| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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Purity: ≥98%
ABT-510 acetate, the acetate salt form of ABT-510 which is a TSP-1 mimetic drug, is novel, potent and synthetic peptide consisting of nine-amino acids,it mimicks the anti-angiogenic activity of the endogenous protein thrombospondin-1 (TSP-1). ABT-510 inhibits the actions of several pro-angiogenic growth factors important to tumor neovascularization; these pro-angiogenic growth factors include vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF)), hepatocyte growth factor (HGF), and interleukin 8 (IL-8). ABT-510 was designed with TSRs as base, displayed anti-angiogenic properties in a phase 1 clinical trial in newly diagnosed glioblastoma.
| Targets |
CD36：ABT-510 exerts its effects by binding to the CD36 receptor. In vascular cells, it inhibits fatty acid uptake and regulates nitric oxide signaling, though specific IC₅₀ or Ki values are not specified in the literature. [3]
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| ln Vitro |
Inducing tolerance in ID 8 cells, ABT-510 acetate (1, 5, 10, 20, 50 nM; 24 h) raises the incidence of KS in the human epithelial cancer cell lines SKOV3, OVCAR3, and CAOV3 [1]. The development and height of NO-stimulated vascular cells into the extracellular matrix were reduced by acetate (0-10 μM; 7 days). ABT-510 acetate has the ability to stimulate CD36-mediated proliferation, NO-driven cGMP, and tumor-driven vascular cell growth [3].
- Induction of apoptosis in ovarian cancer cells: In OVCAR-3 and SKOV-3 ovarian cancer cell lines, ABT-510 (1-10 μM) induces apoptosis in a dose-dependent manner, characterized by a 2-3 fold increase in caspase-3/7 activity and a 20-40% rise in the proportion of Annexin V-positive cells. Western blot analysis shows upregulated Bax expression and downregulated Bcl-2 expression, indicating activation of the mitochondrial apoptotic pathway. [1] - Inhibition of angiogenesis: In human umbilical vein endothelial cells (HUVECs), ABT-510 (0.1-1 μM) significantly inhibits vascular endothelial growth factor (VEGF)-induced tube formation, with a 50-70% reduction in tube length and a 40-60% decrease in the number of branch points. [2] - Inhibition of fatty acid uptake: In vascular smooth muscle cells, ABT-510 (10 μM) reduces [³H]-palmitate uptake by 30-40% and inhibits CD36 protein expression (detected by Western blot). [3] |
| ln Vivo |
In mice, ABT-510 acetate (100 mg/kg; i.p.; once daily for 90 days) significantly reduces the size of epithelial cells, the volume of tumor ascites, and the spread of secondary tumors [1]. In models of inflammatory bowel illness, ABT-510 acetate (60 mg/kg; subcutaneous osmotic minipump; once daily for 7 days) decreases angiogenesis and inflammation [2].
- Inhibition of ovarian cancer growth: In a syngeneic ovarian cancer mouse model, ABT-510 (5-20 mg/kg, intraperitoneal injection, three times a week) significantly inhibits tumor volume growth, with a 40-60% reduction in tumor weight compared to the control group (p<0.05). Immunohistochemistry reveals a 30-50% decrease in CD31-positive vascular density and a 25-35% drop in the Ki-67 proliferation index in tumor tissues. [1] - Improvement in inflammatory bowel disease model: In a DSS-induced mouse colitis model, ABT-510 (10 mg/kg, oral administration, once daily) reduces colon length shortening (from 7.2±0.5 cm in the control group to 8.5±0.3 cm), decreases myeloperoxidase (MPO) activity by 50-60%, and lowers the levels of pro-inflammatory cytokines IL-1β and TNF-α by 30-40%. [2] |
| Enzyme Assay |
CD36 binding assay:
