2. GPCR/G Protein MAPK/ERK Pathway TGF-beta/Smad Stem Cell/Wnt Metabolic Enzyme/Protease
  3. Angiotensin Receptor p38 MAPK TGF-β Receptor TGF-beta/Smad MMP
  4. Buloxibutid hydrochloride

Buloxibutid hydrochloride  (Synonyms: AT2 receptor agonist C21 hydrochloride)

Cat. No.: HY-100113A
Handling Instructions Technical Support

Buloxibutid (AT2 receptor agonist C21) hydrochloride is an orally active, selective angiotensin II type 2 receptor (AT2R) agonist, with a Ki value of 0.4 nM for porcine AT2R. Buloxibutid hydrochloride exerts vasodilatory, anti-inflammatory, antifibrotic (promoting the expression of collagenase MMP-13) and tissue repair effects mainly by activating the NO/cGMP pathway, inhibiting the pro-proliferative MAPK signaling, and suppressing the pro-fibrotic TGF-β/Smad pathway and inflammatory NF-κB pathway. Buloxibutid hydrochloride can be used in research related to idiopathic pulmonary fibrosis, hypertension, systemic sclerosis and other conditions.

For research use only. We do not sell to patients.

Buloxibutid hydrochloride

Buloxibutid hydrochloride Chemical Structure

CAS No. : 1947313-60-1

Size Stock
50 mg   Get quote  
100 mg   Get quote  
250 mg   Get quote  

* Please select Quantity before adding items.

This product is a controlled substance and not for sale in your territory.

Other In-stock Forms of Buloxibutid hydrochloride:

Other Forms of Buloxibutid hydrochloride:

Buloxibutid hydrochloride Related Antibodies

Top Publications Citing Use of Products

View All Angiotensin Receptor Isoform Specific Products:

View All Isoforms
AT1 Receptor AT2 Receptor

View All p38 MAPK Isoform Specific Products:

View All Isoforms
p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

View All TGF-β Receptor Isoform Specific Products:

View All Isoforms
ALK1 ALK2 ALK3 ALK4 ALK5 ALK6 ALK7 TGFβR2 ACVR2A ACVR2B BMP

View All MMP Isoform Specific Products:

View All Isoforms
MMP-1 MMP-2 MMP-3 MMP-8 MMP-9 MMP-13 MMP-14 MMP-17 ADAM10 ADAM17 MMP-7 MMP-12 MMP-10 MMP ADAM8 MMP-19

  • Biological Activity

  • Purity & Documentation

  • References

  • Customer Review

Description

Buloxibutid (AT2 receptor agonist C21) hydrochloride is an orally active, selective angiotensin II type 2 receptor (AT2R) agonist, with a Ki value of 0.4 nM for porcine AT2R. Buloxibutid hydrochloride exerts vasodilatory, anti-inflammatory, antifibrotic (promoting the expression of collagenase MMP-13) and tissue repair effects mainly by activating the NO/cGMP pathway, inhibiting the pro-proliferative MAPK signaling, and suppressing the pro-fibrotic TGF-β/Smad pathway and inflammatory NF-κB pathway. Buloxibutid hydrochloride can be used in research related to idiopathic pulmonary fibrosis, hypertension, systemic sclerosis and other conditions[1][2][3][4].
IC50 & Target[4]

AT2 Receptor

0.4 nM (Ki)

AT1 Receptor

> 10 μM (Ki)

In Vitro

Buloxibutid (1-10 μM) hydrochloride inhibits the expression and signaling of proinflammatory pathways in LPS (HY-D1056)-induced THP-1 macrophages in a time- and concentration-dependent manner at concentrations of 1 and 10 μM[2].
Buloxibutid (Compound 21) (0.1-0.1 μM; 3 days) hydrochloride induces neurite outgrowth in NG108-15 cells by activating AT2 receptors. After treatment with 0.1 μM for 3 days, it increases the proportion of neurite-positive cells to 19.9%, and its signal transduction depends on the MAPK, cGMP and cGMP-dependent protein kinase pathways[4].
Buloxibutid (100 nM; 0-1 h) hydrochloride transiently activates p42/p44mapk in NG108-15 cells via activation of the AT2 receptor, and its phosphorylation level increases by 2.2-fold after treatment with 0.1 μM for 30 min[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Buloxibutid hydrochloride Related Antibodies

