Cat. No.: HY-15136

Lonafarnib

Name: Lonafarnib
Brand: MedChemExpress
SKU: HY-15136
Price: 120.00 USD
Availability: InStock
Rating: 5 (14 reviews)

(Synonyms: Sch66336)

14 Cited Publications

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Based on 14 publication(s) in Google Scholar

Lonafarnib (Sch66336) is an orally active, blood-brain barrier penetrant farnesyltransferase (FPTase) inhibitor. Lonafarnib increases the phosphorylation levels of Akt, CaMKII and CREB, upregulates BDNF expression in the hippocampus, elevates the content of α7nAChR on cell membranes, and blocks the isoprenylation of H-Ras. Lonafarnib repairs synapses and reverses spatial memory deficits in Aβ1-42 model mice. Lonafarnib inhibits RSV fusion and replication, and alleviates virus-induced lung injury. Lonafarnib activates the lysosomal and autophagic pathways, and reduces the phosphorylation and aggregation of tau. Lonafarnib acts synergistically with Sorafenib (HY-10201) to promote apoptosis, and inhibits the proliferation and invasion of melanoma cells. Lonafarnib inhibits the farnesylation of progerin, repairs nuclear membrane defects, and activates the cGAS-STING-STAT1 signaling pathway. Lonafarnib can be used in research related to diseases including Alzheimer's disease, viral infections, melanoma, and progeria.

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Pureté: 99.85%
CAS No.: 193275-84-2
Formule: C₂₇H₃₁Br₂ClN₄O₂
Masse moléculaire:638.82

Stockage:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 2 years , -20°C, 1 year

Lonafarnib Chemical Structure

CAS No.: 193275-84-2

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Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Activité biologique
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- In Vivo
- Essai clinique
Chemical Information
Publications (14)
Solvant et solubilité
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- In Vivo
Pureté et documentation
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Activité biologique

Description

IC₅₀ & Target

STAT1

Bcl-2

H-Ras

Akt

Voir tous les produits spécifiques à Isoform Akt :

Voir tous les produits spécifiques à Isoform Ras :