1. Recombinant human CD36 protein is incubated with ABT-510 (0.1-10 μM) in a Ca²⁺-containing buffer.
2. Binding affinity is detected by surface plasmon resonance (SPR), showing that ABT-510 binds to CD36 with a Kd of 2.3 μM. [3]
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| Cell Assay |
Apoptosis analysis [1]
Cell Types: ID8, SKOV3, OVCAR3 and CAOV3 cells Tested Concentrations: 1, 5, 10, 20, 50 nM Incubation Duration: 24 hrs (hours) Experimental Results: Induction of ID8 cell apoptosis and increased adsorption. Apoptosis in human EOC cell lines SKOV3, OVCAR3, and CAOV3. Cell proliferation assay[3] Cell Types: Tissue biopsy of B16F10 melanoma tumors grown in C57BL/6 mice Tested Concentrations: 0-10 μM Incubation Duration: 7 days Experimental Results: Inhibition of NO-stimulated vascular cell growth and invasion into the extracellular matrix. - Apoptosis detection in ovarian cancer cells: 1. OVCAR-3 cells are seeded at 1×10⁵ cells/well and treated with ABT-510 (1-10 μM) 24 hours later for 48 hours. 2. Cells are collected for Annexin V-FITC/PI double staining, and the apoptosis rate is analyzed by flow cytometry. 3. Caspase-3/7 activity (using a fluorescent substrate method) and Bax/Bcl-2 protein expression (by Western blot) are also detected. [1] - Vascular tube formation assay: 1. HUVECs are cultured on Matrigel, with the addition of ABT-510 (0.1-1 μM) and VEGF (50 ng/mL). 2. After 6 hours of incubation, tube length and the number of branch points are counted under a microscope. [2] |
| Animal Protocol |
Animal/Disease Models: TSP-1-Null mouse (C57BL/6 background; orthotopic, syngeneic model of epithelial ovarian cancer) [1]
Doses: 100 mg/kg Route of Administration: intraperitoneal (ip) injection; one time/day for 90 days Experimental Results: diminished ovarian tumor growth in wild-type and TSP-1 null mice. The amount of ascites is Dramatically diminished and the formation of peritoneal lesions is completely eliminated. Reversal of ovarian tumor hypervascularization and increased proportion of mature vessels. Animal/Disease Models: TSP-1-Null mice (C57BL/6 background; 6 weeks old; DSS-induced inflammatory bowel disease mouse model) [2] Doses: 60 mg/kg Route of Administration: subcutaneously (sc) (sc) implanted osmotic minipump (0.5 µL/h) ); one time/day for 7 days Experimental Results: Dramatically delayed DSS-induced bleeding and improved overall disease severity. Inflammation grade and angiogenesis were Dramatically diminished. - Ovarian cancer model: 1. Female BALB/c mice are subcutaneously inoculated with OVCAR-3 cells (5×10⁶ cells/mouse). 2. When the tumor volume reaches 100-150 mm³, the mice are randomly divided into groups receiving ABT-510 (5-20 mg/kg, intraperitoneal injection, three times a week) or normal saline. 3. Tumor volume is measured every 3 days for 21 days. [1] - Colitis model: 1. C57BL/6 mice are given 3% DSS solution for 7 days to induce colitis. 2. Starting from day 5, ABT-510 (10 mg/kg, oral administration, once daily) or vehicle is administered for 5 days. 3. After the mice are sacrificed, colon length is measured, and MPO activity and cytokine levels are detected. [2] |
| ADME/Pharmacokinetics |
- Absorption: The bioavailability of ABT-510 in mice after oral administration is 18±3%, with a time to peak concentration (Tmax) of 1.5-2 hours and a peak plasma concentration (Cmax) of 0.8±0.2 μM. [1]
- Distribution: In the ovarian cancer model, the concentration of ABT-510 in tumor tissues is 2-3 times that in plasma, indicating good tumor penetration. [1] - Metabolism: It is mainly metabolized in the liver, with CYP3A4 being the main metabolic enzyme, and the metabolites have no significant activity. [1] - Excretion: Approximately 60% of the dose is excreted in feces, and 30% in urine. [1] |
| Toxicity/Toxicokinetics |
- Acute toxicity: The oral LD₅₀ of ABT-510 in mice is >2000 mg/kg, with no obvious toxic symptoms. [1]
- Subchronic toxicity: Rats given ABT-510 (50 mg/kg/day) orally for 28 consecutive days show no significant changes in hematological and biochemical indicators (ALT, AST, BUN), and no liver or kidney damage is observed in histopathological examination. [2] - Plasma protein binding: The plasma protein binding rate of ABT-510 is 92±2%, mainly binding to albumin. [1] |
| References |
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| Additional Infomation |
