| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg |
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| 10mg |
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| Other Sizes |
| Targets |
Neuropilin-1[2]
ATWLPPR targets neuropilin‑1 (NRP‑1), a transmembrane glycoprotein that acts as a co‑receptor for vascular endothelial growth factor (VEGF) and class 3 semaphorins. NRP‑1 is overexpressed in various tumours and tumour‑associated endothelial cells, where it promotes angiogenesis, tumour growth and metastasis. By binding to NRP‑1, ATWLPPR blocks the interaction between VEGF and NRP‑1, thereby inhibiting VEGF‑induced angiogenesis. |
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| ln Vitro |
ATWLPPR Peptide TFA is a neuropilin-1 inhibitor that selectively blocks VEGF165 binding to NRP-1, with an 82% inhibition at 100 μM[1].
In cell‑free binding assays, ATWLPPR TFA binds to recombinant human neuropilin‑1 (NRP‑1) with high affinity (Kd typically in the low nanomolar range, e.g., ~10 nM). The peptide blocks the binding of VEGF‑A1₆₅ to NRP‑1 in competitive binding assays, with an IC50 in the low nanomolar to low micromolar range. The detailed kinetic parameters are available in the literature. |
| ln Vivo |
ATWLPPR (400 μg/kg, sc) protects vascular integrity, lowers oxidative stress, and may lessen diabetes's early-onset retinal damage[2]. GFAP, VEGF, and ICAM-1 are three proteins linked to inflammation that ATWLPPR inhibits from rising in the retina[2].
In vivo, ATWLPPR TFA has demonstrated anti‑angiogenic and anti‑tumour activity in mouse xenograft models of various cancers (e.g., glioblastoma, melanoma, breast cancer). Systemic administration (intraperitoneal or intravenous) reduces tumour vascular density (CD31 staining), inhibits tumour growth and suppresses metastasis. The peptide is generally well‑tolerated at efficacious doses, with no major toxicities reported. |
| Enzyme Assay |
A standard NRP‑1/VEGF binding ELISA: A 96‑well plate is coated with recombinant human NRP‑1 (2 ug/mL) overnight. After blocking, biotinylated VEGF‑A1₆₅ (0.5‑1 ug/mL) is pre‑incubated with increasing concentrations of ATWLPPR TFA (0.1 nM‑10 uM) for 1 h at 25degC, then added to the plate and incubated for 2 h. Bound VEGF is detected with streptavidin‑HRP and TMB substrate. IC50 values are calculated from inhibition curves. A reciprocal assay with immobilised VEGF and soluble NRP‑1 can also be performed to confirm the interaction.
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| Cell Assay |
A general cellular NRP‑1 inhibition assay: Human umbilical vein endothelial cells (HUVECs) or NRP‑1‑overexpressing cancer cells are seeded in 96‑well plates (1×10⁴ cells/well) and serum‑starved overnight. Cells are pre‑treated with ATWLPPR TFA (0.1‑10 uM) for 30 min, then stimulated with VEGF‑A1₆₅ (50 ng/mL) for 10‑15 min. NRP‑1‑mediated signalling is assessed by western blot for phosphorylated VEGFR2 (p‑VEGFR2) or downstream effectors such as Akt, Erk and FAK. Endothelial cell migration can be assessed using a scratch wound assay or Boyden chamber assay. Matrigel tube formation assay is also used to quantify angiogenesis inhibition. IC50 values for signalling inhibition are typically in the low micromolar range.
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| Animal Protocol |
A general in vivo angiogenesis model (Matrigel plug assay): Male C57BL/6 mice (n=5/group) are injected subcutaneously with 0.5 mL of growth factor‑reduced Matrigel containing VEGF‑A1₆₅ (200 ng/mL) with or without ATWLPPR TFA (10‑50 uM). After 7‑10 days, the Matrigel plugs are excised and processed for haemoglobin content measurement (Drabkin's reagent) or for CD31 immunohistochemistry to quantify neovascularisation. For tumour xenograft models: Female BALB/c nude mice are implanted subcutaneously with human cancer cells (e.g., U87 glioblastoma, A375 melanoma). When tumours reach ~100 mm3, mice are treated with ATWLPPR TFA (2‑20 mg/kg, intraperitoneal or intravenous) daily or every other day for 14‑21 days. Tumour volumes are measured by calipers. At endpoint, tumours are excised for immunohistochemistry (CD31 for vessel density, Ki‑67 for proliferation) and western blot analysis of NRP‑1 signalling.
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| ADME/Pharmacokinetics |
As a heptapeptide, ATWLPPR TFA has a short plasma half‑life (minutes to a few hours) due to rapid proteolytic degradation when administered systemically. To improve stability, the peptide is often modified (e.g., cyclisation, D‑amino acid substitution, PEGylation) or administered via continuous infusion. The TFA salt provides good water solubility (>10 mg/mL) and facilitates formulation in saline or PBS for intraperitoneal or intravenous injection. ATWLPPR TFA is a research‑grade peptide and is not intended for human therapeutic use. In preclinical studies, the peptide is well‑tolerated at doses up to 20 mg/kg (i.p.) in mice, with no observed acute toxicity or weight loss. At higher doses (>30 mg/kg), mild lethargy or transient diarrhoea may occur. No genotoxicity data are available. Standard safety precautions (gloves, lab coat) should be used when handling.
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| References |
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| Additional Infomation |
ATWLPPR is a heptapeptide that was originally identified by phage‑display biopanning against NRP‑1. The sequence (Ala‑Thr‑Trp‑Leu‑Pro‑Pro‑Arg) is specific for NRP‑1 binding. ATWLPPR is widely used as a research tool to study the role of NRP‑1 in angiogenesis, tumour progression, and neurological development. The peptide is also used as a positive control in screening assays for novel NRP‑1 antagonists. For research use only; not for diagnostic or therapeutic applications.
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| Molecular Formula |
C42H62F3N11O11
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| Molecular Weight |
954.00
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| Related CAS # |
ATWLPPR Peptide;272121-15-0
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| Appearance |
White to off-white solid powder
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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 (~104.82 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: 100 mg/mL (104.82 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.0482 mL | 5.2411 mL | 10.4822 mL | |
| 5 mM | 0.2096 mL | 1.0482 mL | 2.0964 mL | |
| 10 mM | 0.1048 mL | 0.5241 mL | 1.0482 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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