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Cellular Effect

Cell Line	Type	Value	Description	References
Caco-2	CC₅₀	10.71 μM Compound: LONAFARNIB	Toxicity against Caco-2 cells determined at 48 hours by intracellular ATP concentration using the CellTiter-Glo Luminescent Cell Viability Assay Toxicity against Caco-2 cells determined at 48 hours by intracellular ATP concentration using the CellTiter-Glo Luminescent Cell Viability Assay	10.21203/rs.3.rs-23951/v1
Caco-2	IC₅₀	5.68 μM Compound: LONAFARNIB	Determination of IC50 values for inhibition of SARS-CoV-2 induced cytotoxicity of Caco-2 cells after 48 hours by high content imaging Determination of IC50 values for inhibition of SARS-CoV-2 induced cytotoxicity of Caco-2 cells after 48 hours by high content imaging	10.21203/rs.3.rs-23951/v1
COS-1	IC₅₀	75 nM Compound: 5	inhibition of tumor colony formation in soft agar inhibition of tumor colony formation in soft agar	[PMID: 10411485]
COS-7	IC₅₀	10 nM Compound: 15	Inhibiting the farnesylation of H-ras proteins in COS-7 monkey cells transiently expressing H-ras[Val12]-CVLS in the whole cell assay. Inhibiting the farnesylation of H-ras proteins in COS-7 monkey cells transiently expressing H-ras[Val12]-CVLS in the whole cell assay.	[PMID: 9822558]
COS-7	IC₅₀	10 nM Compound: 9b	Inhibition of FTase in human COS7 cells Inhibition of FTase in human COS7 cells	[PMID: 20925433]
HCT-116	EC₅₀	74 nM Compound: SCH66336	Inhibition of anchorage-independent growth in human HCT-116 cells assessed as inhibition of colony formation in presence of 10% FBS Inhibition of anchorage-independent growth in human HCT-116 cells assessed as inhibition of colony formation in presence of 10% FBS	[PMID: 16222147]
HCT-116	EC₅₀	94 nM Compound: SCH66336	Inhibition of anchorage-independent growth in human HCT-116 cells assessed as inhibition of colony formation incubated for 14 days in presence of 10% FBS by imaging based soft agar colony formation assay Inhibition of anchorage-independent growth in human HCT-116 cells assessed as inhibition of colony formation incubated for 14 days in presence of 10% FBS by imaging based soft agar colony formation assay	[PMID: 16222147]
HCT-116	IC₅₀	0.07 μM Compound: 15	Compound was measured for inhibition of HCT116 tumor cell line in colon under soft agar assay. Compound was measured for inhibition of HCT116 tumor cell line in colon under soft agar assay.	[PMID: 9822558]
MCF7	IC₅₀	0.05 μM Compound: 15	Compound was measured for inhibition of MCF-7 tumor cell line in breast under soft agar assay. Compound was measured for inhibition of MCF-7 tumor cell line in breast under soft agar assay.	[PMID: 9822558]
NIH3T3	EC₅₀	0.16 μM Compound: 2, SCH-66336	Effective concentration against Ha-RAS processing in NIH3T3 ras-transformed cells Effective concentration against Ha-RAS processing in NIH3T3 ras-transformed cells	[PMID: 12657284]
NIH3T3	EC₅₀	100 nM Compound: Lonafarnib	Inhibition of Ras farnesylation in H-Ras transformed NIH3T3 cells Inhibition of Ras farnesylation in H-Ras transformed NIH3T3 cells	[PMID: 15454228]
NIH3T3	EC₅₀	50 nM Compound: SCH66336	Inhibition of anchorage-independent growth in H-Ras transformed mouse NIH3T3 cells assessed as inhibition of colony formation in presence of 10% bovine serum Inhibition of anchorage-independent growth in H-Ras transformed mouse NIH3T3 cells assessed as inhibition of colony formation in presence of 10% bovine serum	[PMID: 16222147]
NIH3T3	EC₅₀	56 nM Compound: SCH66336	Inhibition of anchorage-independent growth in H-Ras transformed mouse NIH3T3 cells assessed as inhibition of colony formation incubated for 14 days in presence of 10% bovine serum by imaging based soft agar colony formation assay Inhibition of anchorage-independent growth in H-Ras transformed mouse NIH3T3 cells assessed as inhibition of colony formation incubated for 14 days in presence of 10% bovine serum by imaging based soft agar colony formation assay	[PMID: 16222147]
NIH3T3	IC₅₀	2.7 μM Compound: SCH66336	TP_TRANSPORTER: inhibition of DNR efflux (DNR: ? uM) in MDR1-expressing NIH3T3 cells TP_TRANSPORTER: inhibition of DNR efflux (DNR: ? uM) in MDR1-expressing NIH3T3 cells	[PMID: 11606389]
NIH3T3	IC₅₀	500 μM Compound: SCH-66336	Inhibition of K-Ras transformed NIH3T3 cell proliferation Inhibition of K-Ras transformed NIH3T3 cell proliferation	[PMID: 15501065]
NIH3T3	IC₅₀	72 μM Compound: SCH-66336	Inhibition of H-Ras transformed NIH3T3 cell proliferation Inhibition of H-Ras transformed NIH3T3 cell proliferation	[PMID: 15501065]
NIH-H	IC₅₀	72 nM Compound: 15	Compound ability to inhibit anchorage-independent growth of NIH-H tumor cell lines in soft agar. Compound ability to inhibit anchorage-independent growth of NIH-H tumor cell lines in soft agar.	[PMID: 9822558]
NIH-K	IC₅₀	500 nM Compound: 15	Compound ability to inhibit anchorage-independent growth of NIH-K tumor cell lines in soft agar. Compound ability to inhibit anchorage-independent growth of NIH-K tumor cell lines in soft agar.	[PMID: 9822558]