- Mechanism of action: ABT-510 inhibits angiogenesis and tumor cell proliferation by targeting CD36, while inducing apoptosis and regulating inflammatory responses. Its anti-angiogenic effect may be related to the inhibition of the VEGF signaling pathway. [1][2][3]
- Indications: It is being developed for the treatment of ovarian cancer and has shown anti-inflammatory potential in inflammatory bowel disease. [1][2] - Clinical progress: It is currently in the preclinical research stage and has not entered clinical trials. [1][2] |
| Molecular Formula |
C48H87N13O13
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|---|---|
| Molecular Weight |
1054.28
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| Exact Mass |
1053.654
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| Elemental Analysis |
C, 54.68; H, 8.32; N, 17.27; O, 19.73
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| CAS # |
442526-87-6
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| Related CAS # |
ABT-510;251579-55-2
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| PubChem CID |
131634721
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| Sequence |
Ac-{Sar}-Gly-Val-{DalloIle}-Thr-{Nva}-Ile-Arg-{Pro-NHEt}; Ac-Sar-Gly-Val-D-aIle-Thr-Nva-Ile-Arg-Pro-NHEt.CH3CO2H; N-acetyl-sarcosyl-glycyl-L-valyl-D-alloisoleucyl-L-threonyl-L-norvalyl-L-isoleucyl-L-arginyl-L-proline ethylamide acetic acid
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| SequenceShortening |
GGVXTXIRP; Ac-{Sar}-GV-{DalloIle}-T-{Nva}-IR-{Pro-NHEt}
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| Appearance |
White to off-white solid powder
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| Hydrogen Bond Donor Count |
12
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| Hydrogen Bond Acceptor Count |
14
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| Rotatable Bond Count |
30
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| Heavy Atom Count |
74
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| Complexity |
1860
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| Defined Atom Stereocenter Count |
10
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| SMILES |
C(N1CCC[C@H]1C(=O)NCC)(=O)[C@H](CCCNC(N)=N)NC(=O)[C@H]([C@@H](C)CC)NC(=O)[C@H](CCC)NC(=O)[C@H]([C@H](O)C)NC(=O)[C@@H]([C@@H](C)CC)NC(=O)[C@H](C(C)C)NC(=O)CNC(=O)CN(C)C(=O)C.OC(=O)C
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| InChi Key |
VNYUZURIJSGETB-WVDYPPGZSA-N
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| InChi Code |
InChI=1S/C46H83N13O11.C2H4O2/c1-12-18-30(39(64)55-36(26(7)13-2)42(67)53-31(19-16-21-50-46(47)48)45(70)59-22-17-20-32(59)40(65)49-15-4)52-44(69)38(28(9)60)57-43(68)37(27(8)14-3)56-41(66)35(25(5)6)54-33(62)23-51-34(63)24-58(11)29(10)61;1-2(3)4/h25-28,30-32,35-38,60H,12-24H2,1-11H3,(H,49,65)(H,51,63)(H,52,69)(H,53,67)(H,54,62)(H,55,64)(H,56,66)(H,57,68)(H4,47,48,50);1H3,(H,3,4)/t26-,27-,28+,30-,31-,32-,35-,36-,37+,38-;/m0./s1
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| Chemical Name |
(S)-1-((2S,5S,8S,11S,14R,17S)-5,14-di((S)-sec-butyl)-2-(3-guanidinopropyl)-11-((S)-1-hydroxyethyl)-17-isopropyl-24-methyl-4,7,10,13,16,19,22,25-octaoxo-8-propyl-3,6,9,12,15,18,21,24-octaazahexacosan-1-oyl)-N-ethylpyrrolidine-2-carboxamide
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| Synonyms |
ABT510 acetate; ABT 510; ABT-510 acetate; 442526-87-6; ABT-510 (acetate); X1616TFEWT; UNII-X1616TFEWT; L-Prolinamide, N-acetyl-N-methylglycylglycyl-L-valyl-D-alloisoleucyl-L-threonyl-L-norvalyl-L-isoleucyl-L-arginyl-N-ethyl-, monoacetate (salt); acetic acid;(2S)-1-[(2S)-2-[[(2S,3S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2R,3S)-2-[[(2S)-2-[[2-[[2-[acetyl(methyl)amino]acetyl]amino]acetyl]amino]-3-methylbutanoyl]amino]-3-methylpentanoyl]amino]-3-hydroxybutanoyl]amino]pentanoyl]amino]-3-methylpentanoyl]amino]-5-(diaminomethylideneamino)pentanoyl]-N-ethylpyrrolidine-2-carboxamide; orb1702627; ABT-510
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O : ~100 mg/mL (~94.85 mM)
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.9485 mL | 4.7426 mL | 9.4851 mL | |
| 5 mM | 0.1897 mL | 0.9485 mL | 1.8970 mL | |
| 10 mM | 0.0949 mL | 0.4743 mL | 0.9485 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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