PDGFR-IN-1 (BALB/c mice, MNNG/HOS xenograft mouse, 15, 30 mg/kg, orally, daily for 14 days) significantly suppresses tumor growth, exhibits a stronger antitumor efficacy with low toxicity[1].
PDGFR-IN-1 (C57/BL6 mice, 40, 80 mg/kg, orally, daily for 10 days) is safe for in vivo investigations[1].
PDGFR-IN-1 (Sprague-Dawley rats, 20 mg/kg PO or 4 mg/kg IP, once) shows a favorable profile with a high maximum concentration and exposure, an acceptable half-life , and a good oral bioavailability[1].
Pharmacokinetic Parameters of PDGFR-IN-1 in male Sprague-Dawley rats[1].
| 7m | |
| route | IP | PO |
| dose (mg/kg) | 4 | 20 |
| Cmax (ng/mL) | 78.3 | 75.2 |
| t1/2 (h) | 2.86 | 2.12 |
| AUC0-∞ (ng/mL*h) | 211.3 | 664.7 |
| F (%) | | 62.9 |
| Animal Model: | Sprague-Dawley rats (male, 200-260 g, Six rats, two groups)[1] |
| Dosage: | 20 mg/kg (PO) or 4 mg/kg (IP) |
| Administration: | PO, IP, once (Pharmacokinetic Analysis) |
| Result: | Showed a favorable profile with a high maximum concentration and exposure, an acceptable half-life , and a good oral bioavailability. |
| Animal Model: | BALB/c mice (18-20 g, MNNG/HOS xenograft mouse, eight groups)[1] |
| Dosage: | 15, 30 mg/kg |
| Administration: | Orally, daily for 14 days |
| Result: | Significantly suppressed tumor growth, exhibited a stronger antitumor efficacy, did not cause significant body weight or organ weight (heart, lung, liver, spleen, or kidney) changes, strongly suppressed the proliferation of tumor cells and induced apoptosis in tissues of the tumor. |
| Animal Model: | C57/BL6 mice[1] |
| Dosage: | 40, 80 mg/kg |
| Administration: | Orally, daily for 10 days |
| Result: | Did not reveal any obvious morphological aberration in organ tissues. |