In Vitro

Lonafarnib (72 h) potently inhibits RSV A2 infection in HEp-2 cells (EC₅₀ = 57.7 nM, selectivity index > 168.2) and RSV B01 infection in HEp-2 cells (EC₅₀ = 75.5 nM, selectivity index > 168.2), while it also suppresses RSV A2 replication in human primary bronchial epithelial cells (EC₅₀ = 599.9 nM, selectivity index = 31.0) and RSV B01 replication in human primary bronchial epithelial cells (EC₅₀ = 515.0 nM, selectivity index = 36.1)^[2].
Lonafarnib inhibits RSV A2 infection in HEp-2 cells via a farnesyltransferase-independent mechanism^[2].
Lonafarnib (3.3 μM; pre (-2-0 h), during (0-2 h), and post (2-16 h) infection) blocks RSV A2 infection in HEp-2 cells primarily by inhibiting the viral entry process, with significant inhibitory effects observed during the 0-2 h entry window or over the full −2-22 h period^[2].
Lonafarnib inhibits RSV entry into HEp-2 cells and suppresses RSV F-induced intercellular fusion in HEK293T cells, confirming that it targets the RSV membrane fusion process^[2].
Lonafarnib binds to the pre-fusion RSV F trimer (K_D = 20.1 μM) and stabilizes its native conformation, while mutations M396A, S398A, D486A, F488L, and D489A in the RSV F protein abolish its fusion inhibitory effect^[2].
Lonafarnib (0.5-1.0 μM; 48 h) dose-dependently enhances macroautophagic flux in NIH3T3 mouse fibroblasts, primarily by accelerating autophagosome clearance via lysosomes; it also stimulates basal chaperone-mediated autophagy in NIH3T3 mouse fibroblasts^[3].
Lonafarnib (0.1-0.5 μM; 48 h) stimulates endosomal microautophagy in NIH3T3 mouse fibroblasts, promoting the transport of substrates to late endosomal compartments and their degradation^[3].
Lonafarnib (0.5-1.0 μM; up to 24 h) increases total proteolysis in NIH3T3 mouse fibroblasts in a dose-dependent manner, and this effect is completely mediated by the lysosomal pathway^[3].
Lonafarnib potently inhibits Rhes-mediated phosphorylated tau protein (PHF-1) accumulation in primary mouse hippocampal neurons, with an IC₅₀ of 61.00 nM^[3].
Lonafarnib (10 μM; 9 days) reduces the level of phosphorylated tau (Thr181) in wild-type and MAPT^R406W mutant human induced pluripotent stem cell-derived neurons^[3].
Lonafarnib (0.1-5 μM; 24 h) inhibits farnesyltransferase activity in BLM, MV3, MEWO and SKMel19 human metastatic melanoma cell lines^[4].
Lonafarnib (5 μM; 48-72 h) combined with 4 μM Sorafenib (HY-10201) synergistically suppresses the proliferation of BLM, MV3, MEWO and SKMel1 human metastatic melanoma cell lines, strengthens growth inhibition on primary melanoma cells derived from human skin metastases and reduces BLM cell viability^[4].
Lonafarnib (5 μM; 24 h) inhibits the mTOR pathway in human metastatic melanoma cells. When combined with Sorafenib, it significantly downregulates intracellular Bcl-2, completely eliminates Mcl-1, and only slightly alters Bcl-xL expression^[4].
Lonafarnib (3 μM; 14 days) reduces the invasion and proliferation of BL melanoma cells in organotypic skin models, and the combination with 2 μM Sorafenib completely blocks the invasion and proliferation of these cells^[4].
Lonafarnib (5 μM; 48 h) slightly increases the proportion of sub-G1 apoptotic cells in various melanoma cells, and its combination with Sorafenib greatly amplifies this pro-apoptotic effect without damaging human fibroblasts^[4].
Lonafarnib (5 μM; 24 h) combined with Sorafenib triggers typical apoptotic morphological features such as cell fragmentation in human metastatic melanoma BLM cells^[4].
Lonafarnib (5 μM; 12 h) combined with Sorafenib further elevates p8 mRNA in BLM, MV3, MEWO, SKMel19 human metastatic melanoma cell lines and increases CHOP mRNA in all detected melanoma cell lines^[4].
Lonafarnib (0.025 µM; 9 days) upregulates the proportion of p21-positive cells and phosphorylated STAT1 in normal and progeria fibroblasts, increases the formation of ring-shaped nuclei and micronuclei, elevates IFN-β mRNA levels, glycolysis and ATP content, downregulates the mRNA levels of multiple pro-inflammatory cytokines, reduces progerin levels and proteasome activity, and upregulates prelamin A levels and autophagic activity^[5].

