials and methods > Mouse model of medication overuse headache (S20); Results > The endogenous CCL2-CCR2 signaling pathway is not required for repeated sumatriptan-induced behavioral sensitization (S105, S106)

Sumatriptan succinate 0.6 mg/kg · Materials and methods > Mouse model of medication overuse headache (S19); Results > The endogenous CCL2-CCR2 signaling pathway is not required for repeated sumatriptan-induced behavioral sensitization (S105, S106)

Sumatriptan alleviates allodynia following optogenetic CSD induction

Animal study · Male C57BL/6 J wild-type mice (8–12 weeks); optogenetic CSD induction; CSD + Suma (n = 8) [3]

In male wild-type mice undergoing optogenetic CSD induction, Sumatriptan was administered intraperitoneally immediately after a single light stimulus. Hind-paw and periorbital allodynia were alleviated to varying degrees in the CSD + Suma group relative to the CSD + NS group.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
hind-paw (A) and periorbital (B) withdrawal thresholdsReported result Both hind-paw (2.5 h, left: p = 0.008, right: p = 0.028; Fig. 6A) and periorbital (3 h, left: p = 0.028, right: p = 0.011; Fig. 6B) allodynia were alleviated at varying degrees in the CSD + Suma group, relative to the CSD + NS group.[3]

Conditions shared by the study groups

Route
intraperitoneal injection
Treatment course
immediately after a single light stimulus; hind-paw (2.5 h, left: p = 0.008, right: p = 0.028; Fig. 6A)
Vehicle
0.9% normal saline
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Sumatriptan 2 mg/kg, 0.02 ml/g of body weightCSD + NS groupBoth hind-paw (2.5 h, left: p = 0.008, right: p = 0.028; Fig. 6A) and periorbital (3 h, left: p = 0.028, right: p = 0.011; Fig. 6B) allodynia were alleviated at varying degrees in the CSD + Suma group, relative to the CSD + NS group.[3]
Sumatriptan 2 mg/kg, 0.02 ml/g of body weight
Model: Male C57BL/6 J wild-type mice (8–12 weeks); optogenetic CSD induction; CSD + Suma (n = 8)
Methods and source locations

Compound reported in the paper: Sumatriptan

The paper names Sumatriptan without stating the salt or form; not verified as the succinate form supplied as A10879. No dose conversion or lot validation.

Methods > Animals (S1); Methods > Virus injection (S10, S14); Methods > Fiber-optic implantation and optogenetic CSD induction (S19, S39); Results > Sumatriptan alleviates optogenetic-induced migraine-like pain and anxiety behaviors (S104, S106); Fig. 1 legend (S122); Fig. 6 legend (S151, S152, S154)

hind-paw (A) and periorbital (B) withdrawal thresholds: hind-paw (A) and periorbital (B) withdrawal thresholds; comparator: CSD + NS group — Results > Sumatriptan alleviates optogenetic-induced migraine-like pain and anxiety behaviors (S106); Fig. 6 legend (S152)

Sumatriptan 2 mg/kg, 0.02 ml/g of body weight · Methods > Fiber-optic implantation and optogenetic CSD induction (S39); Results > Sumatriptan alleviates optogenetic-induced migraine-like pain and anxiety behaviors (S104, S106)

Specifications

Manufacturer Adooq Bioscience
Actions Agonist
CAS Number 103628-48-4
Applications 5-HT1 Receptor Agonist
Formula C18H27N3O6S
Molecular Weight 413.49
Synonyms GR 43175 succinate
SMILES
O=C(O)CCC(O)=O.O=S(CC1=CC2=C(NC=C2CCN(C)C)C=C1)(NC)=O

Storage & Solubility

In Vitro Solubility

Reported Solubility

No reported solubility data are available for this product.

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Peng J, Sanchez BT, Chirila AM, et al. Targeting Gi/o-coupled GPCRs to inhibit nociceptors: Insights from the serotonin receptor Htr1b and triptans. Cell Rep Med (2026). PMID: 42532046 DOI: 10.1016/j.xcrm.2026.102949 Source material
  2. [2] Ryu S, Zhang J, Simoes R, et al. Regulatory T cells require peripheral CCL2-CCR2 signaling to facilitate the resolution of medication overuse headache-related behavioral sensitization. J Headache Pain (2024). PMID: 39528947 DOI: 10.1186/s10194-024-01900-5 Source material
  3. [3] Yuan H, Na W, Li B, et al. Optogenetic cortical spreading depression originating from the primary visual cortex induces migraine-like pain and anxiety behaviors in freely moving C57BL/6 J mice. J Headache Pain (2025). PMID: 40011818 DOI: 10.1186/s10194-025-01983-8 Source material

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