Cell Differentiation Assay[4]

Cell Line: NG108-15 neuroblastoma-glioma hybrid cells
Concentration: 0.1 nM, 1 nM, 0.1 μM, 1 μM
Incubation Time: 3 days
Result: Increased the percentage of neurite-positive cells from 5.5% (control) to 19.9% at 0.1 μM treatment.
Induced neurite outgrowth at concentrations ≥ 0.1 nM.
Had its neurite outgrowth effect abolished by co-incubation with PD 123,319.
Had its neurite outgrowth effect reduced by co-incubation with PD 98,059, LY-83,583, or KT 5823.

Western Blot Analysis[4]

Cell Line: NG108-15 neuroblastoma-glioma hybrid cells
Concentration: 100 nM
Incubation Time: 0, 30 and 60 min
Result: Induced a 2.2-fold increase in phosphorylated p42/p44mapk levels relative to control within 30 min.
Decreased phosphorylated p42/p44mapk levels to basal levels by 60 min.
Had its 30-min activation abolished by pre-incubation with PD 123,319.
In Vivo

Buloxibutid (0.03 mg/kg/day; i.p.; daily administration; for 2 consecutive weeks) hydrochloride prevents and reverses bleomycin (HY-108345)-induced pulmonary fibrosis, vascular remodeling and inflammatory responses in Sprague-Dawley rats[2].
Buloxibutid (0.3 mg/kg/day; mini pump; daily administration; for 7 consecutive days) hydrochloride alleviates bleomycin-induced pulmonary fibrosis in rats[2].
Buloxibutid (1 mg/kg; i.p.; single administration) hydrochloride attenuates lung injury and inflammation induced by ventilator-induced lung injury (VILI) in Sprague-Dawley rats[2].
Buloxibutid (0.3 mg/kg/day; i.p.; daily) hydrochloride alleviates LPS-induced acute lung injury in C57Bl/6 mice[2].
Buloxibutid (0.3 mg/kg/day; i.p.; daily administration) hydrochloride alleviates hyperoxia-induced acute lung injury in C57Bl/6 mice[2].
Buloxibutid (0.1-1 mg/kg/day; i.p.; administered daily for 7 consecutive days) hydrochloride reduces acute cigarette smoke-induced inflammation in female BALB/c mice, with the maximum efficacy observed at a dose of 0.3 mg/kg/day[2].
Buloxibutid (0.3 mg/kg/day; i.p.; daily administration; for 3 consecutive weeks) hydrochloride reduces chronic cigarette smoke-induced inflammation, epithelial injury and profibrotic responses, while improving pulmonary function in BALB/c mice[2].
Buloxibutid (0.03 mg/kg/day; i.p.; daily administration for 2 consecutive weeks) hydrochloride reverses monocrotaline-induced pulmonary fibrosis and myocardial fibrosis in male Sprague-Dawley rats[2].
Buloxibutid (0.03 mg/kg; i.p.; once daily; for 14 consecutive days) hydrochloride significantly reduces systolic blood pressure, diastolic blood pressure, and mean blood pressure by 34.4%, 40.2%, and 38.0%, respectively, in male Sprague Dawley rats with hypertension induced by L-NAME/NaCl. It also improves the antioxidant status of the heart and aorta, alleviates histopathological damage to cardiac tissue, and restores normal aortic structure[3].
Buloxibutid (0.03 mg/kg; i.p.; daily; 14 days) hydrochloride combined with Empagliflozin (HY-15409) significantly improves the antioxidant status of the heart and aorta in male Sprague Dawley rats with hypertension induced by L-NAME/NaCl, reduces aortic MDA levels by 27.5%, restores normal aortic structure, alleviates cardiac histopathological damage, and exerts a synergistic effect on aortic SOD and CAT activities[3].
Buloxibutid (Compound 21) (0.003-0.3 mg/kg/h; i.v.; continuous infusion; 100 μM; intraluminal perfusion) hydrochloride dose-dependently enhances duodenal mucosal alkaline secretion in male Sprague-Dawley rats via activation of the AT2 receptor, with the maximal effect observed at an intravenous dose of 0.3 mg/kg/h[4].
Buloxibutid (0.008-4 mg/kg; i.v.; single bolus) hydrochloride induces a significant AT2 receptor-mediated reduction in mean arterial pressure at intravenous doses of 0.008 mg/kg and 0.05 mg/kg in anesthetized spontaneously hypertensive rats[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Sprague-Dawley[2]
Dosage: 0.03 mg/kg/day
Administration: i.p.; daily; 14 days
Result: Attenuated bleomycin-induced increases in right ventricular systolic pressure (RVSP), associated with reduced cardiac and pulmonary vascular remodeling.
Caused significant reductions in percentage fibrotic area, Ashcroft score, and hydroxyproline content.
Prevented or reversed bleomycin-induced increases in Col1a/3a1, CTGF, MMP-12, TIMP-1, and IL-13 gene expression to baseline levels.
Reduced pro-inflammatory gene expression (CCL2, IL-6, TLR4) and CD68+ macrophage infiltration.