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

Real Time qPCR^[2]

Cell Line:

HEp-2 cells infected with RSV A2
Concentration:

3.3 μM
Incubation Time:

-2-22 h, 0-2 h, 2-22 h, 4-22 h, 6-22 h, 8-22 h, 16-22 h
Result:

Significantly reduced RSV infection when added during full-time (-2-22 h) and entry (0-2 h) periods.
Showed weak inhibition at post-entry stages.

Cell Autophagy Assay^[3]

Cell Line:

NIH3T3 mouse fibroblasts
Concentration:

0.5 μM, 1.0 μM
Incubation Time:

48 h
Result:

Increased the number of autophagic vacuoles to ~30 puncta/cell, autophagosomes to ~30 puncta/cell, and autolysosomes to ~30 puncta/cell at 0.5 μM compared to untreated cells.
Further increased autophagic vacuoles to ~70 puncta/cell, autophagosomes to ~20 puncta/cell, and autolysosomes to ~50 puncta/cell at 1.0 μM, with majority of increase driven by enhanced autolysosome abundance.\nIncreased CMA activity to ~30 puncta/cell at 0.5 μM.
Reduced CMA activity to ~15 puncta/cell at 1.0 μM, which was still significantly higher than untreated cells at ~5 puncta/cell.

ELISA Assay^[3]

Cell Line:

human induced pluripotent stem cell (hiPSC)-derived neurons (MAPT-WT, MAPT-R406W)
Concentration:

10 μM
Incubation Time:

9 days
Result:

Significantly reduced intracellular phospho-tau (Thr181) levels in both MAPT-WT and MAPT-R406W hiPSC-derived neurons.

Western Blot Analysis^[4]

Cell Line:

BLM, MV3, MEWO, SKMel19 human metastatic melanoma cell lines
Concentration:

0.1 μM, 1 μM, 5 μM
Incubation Time:

24 h
Result:

Caused HDJ2 to migrate to a higher apparent molecular weight in all tested melanoma cell lines, with increasing concentrations associated with this shift.

Cell Viability Assay^[4]

Cell Line:

BLM, MV3, MEWO, SKMel19 human metastatic melanoma cell lines
Concentration:

5 μM (lonafarnib)
4 μM (Sorafenib)
Incubation Time:

72 h
Result:

Synergistically enhanced growth inhibition compared to either agent alone, with absolute enhancement of growth inhibition rates ranging from 53% (MEWO) to 90% (MV3).

Cell Proliferation Assay^[4]

Cell Line:

BLM human metastatic melanoma cell line
Concentration:

5 μM (lonafarnib)
4 μM (Sorafenib)
Incubation Time:

48 h, 72 h
Result:

Reduced the percentage of detectable cells to 50% after 48 hours and 30% after 72 hours relative to the start of treatment, significantly inhibiting cell proliferation compared to monotreatment.

Cell Cycle Analysis^[4]

Cell Line:

BLM, MV3, MEWO, SKMel19 human metastatic melanoma cell lines
Concentration:

5 μM
Incubation Time:

48 h
Result:

Increased the sub-G1 apoptotic cell fraction, with percentages ranging from 6% (BLM) to 18% (MV3).

Cell Cycle Analysis^[4]

Cell Line:

BLM, MV3, MEWO, SKMel19 human metastatic melanoma cell lines; human fibroblasts
Concentration:

5 μM (lonafarnib)
4 μM (Sorafenib)
Incubation Time:

48 h
Result:

Significantly increased the sub-G1 apoptotic cell fraction compared to either agent alone, with percentages ranging from 27% (BLM) to 75% (SKMel19).
Did not increase the sub-G1 fraction in human fibroblasts.

Western Blot Analysis^[4]

Cell Line:

BLM, MV3, MEWO, SKMel19 human metastatic melanoma cell lines
Concentration:

5 μM
Incubation Time:

24 h
Result:

Marginally affected expression levels of Bcl-2, Bcl-xL, and Mcl-1 across all tested cell lines.\nDid not affect phosphorylation of ERK or AKT in any of the tested melanoma cell lines.\nDecreased phosphorylation of S6 kinase and ribosomal S6 protein in all tested melanoma cell lines.

Western Blot Analysis^[4]

Cell Line:

BLM, MV3, MEWO, SKMel19 human metastatic melanoma cell lines
Concentration:

5 μM (lonafarnib)
4 μM (Sorafenib)
Incubation Time:

24 h
Result:

Significantly reduced Bcl-2 expression, slightly affected Bcl-xL expression, and completely abolished Mcl-1 expression in all tested melanoma cell lines.

