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Fig. 1 · Structure
Cat. No.
A11091
CAS No.
147536-97-8
Formula
C27H29N5O6S
Mol. Weight
551.6

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Bosentan

Cat. No. A11091 CAS 147536-97-8

ETAR/ETBR inhibitor

Bosentan is a competitive antagonist of endothelin-1 at the endothelin-A (ET-A) and endothelin-B (ET-B) receptors.

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Biological Activity

Target & Activity

Target Activity Value
ET-A Ki 4.7 nM
ET-B Ki 95 nM

Cellular Effect

Cell Line Activity Value Description Reference
A-375 IC50 67.36 μM Cytotoxicity against human A-375 cells assessed as reduction in cell viability incubated for 24 hrs by CCK-8 assay [PMID: 34473510]
B16 IC50 > 80 μM Cytotoxicity against mouse B16 cells assessed as reduction in cell viability incubated for 24 hrs by CCK-8 assay [PMID: 34473510]
CHO IC50 202 nM Displacement of [I125]ET1 from recombinant ETB receptor expressed in CHO cells after 2 hrs by TopCount analysis [PMID: 22862294]
CHO IC50 45 nM Displacement of [I125]ET1 from recombinant ETA receptor expressed in CHO cells after 2 hrs by TopCount analysis [PMID: 22862294]
CHO-K1 IC50 195.9 μM Cytotoxicity against CHOK1 cells assessed as decrease in cell viability after 24 hrs by MTT assay [PMID: 27318985]
HepG2 EC50 12.6 μM Activation of human PXR expressed in human HepG2 (DPX-2) cells assessed as induction of CYP3A4 after 24 hrs by luminescent analysis [PMID: 20966043]
HepG2 EC50 14.1 μM Activation of human PXR expressed in human HepG2 (DPX-2) cells after 24 hrs by luciferase reporter gene based luminescent analysis [PMID: 20966043]
SK-MEL-28 IC50 53.65 μM Cytotoxicity against human SK-MEL-28 cells assessed as reduction in cell viability incubated for 24 hrs by CCK-8 assay [PMID: 34473510]

In Vitro Studies

In sandwich-cultured human hepatocytes, Bosentan reduced total d8-TCA accumulation compared to untreated controls. Bosentan also produced dose-dependent reductions in d8-TCA biliary clearance compared to untreated controls. [1]

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

Total accumulation in cultured human hepatocytes

Cell-based study · sandwich-cultured human hepatocytes; n = 3 donors [1]

Sandwich-cultured human hepatocytes were co-incubated with Bosentan at 11, 33, and 100 µM. Total d8-TCA accumulation was 68.6±1.5%, 62.6±6.6%, and 31.7±5.9% of control, respectively, with all P<0.05 compared to untreated controls.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
d8-TCA total accumulationd8-TCA total accumulation 68.6±1.5%, 62.6±6.6%, and 31.7±5.9%[1]

Literature-Reported Treatment Conditions

Treatment concentration
11, 33, and 100 µM
Exposure duration
conditioned for 10 min; incubated for 10 min at 37°C
Method
co-incubation solutions
Vehicle
Plus (+) Buffer and Minus (−) Buffers
Methods and source locations

Compound reported in the paper: Bosentan

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

Materials and Methods > ERA Effect on Hepatobiliary Disposition of d8-Taurocholate (S9, S10, S12, S13); Results > ERA Effect on Hepatobiliary Disposition of d8-Taurocholate (S92, S95); Figure 2 legend (S127, S129)

d8-TCA total accumulation: d8-TCA total accumulation; comparator: untreated control samples — Results > ERA Effect on Hepatobiliary Disposition of d8-Taurocholate (S95)

Biliary clearance in cultured human hepatocytes

Cell-based study · sandwich-cultured human hepatocytes; n = 3 donors [1]

