CXCR4 antagonist 4 is a potent, orally active CXCR4 antagonist (IC50=24 nM) with diminished CYP 2D6 activity, improved PAMPA permeability, potent inhibition of human immunodeficiency virus entry (IC50=7 nM)[1].
IC50 Target
CXCR4
24 nM (IC50)
HIV
7 nM (IC50)
体外研究 (In Vitro)
CXCR4 antagonist 4 (Compound 30, 0.1~10 µM, 48 hours) displays the inhibition potencies against the X4 virus in TZM-bl cells (IC50=7 nM) [1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Cytotoxicity Assay[1]
Cell Line:
TZM-bl cells
Concentration:
0.1, 1, 10 µM
Incubation Time:
48 hours
Result:
Displayed inhibition potencies against the X4 virus (IC50=7 nM)
体内研究 (In Vivo)
CXCR4 antagonist 4 (3, 10, 30 mg/kg) demonstrates better oral Bioavailability in a dose dependent and reached 27% for the 30 mg/kg[1]. Pharmacokinetic Parameters of CXCR4 antagonist 4 in mice[1]
Route
Dose(mg/kg)
T1/2(h)
Cmax(ng/mL)
C12h (ng/mL)
AUC0-8h(h*ng/mL)
% FPO (0-8 h)
Cl (L/h/kg)
Vd (L/kg)
iv
3
5.89
116
265
11.3
96.3
po
3
12.8
1.50
34.3
12.9
po
10
54.8
14.3
190
215
po
30
169
34.8
717
27.1
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
mice[1]
Dosage:
3, 10, 30 mg/kg
Administration:
Result:
Demonstrated better oral bioavailability in a dose dependent and reached 27% for the 30 mg/kg.
分子量
497.67
Formula
C29H41F2N5
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.
参考文献
[1]. Jecs E, et al. Synthesis and Evaluation of Novel Tetrahydronaphthyridine CXCR4 Antagonists with Improved Drug-like Profiles. J Med Chem. 2022, 65(5):4058-4084.
Antagonist G TFA 是有效的后叶加压素 (vasopressin) 的拮抗剂。Antagonist G 也是弱的GRP 和缓激肽的弱拮抗剂。Antagonist G 可诱导 AG-1 的转录，是癌细胞对化疗增敏。
Antagonist G TFA Chemical Structure
规格
是否有货
100 mg
;
询价
;
250 mg
;
询价
;
500 mg
;
询价
;
* Please select Quantity before adding items.
Antagonist G TFA 的其他形式现货产品:
Antagonist G
生物活性
Antagonist G TFA is a potent vasopressin antagonist. Antagonist G is also a weak antagonist of GRP and Bradykinin. Antagonist G induces AP-1 transcription and sensitizes cells to chemotherapy[1][2].
体外研究 (In Vitro)
Antagonist G (0-100 μM) induces apoptosis is redox-sensitive and caspase-dependently in SCLC cells[2]. Antagonist G activates JNK1 in SCLC cells[2]. Antagonist G is not intrinsically a free radical oxygen donor but stimulates free radical generation specifically within SCLC cells (6.2-fold) and increases the activity of the redox-sensitive transcription factor AP-1 by 61%[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[2]
Cell Line:
SCLC cell lines NCI-H69, NCI-H510 and CHO-K1 cells.
Concentration:
0-100 μM.
Incubation Time:
24 h.
Result:
Inhibited cell growh.
分子量
1065.21
Formula
C51H67F3N12O8S
Sequence Shortening
RW-{Me-Phe}-WLM-NH2
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.
Solvent Solubility
In Vitro:;
H2O
Peptide Solubility and Storage Guidelines:
1.;;Calculate the length of the peptide.
2.;;Calculate the overall charge of the entire peptide according to the following table:
;
Contents
Assign value
Acidic amino acid
Asp (D), Glu (E), and the C-terminal -COOH.
-1
Basic amino acid
Arg (R), Lys (K), His (H), and the N-terminal -NH2
+1
Neutral amino acid
Gly (G), Ala (A), Leu (L), Ile (I), Val (V), Cys (C), Met (M), Thr (T), Ser (S), Phe (F), Tyr (Y), Trp (W), Pro (P), Asn (N), Gln (Q)
0
3.;;Recommended solution:
Overall charge of peptide
Details
Negative (lt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, add NH4OH (lt;50 μL). 3.;;If the peptide still does not dissolve, add DMSO (50-100 μL) to solubilize the peptide.
Positive (gt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, try dissolving the peptide in a 10%-30% acetic acid solution. 3.;;If the peptide still does not dissolve, try dissolving the peptide in a small amount of DMSO.
Zero (=0)
1.;;Try to dissolve the peptide in organic solvent (acetonitrile, methanol, etc.) first. 2.;;For very hydrophobic peptides, try dissolving the peptide in a small amount of DMSO, and then dilute the solution with water to the desired concentration.
