Apoptosis Autophagy Metabolic Enzyme/Protease Immunology/Inflammation NF-κB Epigenetics Cell Cycle/DNA Damage Protein Tyrosine Kinase/RTK MAPK/ERK Pathway Vitamin D Related/Nuclear Receptor
Apoptosis Autophagy Reactive Oxygen Species (ROS) Mitochondrial Metabolism PARP Caspase Bcl-2 Family VEGFR FAK WDR5 p38 MAPK JNK PPAR
Caudatin

製品番号: HY-N1983

Caudatin

1 Cited Publications

カスタマーレビュー

Based on 1 publication(s) in Google Scholar

Caudatin is an orally active and brain-penetrant C-21 steroidal found in Cynanchum bungei decne with a variety of biological activities. Caudatin can inhibit cell proliferation, migration, invasion, cause cell phase arrest, induce apoptosis, autophagy, ROS prodution and loss of mitochondrial membrane potential. Caudatin activates PARP, caspase-3, -7, -9, upregulates pro-apoptotic Bad and Bax and downregulates anti-apoptotic Bcl-2 and Bcl-XL. Caudatin suppresses VEGF, FAK phosphorylation, upregulates p21, p27, DR5 protein expression, activates the p38 MAPK, JNK and PPARα/TFEB-mediated autophagy-lysosomal signaling pathways. Caudatin can be used for the research of cancer, inflammation and neurological disease, such as glioma and Alzheimer's disease.

商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。

純度: 99.95%
CAS 番号: 38395-02-7
分子式: C₂₈H₄₂O₇
分子量:490.63

保管条件:

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Caudatin 構造式

CAS 番号: 38395-02-7

容量

価格（税別）

在庫状況

数量

Amount: USD 0.00

* アイテムを追加する前、数量をご選択ください

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Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

生物活性
- 製品説明
- IC₅₀ & Target
- Cellular Effect
- 体外実験
- 体内実験
化学情報
Publications (1)
溶剤 & 溶解度
- 体外
- 体内
純度とドキュメンテーション
参考文献
Help & FAQs
関連分類
Bioz

生物活性

製品説明

IC₅₀ & Target^[1]

Caspase 3

Caspase-7

Caspase-9

Bax

Bcl-xL

Bcl-2

bad

PARP アイソフォーム固有の製品をすべて表示 :

Caspase アイソフォーム固有の製品をすべて表示 :

Bcl-2 Family アイソフォーム固有の製品をすべて表示 :

VEGFR アイソフォーム固有の製品をすべて表示 :

p38 MAPK アイソフォーム固有の製品をすべて表示 :

JNK アイソフォーム固有の製品をすべて表示 :

PPAR アイソフォーム固有の製品をすべて表示 :

Cellular Effect

Cell Line	Type	Value	Description	References
HCT-116	IC₅₀	64.11 μM Compound: 1	Antiproliferative activity against human HCT-116 cells after 48 hrs by MTT assay Antiproliferative activity against human HCT-116 cells after 48 hrs by MTT assay	[PMID: 34968813]
HeLa	IC₅₀	>100 μM Compound: 1	Antiproliferative activity against human HeLa cells after 48 hrs by MTT assay Antiproliferative activity against human HeLa cells after 48 hrs by MTT assay	[PMID: 34968813]
HepG2	IC₅₀	65.9 μM Compound: 1	Antiproliferative activity against human HepG2 cells after 48 hrs by MTT assay Antiproliferative activity against human HepG2 cells after 48 hrs by MTT assay	[PMID: 34968813]
HepG2 2.2.15	CC₅₀	244.58 μM Compound: 1	Cytotoxicity against human HepG2(2.2.15) cells by MTT assay Cytotoxicity against human HepG2(2.2.15) cells by MTT assay	[PMID: 22472044]
HepG2 2.2.15	CC₅₀	244.58 μM Compound: 1	Cytotoxicity against human HepG2(2.2.15) cells by modified-MTT assay Cytotoxicity against human HepG2(2.2.15) cells by modified-MTT assay	[PMID: 22687441]
HepG2 2.2.15	IC₅₀	>183.44 μM Compound: 1	Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as suppression of HbeAg secretion by ELISA Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as suppression of HbeAg secretion by ELISA	[PMID: 22472044]
HepG2 2.2.15	IC₅₀	>183.44 μM Compound: 1	Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as inhibition of viral e antigen secretion by ELISA Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as inhibition of viral e antigen secretion by ELISA	[PMID: 22687441]
HepG2 2.2.15	IC₅₀	142.67 μM Compound: 1	Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as suppression of HBsAg secretion by ELISA Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as suppression of HBsAg secretion by ELISA	[PMID: 22472044]
HepG2 2.2.15	IC₅₀	142.67 μM Compound: 1	Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as inhibition of viral surface antigen secretion by ELISA Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as inhibition of viral surface antigen secretion by ELISA	[PMID: 22687441]
HepG2 2.2.15	IC₅₀	40.62 μM Compound: 1	Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as inhibition of viral DNA replication by RT-PCR analysis Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as inhibition of viral DNA replication by RT-PCR analysis	[PMID: 22472044]
HepG2 2.2.15	IC₅₀	40.62 μM Compound: 1	Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as inhibition of viral DNA replication by PCR analysis Antiviral activity against Hepatitis B virus infected in human HepG2(2.2.15) cells assessed as inhibition of viral DNA replication by PCR analysis	[PMID: 22687441]
MCF7	IC₅₀	>100 μM Compound: 1	Antiproliferative activity against human MCF7 cells after 48 hrs by MTT assay Antiproliferative activity against human MCF7 cells after 48 hrs by MTT assay	[PMID: 34968813]

