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Fig. 1 · Structure
Cat. No.
A10144
CAS No.
33570-04-6
Formula
C15H18O8
Mol. Weight
326.3

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Bilobalide

Cat. No. A10144 CAS 33570-04-6

Bilobalide, a biologically active terpenic trilactone (terpinoid), derived from geranylgeranyl pyrophosphate (GGPP) is an inducer of cytochrome P450 enzymes CYP3A1 and CYP1A2. May contain properties to stop apoptosis activation of the phosphatidylinositol 3-Kinase pathway in SH-SY5Y cells.

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Biological Activity

Bioactivity / Mechanism

Bilobalide displaced [35S]-TBPS binding in rat brain membranes and inhibited GABA-evoked chloride uptake in rat synaptoneurosomes. Binding displacement and functional antagonism are distinct endpoints; these assays do not establish a complete mechanism for neuroprotection. [1]

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

Target & Activity

Target Activity Value
Human Endogenous Metabolite  

In Vitro Studies

In rat corticohippocampal synaptoneurosomes, bilobalide inhibited chloride uptake evoked by 100 μM GABA, with an IC50 of 39 μM (95% confidence interval 24–63 μM). This is an assay-specific inhibitory concentration, not a treatment dose. [1]

Displacement of a GABA-associated chloride-channel radioligand

Biochemical assay · Rat corticohippocampal membrane preparation [1]

Bilobalide concentration-dependently displaced specific [35S]-TBPS binding. This binding endpoint does not itself establish functional chloride-channel blockade or a direct binding site. The numerical binding constant is omitted because the paper labels it inconsistently.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Specific [35S]-TBPS bindingConcentration-dependent displacement Displacement observed; numerical constant not adopted[1]

Literature-Reported Treatment Conditions

Treatment concentration
0.3–30 μM
Exposure duration
150 min at 25°C
Method
Radioligand displacement with 2 nM [35S]-TBPS
Vehicle
DMSO negative control; final DMSO concentration not specified
Co-treatment
Radioligand present; non-labelled TBPS (10 μM) used to define specific binding
Reported limits
No salt or separate stereochemical analysis reported; final solvent fraction unspecified.
Methods and source locations

Compound reported in the paper: Bilobalide; Compound label in the paper: bilobalide

Evidence concerns reported bilobalide, not validation of an Adooq lot or a Ginkgo extract.

Results 2.3; Fig. 5 and caption; Discussion 3.2; Methods 4.1, 4.2, 4.5 and 4.7

Specific [35S]-TBPS binding: Four independent experiments, each with triplicate incubations; specific binding 77–85% of total binding — Results 2.3; Fig. 5/caption; Methods 4.5

Inhibition of GABA-evoked chloride uptake

Cell-based study · Rat corticohippocampal synaptoneurosomes [1]

Bilobalide inhibited GABA-evoked 36Cl uptake with an IC50 of 39 μM (95% confidence interval 24–63 μM). GABA increased uptake by 65%; bicuculline and picrotoxin served as antagonist controls. This functional potency should not be substituted for binding potency.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Inhibition of GABA (100 μM)-induced 36Cl uptakeIC50 39 μM (95% confidence interval 24–63 μM)[1]
GABA-evoked increase in 36Cl uptakeChange versus basal uptake +65%; p<0.01; N=12[1]

Literature-Reported Treatment Conditions

Treatment concentration
1–1000 μM; GABA 100 μM
Exposure duration
10 min preincubation at room temperature; subsequent 60 s at 30°C; uptake measured over 5 s
Method
36Cl uptake assay; DMSO negative control and bicuculline/picrotoxin positive controls
Vehicle
DMSO; final fraction not specified
Co-treatment
GABA 100 μM; assay also contained DIDS and furosemide as specified in Methods 4.6
Reported limits
No recombinant subtype assignment; final solvent fraction not specified.
Methods and source locations

Compound reported in the paper: Bilobalide; Compound label in the paper: bilobalide

Evidence concerns reported bilobalide, not validation of an Adooq lot or a Ginkgo extract.

Results 2.4; Fig. 6/caption; Methods 4.1, 4.2, 4.6 and 4.7

Inhibition of GABA (100 μM)-induced 36Cl uptake: Nonlinear regression of six individual experiments; panel A: N=6–12 separate experiments run in triplicate, data ± SEM — Results 2.4; Fig. 6A–B/caption; Methods 4.6–4.7

GABA-evoked increase in 36Cl uptake: GABA 100 μM; bicuculline 100 μM completely inhibited the GABA effect, picrotoxin 100 μM inhibited it by 81% — Results 2.4; Fig. 6A/caption

In Vivo Studies

In female CD-1 mice, bilobalide reduced TTC-defined infarct area 24 h after permanent MCAO when given at 10 mg/kg intraperitoneally 1 h before or 1 h after occlusion. Protection was smaller with dosing 3 h afterward. The 1 mg/kg effect was not significant, and 0.3 mg/kg was ineffective. Long-term protection was not established. [2]