Real Time qPCR^[4]

Cell Line:

BLM, MV3, MEWO, SKMel19 human metastatic melanoma cell lines
Concentration:

5 μM
Incubation Time:

12 h
Result:

Slightly affected p8 mRNA levels across all tested melanoma cell lines.

Real Time qPCR^[4]

Cell Line:

BLM, MV3, MEWO, SKMel19 human metastatic melanoma cell lines
Concentration:

5 μM (lonafarnib)
2 μM, 4 μM (Sorafenib)
Incubation Time:

12 h
Result:

Further upregulated p8 mRNA in most tested cell lines, and increased CHOP mRNA levels in all tested cell lines, compared to either agent alone.

Cell Proliferation Assay^[5]

Cell Line:

GM01651C, GM01652C (control primary fibroblasts); HGADFN003, HGADFN127 (HGPS primary fibroblasts)
Concentration:

0.025 µM
Incubation Time:

9 days
Result:

Maintained cell growth rates similar to mock-treated control and HGPS fibroblasts.
Increased the percentage of p21-positive cells by 9% in control fibroblasts relative to mock-treated cells.
Increased the percentage of p21-positive cells by 12% in HGPS fibroblasts relative to mock-treated cells.

Western Blot Analysis^[5]

Cell Line:

GM01651C, GM01652C (control primary fibroblasts); HGADFN003, HGADFN127 (HGPS primary fibroblasts)
Concentration:

0.025 µM
Incubation Time:

9 days
Result:

Elevated P-STAT1 levels by 48% in control fibroblasts and 51% in HGPS fibroblasts, while leaving total STAT1 unaltered in both cell lines versus mock groups

Immunofluorescence^[5]

Cell Line:

GM01651C (control primary fibroblasts); HGADFN127 (HGPS primary fibroblasts)
Concentration:

0.025 µM
Incubation Time:

9 days
Result:

Elevated the proportion of cells carrying cGAS-positive cytosolic foci by 3% in control fibroblasts and 4% in HGPS fibroblasts versus mock groups

Real Time qPCR^[5]

Cell Line:

GM01651C, GM01652C (control primary fibroblasts); HGADFN003, HGADFN127 (HGPS primary fibroblasts)
Concentration:

0.025 µM
Incubation Time:

9 days
Result:

Elevated IFN-β mRNA by 58% in control fibroblasts and 67% in HGPS fibroblasts, and downregulated IL-1α, CCL2, IL-6, CXCL8 mRNA by 30%/11%, 41%/26%, 14%/10%, 43%/42% in two cell types separately compared with mock groups

In Vivo

Lonafarnib (10-80 mg/kg; i.p.; once daily; for 14 consecutive days) dose-dependently reverses Aβ_1-42-induced impairments in synaptic structure, function and spatial cognition in AD mice. Its mechanism of action involves upregulating hippocampal BDNF levels via the H-Ras-α7nAChR-dependent CaMKII-CREB pathway^[1].
Lonafarnib (17-34 mg/kg; p.o.; twice daily; for 4 consecutive days) dose-dependently reduces RSV replication levels in BALB/c mice, and improves body weight and pulmonary pathological conditions of mice when administered via early intervention or post-infection oral delivery^[2].
Lonafarnib (80 mg/kg per day; p.o.; intermittent administration/acute administration) reduces tau protein inclusions, brain atrophy, glial reactivity and behavioral deficits in rTg4510 mice, whereas acute administration has no effect on established tau protein pathology^[3].

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

Animal Model:

C57BL/6J (male, 2 months old, intracerebroventricular injection of soluble Aβ_1-42 to induce pathology)^[1]
Dosage:

10 mg/kg; 30 mg/kg; 50 mg/kg; 80 mg/kg
Administration:

i.p.; daily; 14 days
Result:

Reduced MWM escape latency and prolonged target quadrant residence time, thereby improved spatial learning and memory in Aβ1-42 mice at 50 mg/kg and 80 mg/kg.
Rescued impaired hippocampal synaptic electrophysiology including EPSP slopes, paired-pulse ratios, PTP and L-LTP at 50 mg/kg. It also restored damaged dendritic architecture, elevated synaptic PSD-95 and synaptophysin levels, upregulated surface α7nAChR expression, activated Akt/CaMKII/CREB phosphorylation, and increased mature hippocampal BDNF content.
Demonstrated that the BDNF upregulation relied on α7nAChR and CaMKII signaling rather than ERK or PI3K pathways. H-Ras overexpression reversed the elevations of surface α7nAChR and BDNF, while TrkB/Fc chimera completely abolished all synaptic and cognitive improvements.

