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Fig. 1 · Structure
Cat. No.
A10497
CAS No.
74050-98-9
Formula
C22H22FN3O3
Mol. Weight
395.43

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Ketanserin (Vulketan Gel)

Cat. No. A10497 CAS 74050-98-9

5-HT2A serotonin receptor antagonist

Ketanserin (Vulketan Gel) is specific 5-HT2A serotonin receptor antagonist with a Ki of 2.5 nM for rat and human 5-HT2A.

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Biological Activity

Bioactivity / Mechanism

Ketanserin antagonized serotonin-induced contraction in isolated rabbit carotid arteries. At 1–100 nM it shifted concentration-response curves rightward while maintaining maximal responses. Schild slopes deviated from unity, particularly in collared arteries, limiting a simple competitive-antagonist interpretation. The paper did not specify the ketanserin salt. [1]

Ketanserin behavior depends on the assay. In pooled human prefrontal cortex membranes, ketanserin tartrate stimulated Gαq/11-associated nucleotide binding; MDL-11,939 blocked this response. A corresponding response was absent in 5-HT2A-knockout mouse cortex membranes. These findings qualify treating ketanserin as a universally neutral antagonist. [2]

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

Target & Activity

Target Activity Value
5-HT2A Ki 2.5 nM
5-HT2C (Rat) Ki 50 nM
5-HT2C (Human) Ki 100 nM

Cellular Effect

Cell Line Activity Value Description Reference
CHO IC50 260 nM Binding affinity by displacement to human cloned 5-hydroxytryptamine 1D receptor in CHO cells by [3H]5-HT displacement. [PMID: 9357514]
CHO IC50 6500 nM Binding affinity to human cloned 5-hydroxytryptamine 1B receptor in CHO cells by [3H]5-HT binding displacement. [PMID: 9357514]
CHO-K1 IC50 0.29 μM Displacement of [3H]Lysergic acid from human recombinant 5HT2B receptor expressed in CHOK1 cells after 60 mins [PMID: 23403082]
CHO-K1 IC50 11 nM Antagonist activity against human recombinant 5-HT2A receptor expressed in CHOK1 cells assessed as reduction in alpha-methylserotonin-induced increase in intracellular Ca2+ levels by aequorin based radiometric and luminescence plate counting method [PMID: 25557493]
CHO-K1 IC50 32 nM Antagonist activity at human 5HT2A receptor expressed in EC80 serotonin-stimulated CHOK1 cells by calcium mobilization assay [PMID: 19328689]
CHO-K1 IC50 80 nM Antagonist activity at 5HT2A receptor (unknown origin) expressed in CHOK1 cells coexpressing Galpha15 assessed as inhibition of agonist-induced response incubated for 60 mins in incubator followed by 15 mins at room temperature by FLIPR assay [PMID: 23675993]
HEK293 IC50 0.52 nM Displacement of [3H]ketanserin from human recombinant 5-HT2A receptor in HEK293 cells after 60 mins by scintillation counting [PMID: 27997171]
HEK293 EC50 1.04 nM Antagonist activity at serotonin-activated human recombinant 5HT-2A receptor expressed in HEK293 cells assessed as decrease in intracellular calcium level after 5 mins measured for 1 min by fluorescence assay [PMID: 23537943]
HEK293 IC50 3.5 x 10 Displacement of [3H]ketanserin from human recombinant 5HT2A receptor expressed in HEK293 cells measured after 60 mins by scintillation counting method [PMID: 27876250]

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In Vitro Studies

Functional antagonism in isolated rabbit carotid artery

Cell-based study · Sham and silicone-collared carotid artery rings from male New Zealand White rabbits; ex vivo organ baths, not in vivo ketanserin dosing. [1]

Ketanserin shifted serotonin contraction curves rightward with maintained maxima. Schild slopes limit a simple competitive interpretation, especially in collared tissue. Figure 2: n = 7 per condition; Methods defines n as rabbits.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Serotonin-induced contractionFunctional antagonism Rightward shifts with maintained maxima at 1, 10 and 100 nM; n = 7 in sham and collared rings[1]
Schild regression slopeSlope Sham: 0.90 ± 0.07 [95% CI 0.83–0.97]; collar: 0.74 ± 0.08 [0.66–0.82][1]

Literature-Reported Treatment Conditions

Treatment concentration
1, 10 and 100 nM
Exposure duration
30 min antagonist incubation before each cumulative agonist curve
Method
Isometric force measurements; responses normalized to 50 mM KCl and corrected by simultaneous antagonist-free time controls.
Vehicle
Stock dissolved in distilled water
Co-treatment
Serotonin challenge. Baths contained uptake/metabolism inhibitors, adrenergic blockers, indomethacin and nitro-L-arginine (Methods: Vascular reactivity).
Reported limits
Salt/form and stock concentration not specified. Tissue-level antagonism does not establish receptor exclusivity.
Methods and source locations

Compound reported in the paper: Ketanserin; Compound label in the paper: Ketanserin supplied by Janssen Research Foundation; salt not specified

Research evidence for the explicitly reported material and model; no claim of Adooq lot performance or salt equivalence.

