| Stereochemistry | ACHIRAL |
| Molecular Formula | C28H34N4O2 |
| Molecular Weight | 458.5952 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CCCN(CCC)C(=O)C1=CC2=CC=C(C=C2N=C(N)C1)C3=CC=C(C=C3)C(=O)N4CCCC4
InChI
InChIKey=QSPOQCXMGPDIHI-UHFFFAOYSA-N
InChI=1S/C28H34N4O2/c1-3-13-31(14-4-2)28(34)24-17-23-12-11-22(18-25(23)30-26(29)19-24)20-7-9-21(10-8-20)27(33)32-15-5-6-16-32/h7-12,17-18H,3-6,13-16,19H2,1-2H3,(H2,29,30)
| Molecular Formula | C28H34N4O2 |
| Molecular Weight | 458.5952 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Motolimod (VTX-2337) is a small molecule, selective Toll-like receptor (TLR) 8 agonist has been used in trials studying phase II for the treatment of peritoneal carcinoma, Ovarian Cancer, Fallopian Tube Cancer, B-cell lymphoma, squamous cell carcinoma of the head and neck among others. Motolimod is designed to mobilize a patient's immune system by directly activating myeloid dendritic cells, monocytes, and natural killer cells. This activation results in the production of a high level of mediators known to orchestrate the integration of both the innate and adaptive anti-tumor responses to a number of cancers.
Originator
Approval Year
Sourcing
PubMed
Patents
Sample Use Guides
Doses of motolimod (2.5, 3.0, or 3.5 mg/m2) were given on days 1, 8, and 15, in combination with fixed weekly doses of cetuximab in 28-day cycles
Low Grade B Cell Lymphoma: sadiation on Day 1. On Day 2, VTX-2337 (MOTOLIMOD) 3.0mg/m2 is administered intratumorally, followed by radiation. VTX-2337 3.0mg/m2 is then given weekly for 3 weeks in a 4 week cycle over 3 cycles.
Route of Administration:
Other
VTX-2337 selectively activates TLR8 with an EC50 of about 100 nmol/L and stimulates production of TNFα and interleukin (IL)-12 from monocytes and myeloid dendritic cells (mDC). VTX-2337 (800 nmol/L) stimulates IFNγ production from NK cells and increases the cytotoxicity of NK cells against K562 and augment antibody-dependent cell-mediated cytotoxicity (ADCC) by rituximab and trastuzumab.