体外実験

Caudatin (25-100 μM; 24-72 h) potently inhibits the viability of human glioma U251 and U87 cells in a time- and dose-dependent manner, with U251 cells showing greater sensitivity (IC₅₀ = 52.1 μM at 72 h)^[1].
Caudatin (25-100 μM; 72 h) induces dose-dependent apoptosis in human glioma U251 cells, with 71.4% of cells undergoing apoptosis after 72 h treatment with 100 μM caudatin^[1].
Caudatin (12.5-100 μM; 72 h) induces dose-dependent PARP cleavage and activation of caspase-3, caspase-7, and caspase-9 in human glioma U251 cells over 72 h^[1].
Caudatin (25-100 μM; 5-30 min) induces time-dependent loss of mitochondrial membrane potential in human glioma U251 cells^[1].
Caudatin (25-100 μM; 1-72 h) disrupts the balance of Bcl-2 family proteins in human glioma U251 cells, dose-dependently upregulating pro-apoptotic Bad and Bax and downregulating anti-apoptotic Bcl-2 and Bcl-XL over 72 h^[1].
Caudatin (25-100 μM; 2-72 h) disturbs intracellular redox homeostasis in human glioma U251 cells by inducing dose-dependent ROS and superoxide accumulation, decreasing mitochondrial mass and GSH content^[1].
Caudatin (6-200 μM; 48 h) inhibits HUVEC proliferation in a dose-dependent manner, with 50, 100, and 200 μM concentrations reducing cell viability to 71.5%, 53.6%, and 38.1% respectively after 48 h of treatment^[2].
Caudatin (100 μM; 48 h) inhibits HUVEC migration after 48 h of treatment^[2].
Caudatin (100 μM; 24 h) inhibits HUVEC invasion after 24 h of treatment^[2].
Caudatin (100 μM; 24 h) inhibits HUVEC capillary-like tube formation after 24 h of treatment^[2].
Caudatin (50-200 μM; 12-48 h) suppresses FAK phosphorylation in HUVECs in both dose-dependent and time-dependent manners^[2].
Caudatin (50-200 μM; 48 h) suppresses the expression of VEGF and phosphorylated VEGFR2 in HUVECs in a dose-dependent manner over 48 h of treatment, without altering total VEGFR2 or AKT levels^[2].
Caudatin (5-100 μg/mL; 24 h) inhibits the viability of human MDA-MB-231 and MCF-7 breast cancer cells in a concentration-dependent manner^[3].
Caudatin (10-50 μg/mL; 24 h) induces G1-phase cell cycle arrest in human MDA-MB-231 and MCF-7 breast cancer cells^[3].
Caudatin (5-50 μg/mL; 24 h) modulates the expression of key cell cycle regulators, including upregulating p21, p27, and p53 and downregulating p-Cdc2, Cdk4, and cyclinB1, in human MDA-MB-231 and MCF-7 breast cancer cells^[3].
Caudatin (5-50 μg/mL; 24 h) induces apoptosis in human MDA-MB-231 and MCF-7 breast cancer cells, as evidenced by dose-dependent cleavage of caspase-8, caspase-9, and PARP^[3].
Caudatin (5-50 μg/mL; 24 h) upregulates DR5 protein expression in a dose-dependent manner in human MDA-MB-231 and MCF-7 breast cancer cells^[3].
Caudatin (5-50 μg/mL; 24 h) activates the endoplasmic reticulum stress response in human MDA-MB-231 and MCF-7 breast cancer cells, as evidenced by dose-dependent upregulation of PERK, BIP, ATF4, and CHOP protein levels^[3].
Caudatin (5-50 μg/mL; 24 h) activates the p38 MAPK and JNK signaling pathways in a dose-dependent manner in human MDA-MB-231 and MCF-7 breast cancer cells, without affecting ERK1/2 phosphorylation^[3].
Caudatin (10-50 μg/mL; 24 h) triggers apoptosis in human MDA-MB-231 and MCF-7 breast cancer cells^[3].
Caudatin binds strongly to the human PPARα ligand binding domain^[4].
Caudatin (25 μM; 24 h) rescues mouse hippocampal neuronal HT-22 cells from Aβ_1-42-induced cytotoxicity^[4].
Caudatin (6.25-25 μM; 24 h) dose-dependently induces autophagy and promotes autophagy flux in mouse neuronal cells^[4].
Caudatin (25 μM; 24 h) induces nuclear translocation of PPARα in mouse microglial cells, an effect blocked by the PPARα inhibitor GW6471 (HY-15372)^[4].
Caudatin (25 μM) reduces phospho-Tau and APP metabolites in mouse microglial cells overexpressing AD-related mutations in a PPARα-dependent manner^[4].
Caudatin (6.25-25 μM) dose-dependently increases TFEB expression and induces TFEB nuclear translocation in mouse neuronal and microglial cells via an MTORC1-independent mechanism^[4].

