Jervine hydriodide  (Synonyms: 11-Ketocyclopamine hydriodide)

Jervine hydriodide is an orally active steroidal alkaloid and Hedgehog signaling pathway inhibitor. Jervine hydriodide can be isolated from Veratrum californicum. Jervine hydriodide regulates Wnt, inhibits the AKT/mTOR signaling pathway, and activates the AMPK signaling pathway. Jervine hydriodide induces DNA damage, Apoptosis, Autophagy, ROS production and Mitochondrial damage. Jervine hydriodide exhibits anti-cancer and anti-inflammatory activities. Jervine hydriodide reduces tumor growth rate and weight in xenograft models. Jervine hydriodide can be used in studies related to triple-negative breast cancer, nasopharyngeal carcinoma and non-small cell lung cancer^[1][2][3].

Jervine (hydriodide) (10-40 μM; 48 h) dose-dependently represses Hedgehog signaling in 5-8F and C666-1 NPC cells, and suppression of GLI1 is necessary for Jervine-induced autophagy, as shown by increased LC3B-II conversion and puncta formation with GLI1 knockdown^[2].
Jervine (1.25-20 μM; 1-4 days) time- and dose-dependently inhibits the proliferation of A549 and H1299 NSCLC cells, with 20 μM jervine causing the strongest reduction after 4 days of incubation^[3].
Jervine (5-10 μM; 48 h) significantly induces apoptosis in A549 and H1299 NSCLC cells, with 10 μM causing a stronger apoptotic response^[3].
Jervine (5-10 μM; 48 h) significantly induces apoptosis in A549 and H1299 NSCLC cells, as detected by Hoechst 33258 staining^[3].
Jervine (5-10 μM; 48 h) dose-dependently upregulates markers of apoptosis (cleaved Caspase-3, cleaved PARP) and autophagy (LC3II) in A549 and H1299 NSCLC cells^[3].
Jervine (5-10 μM; 48 h) dose-dependently represses AKT/mTOR signaling in A549 and H1299 NSCLC cells, as evidenced by reduced p-AKT and p-mTOR expression^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Jervine (20 mg/kg; p.o.; daily; 24 days) significantly suppresses nasopharyngeal carcinoma xenograft tumor growth in BALB/c nude mice by inducing apoptosis and autophagy through inhibition of Hedgehog signaling, with no detectable toxicity^[2].
Jervine (20 mg/kg; p.o.; daily; 24 days)'s suppression of nasopharyngeal carcinoma xenograft tumor growth in BALB/c nude mice is largely dependent on induction of autophagy, as co-treatment with the autophagy inhibitor 3-MA (HY-19312) abrogates its anti-tumor effects^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

553.52

C₂₇H₄₀INO₃

60326-37-6

CC1=C(C([C@@]2([H])[C@@]3([H])CC=C4[C@@]2(CC[C@@H](C4)O)C)=O)[C@@]3([H])CC[C@]15O[C@@]6([H])[C@](NC[C@H](C6)C)([H])[C@H]5C.I

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Eswaran A, et al. Jervine-induced suppression of triple-negative breast cancer (TNBC) cells growth through the regulation of Wnt signaling pathway- an in-silico and in-vitro approach. J Comput Aided Mol Des. 2026 Feb 5;40(1):57.  [Content Brief]

  [2]. Chen J, et al. Jervine exhibits anticancer effects on nasopharyngeal carcinoma through promoting autophagic apoptosis via the blockage of Hedgehog signaling. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2020 Dec;132:110898.  [Content Brief]

  [3]. Lei W, et al. Jervine inhibits non-small cell lung cancer (NSCLC) progression by suppressing Hedgehog and AKT signaling via triggering autophagy-regulated apoptosis. Biochemical and biophysical research communications. 2020 Dec 10;533(3):397-403.  [Content Brief]