In a separate microdialysis experiment, 10 mg/kg bilobalide given intraperitoneally 1 h before permanent MCAO attenuated the striatal glutamate increase. The hippocampal comparison did not reach conventional statistical significance (p=0.06), and glucose profiles were not significantly changed in either region. [2]

Dose and timing dependence of infarct-area protection

Animal study · Female CD-1 mice (28–32 g), permanent middle cerebral artery occlusion; TTC assessment at 24 h [2]

Bilobalide reduced TTC-defined infarct area in a dose- and timing-dependent manner. Reported slice #3 means were 52.1 ± 2.8% for vehicle, 13.1 ± 8.5% for 10 mg/kg given 1 h before MCAO, 16.3 ± 8.6% for 10 mg/kg given 1 h after MCAO, and 31.1 ± 5.1% for 10 mg/kg given 3 h after MCAO (mean ± SEM, N=7 each). The 1 mg/kg effect was not statistically significant and 0.3 mg/kg was ineffective.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
TTC-negative infarct area in striatal slice #3, as percentage of total slice brain areaMean ± SEM; N=7 per group Vehicle 52.1 ± 2.8%; 10 mg/kg: 13.1 ± 8.5% (−1 h), 16.3 ± 8.6% (+1 h), 31.1 ± 5.1% (+3 h)[2]
Dose dependence of infarct-area protectionReported lower-dose response 1 mg/kg: effect not statistically significant; 0.3 mg/kg: ineffective (data not shown)[2]

Conditions shared by the study groups

Route
Intraperitoneal
Frequency
Single injection
Vehicle
10% DMSO in saline
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
10 mg/kg, 1 h before MCAO
10 mg/kg		Vehicle-treated permanent-MCAO miceSlice #3 infarct area 13.1 ± 8.5% versus vehicle 52.1 ± 2.8% (mean ± SEM, N=7 each).[2]
10 mg/kg, 1 h after MCAO
10 mg/kg		Vehicle-treated permanent-MCAO miceSlice #3 infarct area 16.3 ± 8.6% (mean ± SEM, N=7).[2]
10 mg/kg, 3 h after MCAO
10 mg/kg		Vehicle-treated permanent-MCAO miceSlice #3 infarct area 31.1 ± 5.1% (mean ± SEM, N=7); p<0.05 versus control.[2]
1 mg/kg, 1 h before MCAO
1 mg/kg		Vehicle-treated permanent-MCAO miceReduction did not reach statistical significance.[2]
0.3 mg/kg, 1 h before MCAO
0.3 mg/kg		Vehicle-treated permanent-MCAO miceReported ineffective; data not shown.[2]
10 mg/kg, 1 h before MCAO
Model: Female CD-1 mice (28–32 g), permanent middle cerebral artery occlusion; TTC assessment at 24 h
Treatment course: 1 h before MCAO; 24 h endpoint
Reported limits: Long-term outcome not established. Displayed infarct groups: nine mice enrolled, seven analyzed; text attributes exclusions to extensive bleeding or death, captions to two deaths/group. Replicate count for the unillustrated 0.3 mg/kg result not established.
10 mg/kg, 1 h after MCAO
Model: Female CD-1 mice (28–32 g), permanent middle cerebral artery occlusion; TTC assessment at 24 h
Treatment course: 1 h after MCAO; 24 h endpoint
Reported limits: Long-term outcome not established. Displayed infarct groups: nine mice enrolled, seven analyzed; text attributes exclusions to extensive bleeding or death, captions to two deaths/group. Replicate count for the unillustrated 0.3 mg/kg result not established.
10 mg/kg, 3 h after MCAO
Model: Female CD-1 mice (28–32 g), permanent middle cerebral artery occlusion; TTC assessment at 24 h
Treatment course: 3 h after MCAO; 24 h endpoint
Reported limits: Long-term outcome not established. Displayed infarct groups: nine mice enrolled, seven analyzed; text attributes exclusions to extensive bleeding or death, captions to two deaths/group. Replicate count for the unillustrated 0.3 mg/kg result not established.
1 mg/kg, 1 h before MCAO
Model: Female CD-1 mice (28–32 g), permanent middle cerebral artery occlusion; TTC assessment at 24 h
Treatment course: 1 h before MCAO; 24 h endpoint
Reported limits: Long-term outcome not established. Displayed infarct groups: nine mice enrolled, seven analyzed; text attributes exclusions to extensive bleeding or death, captions to two deaths/group. Replicate count for the unillustrated 0.3 mg/kg result not established.
0.3 mg/kg, 1 h before MCAO
Model: Female CD-1 mice (28–32 g), permanent middle cerebral artery occlusion; TTC assessment at 24 h
Treatment course: 1 h before MCAO; 24 h endpoint
Reported limits: Long-term outcome not established. Displayed infarct groups: nine mice enrolled, seven analyzed; text attributes exclusions to extensive bleeding or death, captions to two deaths/group. Replicate count for the unillustrated 0.3 mg/kg result not established.
Methods and source locations

Compound reported in the paper: Bilobalide; Compound label in the paper: bilobalide

Evidence concerns reported bilobalide, not validation of an Adooq lot or a Ginkgo extract.