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

Cell Viability Assay^[1]

Cell Line:

human glioma U251, U87 cells
Concentration:

25, 50, 100 μM
Incubation Time:

24 h; 48 h; 72 h
Result:

Significantly decreased U251 and U87 cell viability in a time- and dose-dependent manner.
Reduced U251 cell viability to 73.5%, 51.3%, and 28.2% after treatment with 25, 50, 100 μM for 72 h, respectively.
Exhibited IC₅₀ values towards U251 cells of 170.3 μM (24 h), 102.2 μM (48 h), and 52.1 μM (72 h).

Apoptosis Analysis^[1]

Cell Line:

human glioma U251 cells
Concentration:

25, 50, 100 μM
Incubation Time:

72 h
Result:

Induced significant dose-dependent apoptosis in U251 cells, as measured by the Sub-G1 peak.
Resulted in 10.2%, 34.7%, and 71.4% apoptotic cells after treatment with 25, 50, 100 μM, respectively.

Western Blot Analysis^[1]

Cell Line:

human glioma U251 cells
Concentration:

12.5, 25, 50, 100 μM
Incubation Time:

72 h
Result:

Dose-dependently induced PARP cleavage (89 KD fragment) and activation of caspase-3, caspase-7, and caspase-9 in U251 cells.
Resulted in PARP cleavage levels (normalized to β-actin) of 0.1, 0.5, 0.9, and 1.0 for 12.5, 25, 50, and 100 μM, respectively.
Resulted in active caspase-3 levels of 0.4, 0.4, 0.5, and 1.0 for 12.5, 25, 50, and 100 μM, respectively.
Resulted in active caspase-7 levels of 0.5, 0.9, and 1.0 for 25, 50, and 100 μM, respectively.
Resulted in active caspase-9 levels of 0.5, 0.7, and 1.0 for 25, 50, and 100 μM, respectively.

Western Blot Analysis^[1]

Cell Line:

human glioma U251 cells
Concentration:

25, 50, 100 μM (72 h treatment); 50 μM (time-course treatment)
Incubation Time:

72 h; 1, 6, 12, 24, 48, 72 h (time-course)
Result:

Dose-dependently upregulated pro-apoptotic Bad and Bax expression, and downregulated anti-apoptotic Bcl-2 and Bcl-XL expression in U251 cells after 72 h treatment.
Decreased Bcl-2 expression (normalized to β-actin) to 0.9, 0.9, 0.8, 0.1, 0.1, and 0.1 at 1, 6, 12, 24, 48, and 72 h, respectively, with 50 μM treatment.
Increased Bad expression to 0.6, 0.7, 0.8, and 1.0 at 12, 24, 48, and 72 h, respectively, with 50 μM treatment.