Reduced bleomycin-induced increases in AT2R gene expression.
Animal Model: Sprague-Dawley[2]
Dosage: 0.3 mg/kg/day
Administration: subcutaneous; daily; 7 days
Result: Reduced bleomycin-induced increases in Ashcroft score and percentage interstitial collagen area, slightly more effectively than β-Pro7 Ang III, and with greater efficacy than pirfenidone for these fibrotic measures.
Reduced lung myofibroblast accumulation and TGFβ expression to a similar degree as β-Pro7 Ang III and pirfenidone.
Tended to increase lung compliance relative to the bleomycin group.
Animal Model: Sprague-Dawley[2]
Dosage: 1 mg/kg
Administration: i.p.; single dose
Result: Significantly attenuated ventilation-induced lung damage (histological scoring).
Reduced cell and protein content in bronchoalveolar lavage fluid (BALF).
Caused a significant increase in the anti-inflammatory cytokines IL-4 and IL-10.
Animal Model: BALB/c (female)[2]
Dosage: 0.1 mg/kg/day; 0.3 mg/kg/day; 1 mg/kg/day
Administration: i.p.; daily; 7 days
Result: Exhibited dose-dependent anti-inflammatory effects, reducing cytokines and cells in BALF, with maximal effects observed at the 0.3 mg/kg dose.
Restored alveolar macrophage phagocytic ability at 0.3 mg/kg/day.
Suppressed cigarette smoke-induced pro-inflammatory marker expression at 0.3 mg/kg/day.
Restored M2 phenotypic marker expression at 0.3 mg/kg/day.
Upregulated AT2R and MasR expression at 0.3 mg/kg/day.
Reversed cigarette smoke-induced reductions in AT2R expression.
Animal Model: BALB/c (female)[2]
Dosage: 0.3 mg/kg/day
Administration: i.p.; daily; 21 days
Result: Significantly reduced cigarette smoke-induced increases in pro-inflammatory cytokines and alveolar epithelial thickening.
Opposed pro-fibrotic responses, reducing active TGFβ1, SMAD2/3, hydroxyproline, MMP-9, and MMP-12 levels, though augmented cigarette smoke-induced increases in TIMP-1.
Elicited significant protective effects in all measured lung function parameters.
Reversed cigarette smoke-induced increases in AT2R expression.
Animal Model: Sprague-Dawley (male)[2]
Dosage: 0.03 mg/kg/day
Administration: i.p.; daily; 14 days
Result: Reversed lung interstitial and peri-vascular fibrosis, as well as cardiac fibrosis; this anti-fibrotic effect was abrogated by co-administration with an AT2R antagonist or MasR antagonist.
Reversed monocrotaline-induced increases in ACE gene expression and decreases in ACE2 gene expression, restoring ACE2 to double control levels.
Did not affect AT1R expression but significantly increased AT2R expression relative to monocrotaline-treated and control rats.
Animal Model: Not specified[2]
Dosage: 2 mg/kg/day; 20 mg/kg/day
Administration: p.o.; daily; 34 days
Result: Significantly improved cardiac function.
Reversed remodeling in vessels of all sizes.
Reduced lung collagen content and percentage dense area.
Animal Model: Sprague Dawley (male, hypertension induced via 40 mg/kg L-NAME i.p. once daily for 28 days plus 1% NaCl in drinking water ad libitum for 28 days)[3]
Dosage: 0.03 mg/kg
Administration: i.p.; once daily; 14 days
Result: Reduced systolic blood pressure to a median of 73.77 mmHg, diastolic blood pressure to a median of 57.82 mmHg, and mean blood pressure to a median of 67.465 mmHg compared to the hypertension-only group.
Decreased heart rate to a median of 215.075 beats/min compared to the control group.
Reduced heart weight to a median of 1.177 g compared to the hypertension-only group.
Increased superoxide dismutase activity to a median of 6.303 U/g protein and glutathione peroxidase activity to a median of 79.698 U/mg protein in cardiac tissue compared to the hypertension-only group.
Increased glutathione level to a median of 51.333 μmol/g tissue, superoxide dismutase activity to a median of 16.511 U/g protein, catalase activity to a median of 42.085 K/g protein, and glutathione peroxidase activity to a median of 104.833 U/mg protein in aortic tissue compared to the hypertension-only group.
Increased serum calcium level to a median of 9.95 mg/dL and reduced serum total cholesterol level to a median of 38.5 mg/dL compared to the hypertension-only group.
Reduced cardiac histopathological damage scores for degenerated cardiomyocytes, hemorrhage, inflammatory infiltration, and collagen deposition compared to the hypertension-only group.
Restored thoracic aortic histology to a state similar to the control group, resolving dilatation and elastic lamella irregularities seen in the hypertension-only group.
Molecular Weight