参考文献
[1]. P J Woll, et al. A neuropeptide antagonist that inhibits the growth of small cell lung cancer in vitro. Cancer Res. 1990 Jul 1;50(13):3968-73.
[2]. A C MacKinnon, et al. [Arg6, D-Trp7,9, NmePhe8]-substance P (6–11) (antagonist G) inducesP-1 transcription and sensitizes cells to chemotherapy. Br J Cancer. 2000 Oct; 83(7): 941–948.
RAGE antagonist peptide is an advanced glycation end products (RAGE) antagonist. RAGE antagonist peptide prevents RAGE from binding with several of its most important ligands, including HMGB-1, S100P, and S100A4. RAGE antagonist peptide (RAP) possesses anti-tumor and anti-inflammatory activities[1][2].
体外研究 (In Vitro)
RAGE antagonist peptide (RAP) reduces the ability of the ligands to stimulate RAGE activation of NFκB in cancer cells in vitro[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
RAGE antagonist peptide (RAP, 100 µg) inhibits RAGE-mediated Basal NFκB Activity in PDAC cells in vivo[1]. RAGE antagonist peptide (RAP) reduces the growth and metastasis of pancreatic tumors and also inhibited glioma tumor growth[1]. In mice bearing asthma, RAGE antagonist peptide (RAP; 4 mg/kg; i.p.) blunts airway reactivity, airway inflammation and goblet cell metaplasia, and decreases release of Th2 cytokines. RAGE antagonist peptide also reduces total, cytoplasmic and nuclear levels of β-catenin, enhanced β-catenin phosphorylation at Ser33/37/Thr41, which triggers ubiquitination, down-regulated expression of β-catenin targeted genes, and tends to keep β-catenin at the cytomembrane, shifting β-catenin from a signalling active pattern to an adhesive function[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Cancer cells expressing the NFκB-luc reporter implanted into immune-deficient mice[1].
Dosage:
100 µg.
Administration:
Intratumoral delivery (or intraperitoneally).
Result:
Systemic administration caused a substantial reduction (p<0.05) in the NFκB signal 5 h after injection.
分子量
1272.56
Formula
C57H101N13O17S
CAS 号
1092460-91-7
Sequence Shortening
Ac-ELKVLMEKEL-NH2
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.
参考文献
[1]. Thiruvengadam Arumugam, et al. S100P-derived RAGE antagonistic peptide reduces tumor growth and metastasis. Clin Cancer Res. 2012 Aug 15;18(16):4356-64.
[2]. Lihong Yao, et al. The receptor for advanced glycation end products is required for β-catenin stabilization in a chemical-induced asthma model. Br J Pharmacol. 2016 Sep;173(17):2600-13.
RAGE antagonist peptide TFA is an advanced glycation end products (RAGE) antagonist. RAGE antagonist peptide TFA prevents RAGE from binding with several of its most important ligands, including HMGB-1, S100P, and S100A4. RAGE antagonist peptide TFA possesses anti-tumor and anti-inflammatory activities[1][2].
体外研究 (In Vitro)
RAGE antagonist peptide TFA (RAP) reduces the ability of the ligands to stimulate RAGE activation of NFκB in cancer cells in vitro[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
RAGE antagonist peptide TFA (RAP, 100 µg) inhibits RAGE-mediated Basal NFκB Activity in PDAC cells in vivo[1]. RAGE antagonist peptide TFA (RAP) reduces the growth and metastasis of pancreatic tumors and also inhibited glioma tumor growth[1]. In mice bearing asthma, RAGE antagonist peptide TFA (RAP; 4 mg/kg; i.p.) blunts airway reactivity, airway inflammation and goblet cell metaplasia, and decreases release of Th2 cytokines. RAGE antagonist peptide TFA also reduces total, cytoplasmic and nuclear levels of β-catenin, enhances β-catenin phosphorylation at Ser33/37/Thr41, which triggers ubiquitination, down-regulated expression of β-catenin targeted genes, and tends to keep β-catenin at the cytomembrane, shifting β-catenin from a signalling active pattern to an adhesive function[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Cancer cells expressing the NFκB-luc reporter implanted into immune-deficient mice[1].
Dosage:
100 µg
Administration:
Intratumoral delivery (or intraperitoneally).
Result:
Systemic administration caused a substantial reduction (p<0.05) in the NFκB signal 5 h after injection.
分子量
1386.58
Formula
C59H102F3N13O19S
Sequence Shortening
Ac-ELKVLMEKEL-NH2
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Thiruvengadam Arumugam, et al. S100P-derived RAGE antagonistic peptide reduces tumor growth and metastasis. Clin Cancer Res. 2012 Aug 15;18(16):4356-64.
[2]. Lihong Yao, et al. The receptor for advanced glycation end products is required for β-catenin stabilization in a chemical-induced asthma model. Br J Pharmacol. 2016 Sep;173(17):2600-13.
