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Fig. 1 · Structure
Cat. No.
A15464
CAS No.
934826-68-3
Formula
C36H42BrO2P
Mol. Weight
617.6

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SKQ1 Bromide

Cat. No. A15464 CAS 934826-68-3

mitochondria-targeted antioxidant

SKQ1 is a potent mitochondria-targeted antioxidant. SKQ1 is also an API (active pharmaceutical ingredient) for making eye drop drug called Visomitin. SKQ1 showed activities (1) to prevent amyloid-beta-induced impairment of long-term potentiation in rat hippocampal slices.

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Publications for SKQ1 Bromide

1 publication citing this product

  1. Massimo Costanza, .et al. , PNAS, 2019, 2019 PMID: 30988194
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Biological Activity

Bioactivity / Mechanism

In isolated rat-heart mitochondria, SkQ1 bromide inhibited iron-dependent mitochondrial lipid peroxidation while leaving the measured hydrogen peroxide signal unchanged. This supports antioxidant action on lipid oxidation downstream of ROS generation under these assay conditions. [1]

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

In Vitro Studies

SkQ1 bromide protected LHON patient-derived fibroblasts against BSO-induced ferroptosis and reduced mitochondrial lipid-probe oxidation. The carrier-only analog C12TPP did not protect. These findings are limited to the tested cellular model. [1]

SkQ1 in BSO-challenged LHON fibroblasts

Cell-based study · Primary skin fibroblasts from one LHON patient; reported 13513G>A mutation. [1]

SkQ1 protected BSO-challenged cells and reduced mitochondrial lipid-probe oxidation. C12TPP lacked protection. Results describe this cellular background, not a patient treatment.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell viabilityqualitative result SkQ1 protected; C12TPP did not. Ferrostatin-1 and deferoxamine protected; zVADfmk did not.[1]
Mitochondrial lipid peroxidationqualitative result 100 nM SkQ1 reduced the oxidized-MitoCLox cell fraction; C12TPP did not.[1]

Literature-Reported Treatment Conditions

Treatment concentration
100 nM SkQ1 for lipid-peroxidation assay; viability concentration series in Figure 2b.
Exposure duration
17 h for MitoCLox assay; 24 h for viability.
Method
Added together with BSO.
Co-treatment
BSO 1 mM; SkQ1 protection assessed against BSO challenge.
Reported limits
Solvent/vehicle not specified in the relevant methods. Viability curve not digitized; no IC50 derived.
Methods and source locations

Compound reported in the paper: SkQ1; Compound label in the paper: SkQ1, 10-(6′-plastoquinonyl)decyltriphenylphosphonium bromide.

Published SkQ1 bromide evidence; the supplied Adooq lot was not tested or validated.

Methods 2.1–2.4, 2.6; Results 3.2–3.3; Figure 2a–d

Cell viability: CellTiterBlue — Results 3.2; Figure 2a–b and caption

Mitochondrial lipid peroxidation: MitoCLox green/red ratio by flow cytometry; Figure 2d: three independent experiments; Methods 2.6: mean with SD. — Methods 2.4, 2.6; Results 3.2–3.3; Figure 2c–d and caption

SkQ1 inhibition of lipid peroxidation in isolated mitochondria

Biochemical assay · Isolated rat-heart mitochondria; iron-dependent lipid-peroxidation assay. [1]

SkQ1 inhibited lipid-probe oxidation without inhibiting the measured hydrogen peroxide production, supporting an effect downstream of ROS generation in this assay.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Lipid peroxidationqualitative result SkQ1 inhibited MitoCLox oxidation in a concentration-dependent manner.[1]
Hydrogen peroxide productionqualitative result 300 nM SkQ1 did not inhibit the complex-I-associated hydrogen peroxide signal.[1]

Literature-Reported Treatment Conditions

Treatment concentration
SkQ1 30, 100 or 300 nM for lipid assay; 300 nM for hydrogen peroxide trace.
Exposure duration
Lipid kinetics displayed through 150 min; 5 min SkQ1 preincubation for hydrogen peroxide assay.
Method
Addition to isolated-mitochondria assay at 25°C.
Co-treatment
Glutamate/malate 5 mM each, rotenone 10 μM and FeSO4 10 μM; mitochondrial protein 0.4 mg/mL.
Reported limits
SkQ1 solvent not specified in relevant methods; exact percent inhibition not tabulated.
Methods and source locations

Compound reported in the paper: SkQ1; Compound label in the paper: SkQ1, 10-(6′-plastoquinonyl)decyltriphenylphosphonium bromide.