Apoptosis Analysis^[1]

Cell Line:

human glioma U251 cells
Concentration:

50 μM (with 20 μM caspase inhibitor pretreatment)
Incubation Time:

72 h
Result:

Reduced 50 μM caudatin-induced apoptosis from 32.4% to 7.4% when cells were pretreated with z-VAD-fmk, and increased cell viability in caudatin-treated cells.
Suppressed caudatin-induced PARP cleavage when cells were pretreated with z-VAD-fmk or z-LEHD-fmk.
Suppressed caudatin-induced activation of caspase-3, caspase-7, and caspase-9 when cells were pretreated with z-VAD-fmk or z-DEVD-fmk.

Cell Viability Assay^[2]

Cell Line:

human umbilical vein endothelial cells (HUVECs)
Concentration:

6, 12, 25, 50, 100, 200 μM
Incubation Time:

48 h
Result:

Slightly promoted HUVEC growth at 6 μM.
Significantly inhibited HUVEC viability in a dose-dependent manner at 25, 50, 100, 200 μM, reducing viability to 71.5% (50 μM), 53.6% (100 μM), and 38.1% relative to control.

Western Blot Analysis^[2]

Cell Line:

human umbilical vein endothelial cells (HUVECs)
Concentration:

50, 100, 200 μM (dose-dependent assay); 100 μM (time-dependent assay)
Incubation Time:

48 h; 12, 24, 48 h (time-dependent assay)
Result:

Reduced p-FAK levels in a dose-dependent manner at 50, 100, 200 μM after 48 h.
Reduced p-FAK levels in a time-dependent manner at 100 μM after 12, 24, and 48 h.

Western Blot Analysis^[2]

Cell Line:

human umbilical vein endothelial cells (HUVECs)
Concentration:

50, 100, 200 μM
Incubation Time:

48 h
Result:

Reduced VEGF and p-VEGFR2 expression in a dose-dependent manner after 48 h, with no significant changes in total VEGFR2 or total AKT levels.

Cell Cycle Analysis^[3]

Cell Line:

human MDA-MB-231 and MCF-7 breast carcinoma cells
Concentration:

10, 50 μg/mL
Incubation Time:

24 h
Result:

Increased the G1-phase population to 64.78±0.98% and decreased the G2/M-phase population to 17.75±0.66% in MDA-MB-231 cells at 10 μg/mL.
Increased the G1-phase population to 69.76±1.83% and decreased the G2/M-phase population to 11.10±1.14% in MDA-MB-231 cells at 50 μg/mL.
Increased the G1-phase population to 57.14±1.11% and decreased the S-phase population to 34.05±1.26% in MCF-7 cells at 10 μg/mL.
Increased the G1-phase population to 73.94±2.01% and decreased the S-phase population to 14.99±1.24% in MCF-7 cells at 50 μg/mL.

Western Blot Analysis^[3]

Cell Line:

human MDA-MB-231 and MCF-7 breast carcinoma cells
Concentration:

5-50 μg/mL
Incubation Time:

24 h
Result:

Caused dose-dependent accumulation of p21 and p27 proteins in both cell lines.
Upregulated p53 protein in MCF-7 cells but not in MDA-MB-231 cells.
Downregulated p-Cdc2, Cdk4, and cyclinB1 proteins in both cell lines.
Left Cdc2 protein levels unchanged in both cell lines.
Caused dose-dependent cleavage of caspase-8, caspase-9, and PARP, hallmark features of apoptosis, in both cell lines.
Caused a dose-dependent increase in DR5 protein levels in both cell lines, with no significant change in DR4 protein levels observed.
Caused a dose-dependent increase in protein levels of PERK, BIP, ATF4, and CHOP, markers of ER stress and the unfolded protein response, in both cell lines.
Caused a dose-dependent increase in phosphorylation of p38 MAPK and JNK in both cell lines, with no significant change in ERK1/2 phosphorylation observed.

Cell Autophagy Assay^[4]

Cell Line:

Mouse hippocampal neuronal HT-22 cells
Concentration:

6.25, 12.5, 25 μM
Incubation Time:

24 h
Result:

Significantly reduced SQSTM1 and increased LC3B-II protein levels in HT-22 cells in a dose-dependent manner.
Promoted autophagy flux in N2A tfLC3 cells, as shown by enhanced RFP puncta.

