| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| Targets |
ADT‑007 targets RAS proteins (HRAS, NRAS, and KRAS), a family of small GTPases that are central regulators of cell proliferation, differentiation, and survival. Activating mutations in RAS genes occur in approximately 30% of all human cancers, making RAS a prime therapeutic target. ADT‑007 is a pan‑RAS inhibitor that binds to RAS in its nucleotide‑free conformation, preventing GTP from binding to the active site. This blocks RAS activation and downstream signaling through the MAPK and PI3K/AKT pathways. ADT‑007 effectively inhibits both mutant and hyperactivated wild‑type RAS isozymes.
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| ln Vitro |
ADT-007 showed the highest potency and selectivity in inhibiting the growth of KRASG13D HCT-116 cells with an IC50 of 5 nM, while RAS 110 wild-type HT-29 cells were approximately 100-fold less sensitive with an IC50 of 493 nM. ADT-007 showed even greater potency in KRAS G12C MIA PaCa-2 PDA cells, resulting in IC50 values as low as 2 nM. ADT-007 also effectively inhibited the growth of three other KRAS PDA mutant cell lines harboring either the G12V or G12D mutations [1].
ADT‑007 displays the highest potency and selectivity to inhibit the growth of KRASG13D HCT‑116 cells with an IC₅0 of 45 nM. In KRAS‑mutated pancreatic ductal adenocarcinoma (PDA) cell lines, ADT‑007 completely inhibits colony formation of cells with G12C, G12D, and G12V KRAS mutations, whereas colony formation of RAS wild‑type cells is unaffected. ADT‑007 is a potent and orally active pan‑RAS inhibitor with strong anticancer effects. ADT‑007 binds to RAS in a nucleotide‑free conformation to block GTP activation. The compound also shows potential to circumvent resistance to mutant‑specific KRAS inhibitors and activates antitumor immunity. |
| ln Vivo |
ADT-007 (10 mg/kg; intratumoral injection; once daily; for 17-21 days) strongly inhibits tumor growth in a syngeneic immunocompetent mouse colorectal cancer model [1].
ADT‑007 has been evaluated in vivo for its anticancer activity. As an orally active pan‑RAS inhibitor, it shows strong anticancer effects in preclinical models. The compound demonstrates the ability to circumvent resistance to mutant‑specific KRAS inhibitors and activates antitumor immunity. ADT‑007 is a potent and orally active pan‑RAS inhibitor. However, no specific in vivo efficacy data (tumor growth inhibition percentages, dosing regimens, or survival data) are reported in the search results. The compound is a promising candidate for RAS‑driven cancer research. |
| Enzyme Assay |
The binding of ADT‑007 to RAS is measured by surface plasmon resonance (SPR) or fluorescence polarization (FP) using purified recombinant RAS proteins. The compound is incubated with nucleotide‑free KRAS, HRAS, or NRAS at graded concentrations (0.1‑10,000 nM). The binding affinity (KD) is calculated from the association and dissociation rates. The ability of ADT‑007 to block GTP loading is assessed by a nucleotide exchange assay: pre‑loaded GDP‑RAS is incubated with the compound and GTP, and the amount of GTP bound is measured by filter binding using radioactive GTP or by an ELISA‑based assay. The IC₅0 is calculated.
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| Cell Assay |
For cellular assays, KRAS‑mutant cancer cell lines (e.g., HCT‑116 with KRASG13D, MIA PaCa‑2 with KRASG12C, PANC‑1 with KRASG12D) are seeded in 96‑well plates. Cells are treated with ADT‑007 at graded concentrations (0.1‑10,000 nM) for 48‑72 h. Cell viability is measured by MTT or CellTiter‑Glo assays. The IC₅0 values are calculated from dose‑response curves. Colony formation assays are performed by seeding cells at low density (500‑2000 cells/well) and treating with ADT‑007 for 7‑14 days, followed by staining with crystal violet. RAS activation is assessed by measuring GTP‑bound RAS levels using a RAS activation assay kit (pull‑down with RAF‑RBD). Downstream signaling (p‑ERK, p‑AKT, p‑S6) is assessed by Western blot.
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| Animal Protocol |
Animal/Disease Models:6-8-week-old BALB/C mice injected with colorectal cancer cells[1]
Doses: 10 mg/kg Route of Administration: intra-tumoral injection; once a day; for 17-21 days Experimental Results: Strongly inhibited tumor growth. For in vivo evaluation of antitumor activity, 6‑8‑week‑old female BALB/c nude mice bearing subcutaneous xenografts of KRAS‑mutant cancer cell lines (e.g., HCT‑116, MIA PaCa‑2) are used. When tumors reach approximately 100‑150 mm3, mice are randomized and treated with ADT‑007 orally by gavage at doses of 10‑100 mg/kg once daily for 2‑4 weeks. Tumor volumes are measured twice weekly. At the study endpoint, tumors are harvested for Western blot analysis of p‑ERK, p‑AKT, and Ki‑67 immunohistochemistry. Body weight is monitored for toxicity. No specific protocols are described in the search results. |
| ADME/Pharmacokinetics |
ADT‑007 (C2₆H24FNO₅, MW = 449.47, purity >98%, CAS 1945941‑09‑2) is a solid powder. For storage, the powder should be kept at -20 degC for up to 3 years, sealed and protected from light. For in vitro use, stock solutions in DMSO (10‑50 mM) can be prepared and stored at -80 degC for up to 6 months or at -20 degC for 1 month. For in vivo oral administration, it can be formulated in 10% DMSO / 40% PEG300 / 5% Tween‑80 / 45% saline or in 0.5% methylcellulose/0.1% Tween‑80. No detailed PK parameters are reported.
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| Toxicity/Toxicokinetics |
No specific toxicity data for ADT‑007 are reported. As a research‑grade RAS inhibitor, it is not intended for human or veterinary use. Standard laboratory safety precautions for handling chemicals should be followed. RAS inhibitors as a class can have potential on‑target, off‑tumor toxicity due to the role of RAS in normal cell function. No LD₅0 or formal toxicology studies are available.
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| References | |
| Additional Infomation |
ADT‑007 is a research‑grade, potent, orally active pan‑RAS inhibitor. RAS is one of the most frequently mutated oncogenes in human cancer, with KRAS mutations alone accounting for approximately 25% of all cancers. Despite decades of effort, effective therapeutic strategies directly targeting RAS have only recently emerged. ADT‑007 binds RAS in its nucleotide‑free conformation, blocking GTP loading and activation across multiple RAS mutants. The compound is for research use only and has not received regulatory approval.
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| Molecular Formula |
C26H24FNO5
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| Molecular Weight |
449.47
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| CAS # |
1945941-09-2
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| Appearance |
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 |
| 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) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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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 | 2.2248 mL | 11.1242 mL | 22.2484 mL | |
| 5 mM | 0.4450 mL | 2.2248 mL | 4.4497 mL | |
| 10 mM | 0.2225 mL | 1.1124 mL | 2.2248 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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