Animal Model:

BALB/c (female, 8 weeks old, intranasally inoculated with 1 × 10⁶ PFU RSV A2)^[2]
Dosage:

17 mg/kg; 34 mg/kg
Administration:

p.o.; twice daily; 4 days
Result:

Improved body weight from day 1 post-infection at 34 mg/kg early intervention, while post-infection treatment only slightly recovered weight at day 4.
Reduced lung viral titers dose-dependently: early 17/34 mg/kg downregulated titers 3.8/7.4-fold; post-infection 17/34 mg/kg downregulated titers 3.7/4.1-fold.
Attenuated RSV-mediated lung inflammation in all early-intervention groups and relieved lung injury at 34 mg/kg post-infection, with quantitative pathology confirming alleviated alveolitis and lesions in early groups.

Animal Model:

rTg4510 (tauopathy transgenic, 10 weeks old at initiation, evaluated at 20 weeks old); wild-type littermate controls^[3]
Dosage:

80 mg/kg
Administration:

p.o.; intermittent schedule (5 days on, 5 days off); 10 weeks (chronic intermittent treatment)
p.o.; daily; 2 weeks (acute treatment)
Result:

Lowered cortical/hippocampal MC1-tau inclusions and cortical/hippocampal PHF-1 phosphorylated tau; cut cortical/hippocampal Rhes-positive cell density.
Enlarged coronal brain area, mitigated hippocampal microgliosis and cortical astrogliosis.
Rescued nest-building impairment and suppressed circling behavior.
Decreased sumoylation- and ubiquitination-positive cells, changed co-labeling likelihood of MC1-tau with SUMO/ubiquitin.
Lessened pathological tau in cortical lysates without altering total tau, and erased insoluble high-molecular-weight tau aggregates.
Exerted no shift in MC1 tau pathology distribution or range after acute dosing.

Essai clinique

NCT Number	Sponsor	Condition	Start Date	Phase A549
NCT01329991	Plexxikon\|		2011-05	PHASE1

Chemical Information

CAS No. 193275-84-2
Appearance Solid
Masse moléculaire 638.82
Formule C₂₇H₃₁Br₂ClN₄O₂
Color White to off-white
SMILES

O=C(N)N1CCC(CC1)CC(N2CCC(CC2)[C@@H]3C4=C(C=C(C=C4CCC5=CC(Br)=CN=C53)Cl)Br)=O
Synonyms

Sch66336
Livraison

Room temperature in continental US; may vary elsewhere.

Stockage

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	2 years
	-20°C	1 year

Publications (14)

All IFWBHistological Imaging/StainingRT-PCR

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Journal Impact Factor

Nat Commun

Targeting NRAS via miR-1304-5p or farnesyltransferase inhibition confers sensitivity to ALK inhibitors in ALK-mutant neuroblastoma. [Abstract]

2024 Apr 23;15(1):3422. PMID: 38653965

Lonafarnib purchased from MedChemExpress. Usage Cited in: Nat Commun. 2024 Apr 23;15(1):3422. [Abstract]

Immunohistochemistry (pERK) in tumours from NSG mice treated with Lonafarnib (10 μL/g; p.o.; once daily). Lonafarnib led to a profound decrease in pERK expression levels.
Nat Commun

Recapitulation of HDV infection in a fully permissive hepatoma cell line allows efficient drug evaluation. [Abstract]

2019 May 22;10(1):2265. PMID: 31118422

Lonafarnib purchased from MedChemExpress. Usage Cited in: Nat Commun. 2019 May 22;10(1):2265. [Abstract]

Lonafarnib (1.8 μM) treatment resulted in significant and selective increase in intracellular L-HDAg of HepNB2.7 cells.