Methods: Vascular reactivity, Calculation, Statistical analysis, Drugs; Results: Effect of serotonergic antagonists and Affinity values; Figure 2; Table 4

Serotonin-induced contraction: Cumulative concentration-response curves; mean ± s.e.mean — Results: Effect of serotonergic antagonists; Figure 2 and caption

Schild regression slope: Schild regression; Table 4 gives mean ± s.e.mean and confidence intervals — Table 4; Results: Affinity values; Methods: Statistical analysis

G protein signaling in human prefrontal cortex membranes

Biochemical assay · Pooled postmortem human dorsolateral prefrontal cortex membranes; six pools for concentration-response experiments, each from 6–8 individuals. [2]

Ketanserin tartrate increased Gαq/11-associated [35S]GTPγS binding. At 10 μM it did not reproduce this activation on Gαi1; MDL-11,939 and altanserin blocked the Gαq/11 response.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Gαq/11-associated [35S]GTPγS bindingEmax 123% ± 3% of basal binding (basal = 100%); mean ± SEM; n = 6 experiments[2]
Gαq/11-associated [35S]GTPγS binding−logEC50 6.8 ± 0.3; mean ± SEM; n = 6 experiments[2]
Signaling and antagonist controlsQualitative response At 10 μM, Gαq/11 activation was blocked by MDL-11,939 or altanserin; ketanserin did not activate Gαi1[2]

Literature-Reported Treatment Conditions

Treatment concentration
10^−10–10^−4 M concentration-response; 10 μM in antagonist-control comparisons
Exposure duration
2 h at 30 °C for initial [35S]GTPγS binding incubation
Method
Antibody-capture scintillation proximity assay; nonspecific binding defined with 100 μM unlabeled GTPγS.
Vehicle
Not specified for ketanserin in the read methods
Co-treatment
Single-agent concentration-response; separate controls co-incubated with MDL-11,939 or altanserin, each 10 μM
Reported limits
Pooling prevents individual-subject inference. Assay activity is not a treatment dose or universal intrinsic efficacy classification.
Methods and source locations

Compound reported in the paper: Ketanserin; Compound label in the paper: Ketanserin tartrate (Tocris Bioscience)

Research evidence for the explicitly reported material and model; no claim of Adooq lot performance or salt equivalence.

Methods 2.1–2.2, 2.5, 2.9–2.10; Results 3.2; Figure 2; Supplement Figure S1, p. 3

Gαq/11-associated [35S]GTPγS binding: Concentration-response fit — Results 3.2; Figure 2A and caption; Methods 2.10

Gαq/11-associated [35S]GTPγS binding: Concentration-response fit; reported log potency retained without conversion — Results 3.2; Figure 2A; Methods 2.10

Signaling and antagonist controls: Single-concentration comparisons; at least three technical replicates per experimental unit — Results 3.2; Figure 2C–D and caption

Receptor knockout validation in mouse cortex membranes

Biochemical assay · Ex vivo cortex membrane pools from wild-type and 5-HT2A receptor-knockout mice, 10 animals per genotype represented in two pools per genotype. [2]

At 10 μM ketanserin tartrate activated Gαq/11-associated [35S]GTPγS binding in wild-type membranes; this response was absent in knockout membranes. No corresponding Gαi1 activation was observed.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Gαq/11-associated [35S]GTPγS bindingGenotype-dependent response Activation in wild-type; absent in 5-HT2A knockout membranes at 10 μM[2]

Literature-Reported Treatment Conditions

Treatment concentration
10 μM
Exposure duration
Initial binding incubation: 2 h at 30 °C (Methods 2.9)
Method
Antibody-capture [35S]GTPγS scintillation proximity assay in cortex membrane preparations
Vehicle
Not specified for ketanserin in the read methods
Co-treatment
Ketanserin and altanserin tested separately; basal binding comparison
Reported limits
Not an in vivo drug-administration experiment. Experiments on pooled membranes do not make individual animals independent assay replicates.
Methods and source locations

Compound reported in the paper: Ketanserin; Compound label in the paper: Ketanserin tartrate (Tocris Bioscience)

Research evidence for the explicitly reported material and model; no claim of Adooq lot performance or salt equivalence.