Published SkQ1 bromide evidence; the supplied Adooq lot was not tested or validated.

Methods 2.1, 2.5–2.6; Results 3.4; Figure 4a–e

Lipid peroxidation: 50 nM MitoCLox; fluorescence ratio 521/596 nm. — Methods 2.5; Results 3.4; Figure 4d and caption

Hydrogen peroxide production: Amplex Red/horseradish peroxidase; trace with and without SkQ1. — Methods 2.5; Results 3.4; Figure 4e and caption

In Vivo Studies

In diabetic male mice, oral SkQ1 (counterion unspecified) reduced wound area on days 6–7 after a 12-week treatment course. Weight gain, glucose, HbA1c and circulating TNF/IL-6 were unchanged. This study does not establish efficacy of a specific bromide formulation or Adooq lot. [2]

Oral SkQ1 and diabetic wound healing

Animal study · Male genetically diabetic C57BL/KsJ-db/db mice; vehicle-treated diabetic and nondiabetic comparator groups. [2]

Oral SkQ1 improved wound-area closure on days 6–7 without correcting the measured diabetic metabolic phenotype or circulating TNF/IL-6.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Wound areaqualitative result Reduced on days 6 and 7 versus diabetic vehicle controls; P < 0.05.[2]
Metabolic and circulating cytokine endpointsqualitative result No effect on weight gain, glucose, HbA1c, TNF or IL-6 was reported.[2]

Conditions shared by the study groups

Route
Oral (per os)
Frequency
Daily
Treatment course
12 weeks, starting at the ninth week of life.
Vehicle
Controls received 20% glycerol.
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Diabetic mice receiving SkQ1
250 nmol/kg body weight/day		Vehicle-treated diabetic mice (n = 9); nondiabetic heterozygous comparator (n = 5).Wound area was reduced on days 6 and 7 versus diabetic controls; metabolic and circulating cytokine measures were unchanged.[2]
Diabetic mice receiving SkQ1
Model: Male C57BL/KsJ-db/db mice; n = 12.
Reported limits: Whether dosing continued during each postwounding observation is not explicitly stated in the retrieved treatment paragraph. No mass-dose conversion.
Methods and source locations

Compound reported in the paper: SkQ1; Compound label in the paper: SkQ1, 10-(6′-plastoquinonyl)decyltriphenylphosphonium; counterion not specified.

Evidence for the named SkQ1 active compound in this model; no bromide-specific formulation or Adooq-lot claim.

Abstract; Methods 2.1–2.5, 2.9; Results; Figures 1 and 5

Wound area: Daily photography and ImageJ; Figure 1: mean ± SEM. — Methods 2.4, 2.9; Results; Figure 1a–b and caption

Metabolic and circulating cytokine endpoints: Body mass, blood glucose and HbA1c; cytokine ELISA on wound-healing day 7. Figure 5a–c: mean ± SEM; 5e: mean ± SD. — Methods 2.3, 2.5, 2.9; Results; Figure 5a–c,e and caption

Diabetic mice receiving SkQ1 · Methods 2.1, 2.3–2.5; Results; Figures 1 and 5

Specifications

Manufacturer Adooq Bioscience
CAS Number 934826-68-3
Applications mitochondria-targeted antioxidant
Formula C36H42BrO2P
Molecular Weight 617.6
Synonyms PDTP; Visomitin
SMILES
O=C(C(CCCCCCCCCC[P+](C1=CC=CC=C1)(C2=CC=CC=C2)C3=CC=CC=C3)=C4)C(C)=C(C)C4=O.[Br-]

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] Lyamzaev KG, Panteleeva AA, Simonyan RA, et al. Mitochondrial Lipid Peroxidation Is Responsible for Ferroptosis Cells (2023). PMID: 36831278 DOI: 10.3390/cells12040611 Source material
  2. [2] Demyanenko IA, Zakharova VV, Ilyinskaya OP, et al. Mitochondria-Targeted Antioxidant SkQ1 Improves Dermal Wound Healing in Genetically Diabetic Mice Oxidative medicine and cellular longevity (2017). PMID: 28761623 DOI: 10.1155/2017/6408278 Source material

Publications

1 publication citing this product

  1. Massimo Costanza, .et al. , PNAS, 2019, 2019 PMID: 30988194

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