体内実験

Caudatin (25-50 mg/kg; i.v.; every other day; 16 days) significantly inhibits U251 human glioma xenograft growth in male nude mice via induction of apoptosis, inhibition of cell proliferation, and suppression of angiogenesis, with no observed effect on mouse body weight^[1].
Caudatin (25-50 mg/kg; i.v.; every other day; 16 days) dose-dependently inhibits subcutaneous U251 glioma xenograft growth in male nude mice, while suppressing angiogenesis via reduced VEGF expression, CD34-positive vessel density, and p-AKT/p-FAK levels^[2].
Caudatin (20-40 mg/kg; p.o.; daily; 8 months) improves cognitive function, reduces Aβ and pathological Tau pathology, activates PPARα/TFEB-mediated autophagy-lysosomal pathway, and mitigates neuroinflammation in 3XTg-AD mice^[4].
Caudatin (20 mg/kg; p.o.; single dose) is brain-permeable in healthy ICR mice, reaching a peak brain concentration of 64.77 ng/g at 15 minutes^[4].

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

Animal Model:

Nude mice with U251 human glioma xenograft (male)^[1]
Dosage:

25 mg/kg; 50 mg/kg
Administration:

i.v.; every other day; 16 days
Result:

Reduced tumor volume and tumor weight compared to control.
Induced tumor cell apoptosis (via caspase-3 activation).
Inhibited tumor cell proliferation (via reduced Ki-67 staining).
Suppressed tumor angiogenesis (via reduced CD-31 staining).
Did not affect mouse body weight.

Animal Model:

Nude mice with U251 human glioma xenograft (male)^[2]
Dosage:

25 mg/kg; 50 mg/kg
Administration:

i.v.; every other day; 16 days
Result:

Reduced mean tumor volume and mean tumor weight.
Dose-dependently reduced phosphorylated AKT (p-AKT) and phosphorylated FAK (p-FAK) levels in tumor tissue.
Dose-dependently decreased immunohistochemical staining of Ki-67, VEGF, and CD34 in tumor tissue.

Animal Model:

3XTg-AD (female, 6 months old, Alzheimer's disease model with K670M/N671L, M146V, P301L mutant gene overexpression); 129/B6/SWJ (female, wildtype littermate)^[4]
Dosage:

20 mg/kg; 40 mg/kg
Administration:

p.o.; daily; 8 months
Result:

Reduced escape latency in the Morris water maze (MWM) task, increased time spent in the target quadrant during the MWM probe trial, increased freezing percentage in the contextual fear conditioning test, reduced time spent in the center of the open field chamber, and increased total distance traveled in the open field test compared to vehicle-treated 3XTg-AD mice.
Reduced AT8-positive neuron load in hippocampal brain slices; significantly lowered sarkosyl-insoluble levels of pathological Tau markers PHF1, AT8, CP13, MC1, and HT7 in brain homogenates.
Reduced the number of 4G8-positive Aβ plaques in hippocampal brain slices; significantly lowered formic acid-soluble Aβ₁-₄₂ and Aβ₁-₄₀ levels in brain homogenates, and reduced SDS-soluble levels of APP metabolites CTFs and pCTFs.
Increased brain homogenate protein levels of PPARα, TFEB, mature CTSD, LAMP1, and LC3B-II, while reducing SQSTM1 levels, compared to vehicle-treated 3XTg-AD mice.
Reduced the number of activated microglia and astrocytes in brain slices, and lowered corresponding protein levels in brain homogenates.

化学情報

CAS 番号 38395-02-7
性状 Solid
分子量 490.63
分子式 C₂₈H₄₂O₇
Color White to off-white
SMILES

C[C@@]([C@@H](C[C@]1([H])[C@]23C)OC(/C=C(C)/C(C)C)=O)([C@]4(O)C(C)=O)[C@@]([C@@]1(CC=C2C[C@@H](O)CC3)O)(CC4)O
Structure Classification
- Steroids
Initial Source
輸送条件

Room temperature in continental US; may vary elsewhere.
保管条件

4°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Publications (1)

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University of Edinburgh

2025 May 29.

溶剤 & 溶解度

体外:

DMSO : 50 mg/mL (101.91 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.0382 mL

10.1910 mL

20.3820 mL

5 mM

0.4076 mL

2.0382 mL

4.0764 mL

10 mM

0.2038 mL

1.0191 mL

2.0382 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (protect from light). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

モル濃度計算機

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

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分子量分子量

希釈計算機

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濃度 _(終了) 濃度 _(終了)

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体内:

Select the appropriate dissolution method based on your experimental animal and administration route.

Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.5 mg/mL (5.10 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: ≥ 2.5 mg/mL (5.10 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (5.10 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

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The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

純度とドキュメンテーション

バッチを選択:

純度: 99.98%

Assay: 99.98%

ee.: 99.98%

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参考文献

[1]. Zhu LZ, et al. Caudatin induces caspase-dependent apoptosis in human glioma cells with involvement of mitochondrial dysfunction and reactive oxygen species generation. Cell Biol Toxicol. 2016;32(4):333-345. [Content Brief]

[2]. Wang X, et al. Antiangiogenic properties of caudatin in vitro and in vivo by suppression of VEGF‑VEGFR2‑AKT/FAK signal axis. Mol Med Rep. 2017 Dec;16(6):8937-8943. [Content Brief]

[3]. Fei HR, et al. Caudatin potentiates the anti-tumor effects of TRAIL against human breast cancer by upregulating DR5. Phytomedicine. 2019;62:152950. [Content Brief]

[4]. Krishnamoorthi S, et al. PPARɑ Ligand Caudatin Improves Cognitive Functions and Mitigates Alzheimer's Disease Defects By Inducing Autophagy in Mice Models. J Neuroimmune Pharmacol. 2023;18(3):509-528. [Content Brief]

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How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	2.0382 mL	10.1910 mL	20.3820 mL	50.9549 mL
	5 mM	0.4076 mL	2.0382 mL	4.0764 mL	10.1910 mL
	10 mM	0.2038 mL	1.0191 mL	2.0382 mL	5.0955 mL
	15 mM	0.1359 mL	0.6794 mL	1.3588 mL	3.3970 mL
	20 mM	0.1019 mL	0.5095 mL	1.0191 mL	2.5477 mL
	25 mM	0.0815 mL	0.4076 mL	0.8153 mL	2.0382 mL
	30 mM	0.0679 mL	0.3397 mL	0.6794 mL	1.6985 mL
	40 mM	0.0510 mL	0.2548 mL	0.5095 mL	1.2739 mL
	50 mM	0.0408 mL	0.2038 mL	0.4076 mL	1.0191 mL
	60 mM	0.0340 mL	0.1698 mL	0.3397 mL	0.8492 mL
	80 mM	0.0255 mL	0.1274 mL	0.2548 mL	0.6369 mL
	100 mM	0.0204 mL	0.1019 mL	0.2038 mL	0.5095 mL

Caudatin

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Caudatin

Apoptosis Compound Library

Cell Cycle/DNA Damage Compound Library

Epigenetics Compound Library

Immunology/Inflammation Compound Library

MAPK Compound Library

Metabolism/Protease Compound Library

NF-κB Signaling Compound Library

Protein Tyrosine Kinase Compound Library

Stem Cell Signaling Compound Library

Natural Product Library

Anti-Cancer Compound Library

CNS-Penetrant Compound Library

Autophagy Compound Library

Anti-Aging Compound Library

Lipid Compound Library

Oxygen Sensing Compound Library

Endoplasmic Reticulum Stress Compound Library

Pyroptosis Compound Library

Cytoskeleton Compound Library

Orally Active Compound Library

Glutamine Metabolism Compound Library

Traditional Chinese Medicine Active Compound Library

Anti-Alzheimer's Disease Compound Library

Anti-Breast Cancer Compound Library

Anti-Lung Cancer Compound Library

Anti-Pancreatic Cancer Compound Library

Anti-Cancer Metabolism Compound Library

Neurodegenerative Disease-related Compound Library

Angiogenesis-Related Compound Library

Mitochondria-Targeted Compound Library

Transcription Factor-Targeted Library

Glucose Metabolism Compound Library

Anti-Cancer Natural Product Library

Anti-inflammatory Traditional Chinese Medicine Active Compound Library

Plant-Sourced Natural Product Library

Human Metabolite Library

Nuclear Receptor Compound Library

Cuproptosis Compound Library

Pain-Related Compound Library

Metabolic Enzyme Compound Library

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Membrane Receptor-targeted Compound Library

Cell Death Library

Multi-Target Compound Library

Mitophagy Compound Library

Bioactive Compound Library Max

MCE Bioactive Compound Library

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Natural Product and Natural Product-Like Compound Library

Bioactive Compound Library

Anti-Brain Cancer Compound Library

Miao Ethnicity Medicine Compound Library

Tibetan Medicine Compound Library

Protein Kinase Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

RO5 Drug-like Natural Product Library

Cell Proliferation Compound Library

High-Throughput Bioactive Compound Library

High-Throughput Natural Product Library

Mass Spectrometry Human Metabolite Library

Natural Product Diversity Scaffold Library

Lactylation Compound Library

Mass Spectrometry Natural Product Library

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