512.09

Formula

C23H30ClN3O4S2
CAS No.
SMILES

O=C(NS(=O)(C1=C(C2=CC=C(CN3C=NC=C3)C=C2)C=C(CC(C)C)S1)=O)OCCCC.Cl
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
  • No file chosen (Maximum size is: 1024 Kb)
  • If you have published this work, please enter the PubMed ID.
  • Your name will appear on the site.

Buloxibutid hydrochloride Related Classifications

  • Molarity Calculator

  • Dilution Calculator

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass   Concentration   Volume   Molecular Weight *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Buloxibutid1947313-60-1AT2 receptor agonist C21Angiotensin Receptorp38 MAPKTGF-β ReceptorTGF-beta/SmadMMPTransforming growth factor beta receptorsTransforming growth factor betaMatrix metalloproteinasesRaynaud's phenomenonangiotensin II type 2 receptorsystemic sclerosisC57Bl/6 miceAT2RBALB/c miceidiopathic pulmonary fibrosishypertensionTHP-1 human macrophagesSprague-Dawley ratsInhibitorinhibitorinhibit

Your Recently Viewed Products:

Inquiry Online

Your information is safe with us. * Required Fields.

Product Name

  

Requested Quantity *

Applicant Name *

 

Salutation

Email Address *

 

Phone Number *

Department

 

Organization Name *

City

State

Country or Region *

      

Remarks

Bulk Inquiry

Inquiry Information

Product Name:
Buloxibutid hydrochloride
Cat. No.:
HY-100113A
Quantity:
MCE Japan Authorized Agent:

Customer Review

Thank You for Your Feedback!

Request for HNMR Report

Please fill out this form to request the QC report. We will send it to your Email address shortly.

Your information is safe with us. * Required Fields.

Product Name

  

Lot #

Applicant Name *

 

Email Address *

Phone Number

 

Department *

Organization Name *

 

Country or Region *

Remarks

SAFETY DATA SHEET (SDS)

Request for HNMR Report

We have received your request and will respond to you as soon as possible.