CRM1

Selinexor (KPT-330) is a small molecule inhibitor of CRM1 with selective and oral activity. Selinexor blocks the cell cycle, induces apoptosis, and has antitumor activity for the treatment of multiple myeloma.

(E)-RN (KPT 330) is a CRM1-selective inhibitor of nuclear export. It inhibits protein trafficking from the nucleus and induces cell cycle arrest and apoptosis in mesothelioma cells.

CBS9106 (SL-801) is a reversible oral CRM1 inhibitor with CRM1 degrading and antitumor activity.CBS9106 inhibits CRM1-dependent nuclear export and reduces CRM1 protein levels.CBS9106 inhibits tumor growth and prolongs the survival of mice bearing tumor xenografts.CBS9106 is an inhibitor of CRM1-dependent nuclear export and reduces CRM1 protein levels.

LFS-1107, a reversible CRM1 inhibitor (Kd: 12.5 pM), selectively targets and eliminates ENKTL cells, offering potential for cancer research applications [1].

CRM1-IN-2 (Compound KL2) is a noncovalent inhibitor that targets CRM1, localizing it to the nuclear periphery, depleting its nuclear presence, and inhibiting its nuclear export function. It demonstrates the capability to inhibit the growth of colorectal cancer cells and induce apoptosis [1].

Leptomycin A, a metabolite derived from Streptomyces, acts as an inhibitor of CRM1 (exportin 1) and effectively suppresses HIV-1 replication. Compared to Leptomycin B, it exhibits lesser potency. Leptomycin A hampers the interaction between CRM1 and nuclear export signals, effectively hindering the nuclear export of a wide array of proteins.

Leptomycin B (LMB) is a potent inhibitor of the nuclear export of proteins and is a potent antifungal antibiotic blocking the eukaryotic cell cycle. Leptomycin B inactivates CRM1/exportin 1 by covalent modification at a cysteine residue.

CRM1-IN-1 (Compound KL1), a noncovalent inhibitor of CRM1, promotes nuclear degradation of CRM1 with an IC50 of 0.27 μM, inhibits CRM1-mediated nuclear export, suppresses cell proliferation, and induces apoptosis in colorectal cancer cells [1].

KPT185 (KPT 185) is a selective CRM1 inhibitor, inducing apoptosis, cell-cycle arrest.

Verdinexor (KPT-335) (KPT-335), a specific XPO1/CRM1 inhibitor, are orally bioavailable.

KPT276 (KPT 276) is an orally bioavailable selective inhibitor of nuclear export (SINE) that irreversibly bind to CRM1 and block the function of CRM1.