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)

目录号: HY-100113A
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Buloxibutid (AT2 receptor agonist C21) hydrochloride 是一种口服有效的、选择性的血管紧张素 II 2 型受体 (AT2R) 激动剂，对猪 AT2R 的 Ki 值为 0.4 nM。Buloxibutid hydrochloride 主要通过促进 NO/cGMP 通路、抑制 MAPK 促增殖信号、抑制 TGF-β/Smad 促纤维化通路及 NF-κB 炎症通路，产生血管舒张、抗炎症、抗纤维化 (促胶原酶 MMP-13 表达) 和组织修复等效应。Buloxibutid hydrochloride 可用于特发性肺纤维化、高血压以及系统性硬化症等相关研究。

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Buloxibutid hydrochloride

Buloxibutid hydrochloride Chemical Structure

CAS No. : 1947313-60-1

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Buloxibutid hydrochloride 相关抗体

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  • 生物活性

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  • 参考文献

生物活性

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)

体外研究
(In Vitro)

Buloxibutid (1-10 μM) hydrochloride 可在 1 和 10 μM 浓度下时间和浓度依赖性地抑制 LPS (HY-D1056) 诱导的 THP-1 巨噬细胞中促炎通路的表达与信号传导[2]。
Buloxibutid (Compound 21) (0.1-0.1 μM; 3 days) hydrochloride 可通过激活 AT2 受体诱导 NG108-15 细胞的神经突生长，在 0.1 μM 处理 3 天后可将神经突阳性细胞比例提升至 19.9%，其信号传导依赖于 MAPK、cGMP 和 cGMP 依赖性蛋白激酶通路[4]。
Buloxibutid (100 nM; 0-1 h) hydrochloride 可通过激活 AT2 受体短暂激活 NG108-15 细胞中的 p42/p44mapk，经 0.1 μM 处理 30 min 后，其磷酸化水平升高 2.2 倍[4]。

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

Buloxibutid hydrochloride 相关抗体:

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.
体内研究
(In Vivo)

Buloxibutid (0.03 mg/kg/天；腹腔注射；每日给药；持续 2 周) hydrochloride 可预防并逆转 Bleomycin (HY-108345) 诱导的 Sprague-Dawley 大鼠肺纤维化、血管重构及炎症反应[2]。
Buloxibutid (0.3 mg/kg/天；微型泵；每日给药；共 7 天) hydrochloride 可减轻 Bleomycin 诱导的大鼠肺纤维化[2]。
Buloxibutid (1 mg/kg；腹腔注射；单次给药) hydrochloride 可减轻 Sprague-Dawley 大鼠中通气相关性肺损伤 (VILI) 诱导的肺损伤与炎症[2]。
Buloxibutid (0.3 mg/kg/天；腹腔注射；每日给药) hydrochloride 可减轻 LPS 诱导的 C57Bl/6 小鼠急性肺损伤[2]。
Buloxibutid (0.3 mg/kg/天；腹腔注射；每日给药) hydrochloride 可减轻高氧诱导的 C57Bl/6 小鼠急性肺损伤[2]。
Buloxibutid (0.1-1 mg/kg/天；腹腔注射；每日给药；连续 7 天) hydrochloride 可减轻雌性 BALB/c 小鼠中急性香烟烟雾诱导的炎症，在 0.3 mg/kg/天剂量下疗效达到最高[2]。
Buloxibutid (0.3 mg/kg/天；腹腔注射；每日给药；持续 3 周) hydrochloride 可减轻慢性香烟烟雾诱导的炎症、上皮损伤及促纤维化反应，同时改善 BALB/c 小鼠的肺功能[2]。
Buloxibutid (0.03 mg/kg/天；腹腔注射；每日给药；持续 2 周) hydrochloride 可逆转野百合碱诱导的雄性 Sprague-Dawley 大鼠肺纤维化和心肌纤维化[2]。
Buloxibutid (0.03 mg/kg；腹腔注射；每日一次；连续 14 天) hydrochloride 可使 L-NAME/NaCl 诱导高血压的雄性 Sprague Dawley 大鼠的收缩压、舒张压和平均血压分别显著降低 34.4%、40.2%和 38.0%，同时还能改善心脏和主动脉的抗氧化状态，减轻心脏组织病理学损伤，并使主动脉结构恢复正常[3]。
buloxibutid (0.03 mg/kg；腹腔注射；每日；14 天) hydrochloride 与 Empagliflozin (HY-15409) 联合使用可显著改善 L-NAME/NaCl 诱导的高血压雄性 Sprague Dawley 大鼠的心脏和主动脉抗氧化状态，使主动脉 MDA 水平降低 27.5%，恢复主动脉结构正常，并减轻心脏组织病理学损伤，且对主动脉 SOD 和 CAT 活性具有协同作用[3]。
Buloxibutid (Compound 21) (0.003-0.3 mg/kg/h；静脉注射；持续输注；100 μM；腔内灌注) hydrochloride 可通过激活 AT2 受体，呈剂量依赖性增强雄性 Sprague-Dawley 大鼠的十二指肠黏膜碱性分泌，在静脉给药剂量为 0.3 mg/kg/h 时观察到最大效应[4]。
Buloxibutid (0.008-4 mg/kg；静脉注射；单次推注) hydrochloride 在麻醉自发性高血压大鼠中，于 0.008 mg/kg 和 0.05 mg/kg 静脉注射剂量下可诱导由 AT2 受体介导的平均动脉压显著降低[4]。

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.
分子量

512.09

Formula

C23H30ClN3O4S2
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

Buloxibutid hydrochloride 相关分类

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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

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