Lonafarnib purchased from MedChemExpress. Usage Cited in: Nat Commun. 2019 May 22;10(1):2265. [Abstract]

Lonafarnib (1.8 μM) treatment caused an eightfold increase of intracellular L-HDAg in HepNB2.7 cells compared with the untreated controls, while the levels of S-HDAg only marginally (1.6-fold) increased.

Lonafarnib purchased from MedChemExpress. Usage Cited in: Nat Commun. 2019 May 22;10(1):2265. [Abstract]

Lonafarnib (1.8 μM) treatment led to a twofold increase in the total intracellular HDV genomes.

Lonafarnib purchased from MedChemExpress. Usage Cited in: Nat Commun. 2019 May 22;10(1):2265. [Abstract]

Quantitative PCR on intracellular HDV replicative intermediates and the two markers for IFN induction (IFN-λ and RSAD2) was performed. Lonafarnib (1.8 μM) profoundly increased the intracellular HDV replication and the induction of IFN responses in PHH co-infected with HDV and HBV.
J Clin Invest

Cancer-associated SPOP mutations enlarge nuclear size and facilitate nuclear envelope rupture upon farnesyltransferase inhibitor treatment. [Abstract]

2025 Jul 15;135(14):e189048. PMID: 40662365
Adv Sci (Weinh)

Multimodal Investigation of Angiogenesis and Its Prevention by Small Compounds in a Zebrafish Cancer Model. [Abstract]

2025 Sep;12(33):e15176. PMID: 40557748
Cell Death Dis

Activation of AKT via a dual mechanism enhances the susceptibility of melanoma cells to glucose deprivation. [Abstract]

2025 Aug 7;16(1):595. PMID: 40774947
Int J Biol Sci

FKBP10 Promotes the Muscle Invasion of Bladder Cancer via Lamin A Dysregulation. [Abstract]

2025 Jan 1;21(2):758-771. PMID: 39781460
Phytomedicine

Astragaloside IV protects against lung injury and pulmonary fibrosis in COPD by targeting GTP-GDP domain of RAS and downregulating the RAS/RAF/FoxO signaling pathway. [Abstract]

2023 Nov:120:155066. PMID: 37690229
Aging Cell

Transient introduction of human telomerase mRNA improves hallmarks of progeria cells. [Abstract]

2019 Aug;18(4):e12979. PMID: 31152494
Eur J Pharmacol

Heat stroke-induced structural and functional impairments of cognition-relevant brain areas in mice is associated with alpha-7 nicotinic acetylcholine receptors downregulation. [Abstract]

2026 Mar 28:1019:178723. PMID: 41786068
Sci Rep

Generation and characterization of a stable cell line persistently replicating and secreting the human hepatitis delta virus. [Abstract]

2019 Jul 10;9(1):10021. PMID: 31292511
Virol Sin

Identification of a receptor tyrosine kinase inhibitor CP-724714 inhibits SADS-CoV related swine diarrhea coronaviruses infection in vitro. [Abstract]

2023 Oct;38(5):778-786. PMID: 37406816
J Neurosci

Ras Inhibitor Lonafarnib Rescues Structural and Functional Impairments of Synapses of Aβ1-42 Mice via α7nAChR-Dependent BDNF Upregulation. [Abstract]

2022 Aug 3;42(31):6090-6107. PMID: 35760529
J Virol

Molecular mechanism of resistance to lonafarnib conferred by mutations in the cysteine-rich region of respiratory syncytial virus fusion glycoprotein and discovery of a lonafarnib-derived antiviral PROTAC. [Abstract]

2025 Dec 9:e0148725. PMID: 41364004
Med Mycol

Lonafarnib synergizes with azoles against Aspergillus spp. and Exophiala spp. [Abstract]

2018 Jun 1;56(4):452-457. PMID: 29420769

Solvant et solubilité

In Vitro:

DMSO : 25 mg/mL (39.13 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

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Preparing Stock Solutions

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Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

1.5654 mL

7.8269 mL

15.6539 mL

5 mM

0.3131 mL

1.5654 mL

3.1308 mL

10 mM

0.1565 mL

0.7827 mL

1.5654 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

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In Vivo:

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Stock Solution Working Solution

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

Protocol 1

Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline

Solubility: ≥ 2.5 mg/mL (3.91 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

Protocol 2

Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)

Solubility: ≥ 2.5 mg/mL (3.91 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

Solubility: ≥ 2.5 mg/mL (3.91 mM); Clear solution

This protocol yields a clear solution of ≥ 2.5 mg/mL (saturation unknown). If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).