Methods 2.1, 2.3, 2.5, 2.9–2.10; Results 3.4; Figure 4; Supplement Figure S1

Gαq/11-associated [35S]GTPγS binding: Basal binding normalized to 100%; no exact bar heights inferred — Results 3.4; Figure 4A–B and caption

In Vivo Studies

Systemic ketanserin treatment was associated with lower day-14 reepithelialization in a mouse burn-wound study. The reported values were 18.2 ± 11.9% with ketanserin versus 34.5 ± 1.7% with vehicle (mean ± SD). The caption reports n = 5, but its relationship to the three experiment repetitions stated in Methods is unclear. This result does not establish the effect of topical ketanserin gel. [3]

Systemic ketanserin in a mouse burn-wound model

Animal study · Male C57BL/6 mice, 6 weeks old, reported body weight 25 g; post-thermal skin injury; day-14 histology. [3]

The ketanserin group had lower reported reepithelialization than vehicle at day 14. This is limiting evidence for systemic treatment in this burn model. Replication reporting is ambiguous: Figure 3 caption n = 5, whereas Methods 4.8 says the in vivo experiment was performed three times per group; the relationship is unspecified.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Day-14 reepithelialization over wound dermal areaPercent reepithelialization Ketanserin: 18.2 ± 11.9%; vehicle: 34.5 ± 1.7%; mean ± SD; Figure 3 caption n = 5 (experimental unit unclear)[3]

Conditions shared by the study groups

Route
Intraperitoneal
Frequency
Daily
Treatment course
Up to two weeks post-burn; day-14 harvest
Vehicle
Not specified in animal methods
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Ketanserin systemic treatment
10 mg/Kg of body weight (as reported)		Vehicle-treated burn group; fluoxetine was a separate comparator groupReported day-14 reepithelialization: 18.2 ± 11.9% versus 34.5 ± 1.7% in vehicle (mean ± SD).[3]
Ketanserin systemic treatment
Model: Male C57BL/6 mice, 6 weeks old, reported body weight 25 g; post-thermal skin injury; day-14 histology.
Reported limits: Total independent animal number and relation of n = 5 to three experiment repetitions unclear. Injectable vehicle composition not specified. No topical-gel or free-base equivalence established.
Methods and source locations

Compound reported in the paper: Ketanserin; Compound label in the paper: Drug list identifies ketanserin (+)-tartrate salt (Sigma-Aldrich); animal group called ketanserin

Research evidence for the explicitly reported material and model; no claim of Adooq lot performance or salt equivalence.

Results 2.3; Figure 3A–B and caption; Methods 4.3.1, 4.4–4.6, 4.8

Day-14 reepithelialization over wound dermal area: Histology of wound cross-sections; Methods 4.8 additionally reports three experiment repetitions per treatment group — Results 2.3; Figure 3A–B and caption; Methods 4.5 and 4.8

Ketanserin systemic treatment · Methods 4.4.2; Results 2.3; Figure 3B caption; Methods 4.8

Specifications

Manufacturer Adooq Bioscience
Actions Antagonist
CAS Number 74050-98-9
Applications 5-HT2A serotonin receptor antagonist
Formula C22H22FN3O3
Molecular Weight 395.43
Synonyms R 41468; Vulketan Gel
SMILES
C1CN(CCC1C(=O)C2=CC=C(C=C2)F)CCN3C(=O)C4=CC=CC=C4NC3=O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 2 mg/mL (5.05 mM)
Water Insoluble
Ethanol Insoluble

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.

In Vivo Preparation

Concentration
1 mg/mL
Vehicle
4% DMSO+40% PEG 300+4% Tween 80+ddH2O

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] Inge S Geerts, Katelijne E Matthys, Arnold G Herman, et al. Involvement of 5-HT1B receptors in collar-induced hypersensitivity to 5-hydroxytryptamine of the rabbit carotid artery British Journal of Pharmacology (1999). PMID: 10455282 DOI: 10.1038/sj.bjp.0702684 Source material
  2. [2] Patricia Miranda-Azpiazu, Carolina Muguruza, Tomasz Maciej Stepniewski, et al. Distinctive patterns of G protein coupling induced by the structurally similar 5-HT2A receptor ligands ketanserin and altanserin in human prefrontal cortex Molecular Pharmacology (2025). PMID: 41135363 DOI: 10.1016/j.molpha.2025.100075 Source material
  3. [3] Alia Sadiq, Ahmed Shah, Marc G Jeschke, et al. The Role of Serotonin during Skin Healing in Post-Thermal Injury International Journal of Molecular Sciences (2018). PMID: 29596386 DOI: 10.3390/ijms19041034 Source material

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