Sandwich-cultured human hepatocytes were co-incubated with Bosentan at 11 µM, 33 µM, and 100 µM. Biliary clearance of d8-TCA showed dose-dependent reductions compared to untreated controls, with reported values of 69.2±0.1%, 58.7±11.4%, and 27.0±9.3%, respectively, all P<0.05.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
in vitro biliary clearance (Clb)Clb 69.2±0.1%; 58.7±11.4%; 27.0±9.3%[1]

Literature-Reported Treatment Conditions

Treatment concentration
11 µM; 33 µM; 100 µM
Exposure duration
conditioned for 10 min; incubated for 10 min at 37°C
Method
co-incubation solutions
Vehicle
Plus (+) Buffer and Minus (−) Buffers
Methods and source locations

Compound reported in the paper: Bosentan

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

Materials and Methods > ERA Effect on Hepatobiliary Disposition of d8-Taurocholate (S9, S10, S12, S13); Results > ERA Effect on Hepatobiliary Disposition of d8-Taurocholate (S93, S100); Figure 3 legend (S130, S132)

in vitro biliary clearance (Clb): in vitro biliary clearance (Clb); comparator: untreated controls — Results > ERA Effect on Hepatobiliary Disposition of d8-Taurocholate (S100)

In Vivo Studies

Adult mice received Bosentan by oral gavage before sciatic nerve crush injury. Bosentan-treated mice had significantly longer axons after injury compared to mice that received vehicle. [2]

Bosentan and Axon Length Following Sciatic Nerve Crush

Animal study · Adult mice; N=5 mice/condition. [2]

Adult mice received Bosentan at 10 mg/kg body weight by oral gavage 2 hr before sciatic nerve crush injury. Bosentan-treated mice had significantly longer axons 1 day after injury compared to mice that received vehicle.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
length of the 10 longest axonsReported result Bosentan (10 mg/kg body weight), 2 hr before the injury: Mice that received Bosentan had significantly longer axons 1 day after SNC compared to mice that received vehicle.[2]

Conditions shared by the study groups

Route
oral gavage
Treatment course
2 hr before the injury, with sample collection taking place 24 hr after the injury
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Bosentan 10 mg/kg body weightmice that received vehicleBosentan (10 mg/kg body weight), 2 hr before the injury: Mice that received Bosentan had significantly longer axons 1 day after SNC compared to mice that received vehicle.[2]
Bosentan 10 mg/kg body weight
Model: Adult mice; N=5 mice/condition.
Reported limits: Not stated in the sentences used: vehicle.
Methods and source locations

Compound reported in the paper: Bosentan

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

Results > Bosentan treatment improves axon regeneration after nerve injury (S32, S37); Materials and methods > Drug administration (S159); Materials and methods > Immunohistochemistry (S203); Figure 3. legend (S315, S320)

length of the 10 longest axons: length of the 10 longest axons; comparator: mice that received vehicle — Results > Bosentan treatment improves axon regeneration after nerve injury (S37); Materials and methods > Drug administration (S159); Figure 3. legend (S315)

Bosentan 10 mg/kg body weight · Results > Bosentan treatment improves axon regeneration after nerve injury (S37); Materials and methods > Drug administration (S159)

Specifications

Manufacturer Adooq Bioscience
Actions Antagonist
CAS Number 147536-97-8
Applications ETAR/ETBR inhibitor
Formula C27H29N5O6S
Molecular Weight 551.6
SMILES
CC(C)(C)C1=CC=C(C=C1)S(=O)(=O)NC2=C(C(=NC(=N2)C3=NC=CC=N3)OCCO)OC4=CC=CC=C4OC

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] Lepist EI, Gillies H, Smith W, et al. Evaluation of the endothelin receptor antagonists ambrisentan, bosentan, macitentan, and sitaxsentan as hepatobiliary transporter inhibitors and substrates in sandwich-cultured human hepatocytes. PLoS One (2014). PMID: 24498134 DOI: 10.1371/journal.pone.0087548 Source material
  2. [2] Feng R, Rosen SF, Ansari I, et al. Endothelin B receptor inhibition rescues aging-dependent neuronal regenerative decline. Elife (2025). PMID: 40924015 DOI: 10.7554/eLife.100217 Source material

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