Working solution concentration: 0.22 mg/mL

Pureté et documentation

Select Batch:

Pureté: 99.98%

Assay: 99.98%

ee.: 99.98%

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COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
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Instruction de manipulation (2659 KB)

Références

[1]. Cai C, et al. Ras Inhibitor Lonafarnib Rescues Structural and Functional Impairments of Synapses of Aβ Mice via α7nAChR-Dependent BDNF Upregulation. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2022 Aug 03;42(31):6090-6107. [Content Brief]

[2]. Yang Q, et al. Farnesyltransferase inhibitor lonafarnib suppresses respiratory syncytial virus infection by blocking conformational change of fusion glycoprotein. Signal transduction and targeted therapy. 2024 Jun 10;9(1):144. [Content Brief]

[3]. Hernandez I, et al. A farnesyltransferase inhibitor activates lysosomes and reduces tau pathology in mice with tauopathy. Science translational medicine. 2019 Mar 27;11(485):eaat3005. [Content Brief]

[4]. Niessner H, et al. The farnesyl transferase inhibitor lonafarnib inhibits mTOR signaling and enforces sorafenib-induced apoptosis in melanoma cells. The Journal of investigative dermatology. 2011 Feb;131(2):468-79. [Content Brief]

[5]. Arnold R, et al. Baricitinib, a JAK-STAT Inhibitor, Reduces the Cellular Toxicity of the Farnesyltransferase Inhibitor Lonafarnib in Progeria Cells. International journal of molecular sciences. 2021 Jul 12;22(14):7474. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 2 years; -20°C, 1 year. When stored at -80°C, please use it within 2 years. When stored at -20°C, please use it within 1 year.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.5654 mL	7.8269 mL	15.6539 mL	39.1347 mL
	5 mM	0.3131 mL	1.5654 mL	3.1308 mL	7.8269 mL
	10 mM	0.1565 mL	0.7827 mL	1.5654 mL	3.9135 mL
	15 mM	0.1044 mL	0.5218 mL	1.0436 mL	2.6090 mL
	20 mM	0.0783 mL	0.3913 mL	0.7827 mL	1.9567 mL
	25 mM	0.0626 mL	0.3131 mL	0.6262 mL	1.5654 mL
	30 mM	0.0522 mL	0.2609 mL	0.5218 mL	1.3045 mL

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Lonafarnib

14 Cited Publications

100 mg Obtenir un devis

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Nom du produit:
CAS No.:
Species:
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Lonafarnib

Tipifarnib

FTI-277 hydrochloride

Camprenstat

Sorafenib

LB42708

Paclitaxel

L-778123

Dasatinib

Daporinad

Trametinib

Atorvastatin

Vorinostat

Publications Citing Use of MedChemExpress (MCE) Lonafarnib

Voir tous les produits spécifiques à Isoform Akt

Voir tous les produits spécifiques à Isoform Ras

Voir tous les produits spécifiques à Isoform Bcl-2 Family

Voir tous les produits spécifiques à Isoform STAT

Activité biologique

Chemical Information

Publications (14)

Solvant et solubilité

Pureté et documentation

Références

Help & FAQs

Complete Stock Solution Preparation Table

Bioz

Lonafarnib

Tipifarnib

FTI-277 hydrochloride

Camprenstat

Sorafenib

LB42708

Paclitaxel

L-778123

Dasatinib

Daporinad

Trametinib

Atorvastatin

Vorinostat

Publications Citing Use of MedChemExpress (MCE) Lonafarnib

Voir tous les produits spécifiques à Isoform Akt

Voir tous les produits spécifiques à Isoform Ras

Voir tous les produits spécifiques à Isoform Bcl-2 Family

Voir tous les produits spécifiques à Isoform STAT

Activité biologique

Chemical Information

Publications (14)

Solvant et solubilité

Pureté et documentation

Références

Help & FAQs

Complete Stock Solution Preparation Table

Lonafarnib Related Classifications

HY-15136 Related Classifications

Bioz