Results 2.1; Figs 1–2/captions; Discussion 3.1; Methods 4.1, 4.3, 4.8; acknowledgements

TTC-negative infarct area in striatal slice #3, as percentage of total slice brain area: TTC staining and image quantification at 24 h; +3 h comparison p<0.05 versus control — Results 2.1; Figs 1–2/captions; Methods 4.1

Dose dependence of infarct-area protection: Same permanent-MCAO infarct experiment; no exact low-dose values inferred from bars — Results 2.1; Fig. 1

10 mg/kg, 1 h before MCAO · Results 2.1; Figs 1–2/captions; Methods 4.3

10 mg/kg, 1 h after MCAO · Results 2.1; Figs 1–2/captions; Methods 4.3

10 mg/kg, 3 h after MCAO · Results 2.1; Figs 1–2/captions; Methods 4.3

1 mg/kg, 1 h before MCAO · Results 2.1; Figs 1–2/captions; Methods 4.3

0.3 mg/kg, 1 h before MCAO · Results 2.1; Figs 1–2/captions; Methods 4.3

Extracellular glutamate and glucose during cerebral ischemia

Animal study · Female CD-1 mice; permanent MCAO; striatal and hippocampal microdialysis, with sham and vehicle controls [2]

Systemic bilobalide attenuated ischemia-associated striatal glutamate elevation (p<0.01). The hippocampal comparison was p=0.06, despite a lower mean profile. Glucose profiles were not significantly changed in either region. These observations do not identify a molecular target or prove that glutamate attenuation causes the infarct-area effect.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Glutamate time course: bilobalide versus vehicleTwo-way repeated-measures ANOVA Striatum F1,10=11.06, p<0.01; hippocampus F1,10=4.48, p=0.06[2]
Glucose time course: bilobalide versus vehicleTwo-way repeated-measures ANOVA Striatum F1,10=0.26, p=0.63; hippocampus F1,10=0.08, p=0.78[2]

Conditions shared by the study groups

Route
Intraperitoneal
Frequency
Single injection
Treatment course
1 h before MCAO; microdialysis through 130 min after MCAO
Vehicle
10% DMSO in saline
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Systemic bilobalide pretreatment
10 mg/kg		MCAO vehicle group; sham groupStriatal glutamate elevation attenuated (p<0.01); hippocampal comparison p=0.06. Neither glucose comparison significant.[2]
Systemic bilobalide pretreatment
Model: Female CD-1 mice; permanent MCAO; striatal and hippocampal microdialysis, with sham and vehicle controls
Reported limits: No exact glutamate peak concentrations inferred from plotted curves. The different regions have distinct statistics; hippocampal result is not claimed significant.
Methods and source locations

Compound reported in the paper: Bilobalide; Compound label in the paper: bilobalide

Evidence concerns reported bilobalide, not validation of an Adooq lot or a Ginkgo extract.

Results 2.3–2.4; Fig. 4/caption; Methods 4.1–4.4, 4.8

Glutamate time course: bilobalide versus vehicle: N=6 per group; values plotted as percentage of baseline, mean ± SEM — Fig. 4C–D/caption; Results 2.4

Glucose time course: bilobalide versus vehicle: N=6 per group; sham, MCAO vehicle and MCAO bilobalide groups; mean ± SEM — Fig. 4A–B/caption; Results 2.3

Systemic bilobalide pretreatment · Results 2.3–2.4; Fig. 4/caption; Methods 4.1–4.4, 4.8

Specifications

Manufacturer Adooq Bioscience
Actions Inducer
CAS Number 33570-04-6
Formula C15H18O8
Molecular Weight 326.3
SMILES
CC(C)(C)[C@@]1(C[C@H]2[C@@]3([C@]14[C@H](C(=O)O[C@H]4OC3=O)O)CC(=O)O2)O

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 62 mg/mL (190.01 mM)
Water Insoluble
Ethanol 62 mg/mL (190.01 mM)

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] Cornelia Kiewert, Vikas Kumar, Oksana Hildmann, et al. Role of GABAergic antagonism in the neuroprotective effects of bilobalide Brain Research (2007). PMID: 17134681 DOI: 10.1016/j.brainres.2006.10.042 Source material
  2. [2] Dorothee Lang, Cornelia Kiewert, Alexander Mdzinarishvili, et al. Neuroprotective effects of bilobalide are accompanied by a reduction of ischemia-induced glutamate release in vivo Brain Research (2011). PMID: 22032877 DOI: 10.1016/j.brainres.2011.10.005 Source material

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