G-Protein antagonist peptide TFA 是一种截短的 substance P 相关肽，与受体竞争 G 蛋白结合。G-Protein antagonist peptide TFA 抑制重组磷脂囊泡中 M2 毒蕈碱胆碱能受体 (M2 mAChR) 激活 Gi 或 Go 或 β 肾上腺素能受体激活 Gs。
G-Protein antagonist peptide TFA Chemical Structure
规格
价格
是否有货
数量
1 mg
￥1500
In-stock
5 mg
￥4000
In-stock
10 mg
￥6400
In-stock
50 mg
;
询价
;
100 mg
;
询价
;
* Please select Quantity before adding items.
生物活性
G-Protein antagonist peptide TFA is a truncated substance P-related peptide, competes with receptor for G protein binding. G-Protein antagonist peptide TFA inhibits the activation of Gi or Go by M2 muscarinic cholinergic receptor (M2 mAChR) or of Gs by beta-adrenergic receptor in the reconstituted phospholipid vesicles, assayed by receptor-promoted GTP hydrolysis[1].
分子量
1207.28
Formula
C59H65F3N12O11S
Sequence
{Glp}-Gln-Trp-Phe-Trp-Trp-Met-NH2
Sequence Shortening
{Glp}QWFWWM-NH2
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Mukai H, et al. G protein antagonists. A novel hydrophobic peptide competes with receptor for G protein binding. J Biol Chem. 1992;267(23):16237-16243.
Antagonist G 是有效的后叶加压素 (vasopressin) 的拮抗剂。Antagonist G 也是弱的 GRP 和缓激肽的弱拮抗剂。Antagonist G 可诱导 AG-1 的转录，是癌细胞对化疗增敏。
Antagonist G Chemical Structure
CAS No. : 115150-59-9
规格
价格
是否有货
数量
1 mg
￥1500
In-stock
5 mg
￥4500
In-stock
10 mg
;
询价
;
50 mg
;
询价
;
* Please select Quantity before adding items.
Antagonist G 相关产品
bull;相关化合物库:
Bioactive Compound Library Plus
Apoptosis Compound Library
GPCR/G Protein Compound Library
Anti-Cancer Compound Library
Transcription Factor Targeted Library
Peptide Library
生物活性
Antagonist G is a potent vasopressin antagonist. Antagonist G is also a weak antagonist of GRP and Bradykinin. Antagonist G induces AP-1 transcription and sensitizes cells to chemotherapy[1][2].
体外研究 (In Vitro)
Antagonist G (0-100 μM) induces apoptosis is redox-sensitive and caspase-dependently in SCLC cells[2]. Antagonist G activates JNK1 in SCLC cells[2]. Antagonist G is not intrinsically a free radical oxygen donor but stimulates free radical generation specifically within SCLC cells (6.2-fold) and increases the activity of the redox-sensitive transcription factor AP-1 by 61%[2].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[2]
Cell Line:
SCLC cell lines NCI-H69, NCI-H510 and CHO-K1 cells.
Concentration:
0-100 μM.
Incubation Time:
24 h.
Result:
Inhibited cell growh.
分子量
951.19
Formula
C49H66N12O6S
CAS 号
115150-59-9
Sequence Shortening
RW-{Me-Phe}-WLM-NH2
运输条件
Room temperature in continental US; may vary elsewhere.
2.;;Calculate the overall charge of the entire peptide according to the following table:
;
Contents
Assign value
Acidic amino acid
Asp (D), Glu (E), and the C-terminal -COOH.
-1
Basic amino acid
Arg (R), Lys (K), His (H), and the N-terminal -NH2
+1
Neutral amino acid
Gly (G), Ala (A), Leu (L), Ile (I), Val (V), Cys (C), Met (M), Thr (T), Ser (S), Phe (F), Tyr (Y), Trp (W), Pro (P), Asn (N), Gln (Q)
0
3.;;Recommended solution:
Overall charge of peptide
Details
Negative (lt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, add NH4OH (lt;50 μL). 3.;;If the peptide still does not dissolve, add DMSO (50-100 μL) to solubilize the peptide.
Positive (gt;0)
1.;;Try to dissolve the peptide in water first. 2.;;If water fails, try dissolving the peptide in a 10%-30% acetic acid solution. 3.;;If the peptide still does not dissolve, try dissolving the peptide in a small amount of DMSO.
Zero (=0)
1.;;Try to dissolve the peptide in organic solvent (acetonitrile, methanol, etc.) first. 2.;;For very hydrophobic peptides, try dissolving the peptide in a small amount of DMSO, and then dilute the solution with water to the desired concentration.
参考文献
[1]. P J Woll, et al. A neuropeptide antagonist that inhibits the growth of small cell lung cancer in vitro. Cancer Res. 1990 Jul 1;50(13):3968-73.
[2]. A C MacKinnon, et al. [Arg6, D-Trp7,9, NmePhe8]-substance P (6–11) (antagonist G) inducesP-1 transcription and sensitizes cells to chemotherapy. Br J Cancer. 2000 Oct; 83(7): 941–948.
