Systemic and tumor disposition of platinum after administration of cisplatin or STEALTH liposomal-cisplatin formulations (SPI-077 and SPI-077 B103) in a preclinical tumor model of melanoma

Zamboni, William C.; Gervais, Anne; Egorin, Merrill J.; Schellens, Jan H.M.; Zuhowski, Elleanor G.; Pluim, Dick; Joseph, Erin; Hamburger, Deborah R.; Working, Peter K.; Colbern, Gail; Tonda, Margaret; Potter, Douglas M.; Eiseman, Julie L.

doi:10.1007/s00280-003-0719-4

Cited by 149 publications

(106 citation statements)

References 31 publications

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“…By microdialysis, we were previously unable to detect released platinum (Pt) in tumor ECF after administration of STEALTH liposomal cisplatin (SPI-077; ref. 18). The results of this study suggested that SPI-077 distributes into tumors but release less unbound Pt into tumor ECF and form fewer Pt-DNA adducts as compared with cisplatin, which was consistent with low antitumor activity of SPI-077 (18).…”

supporting

confidence: 67%

“…Liposomes extravasate through leaky capillary beds of tumors and lodge into the interstitial spaces among tumor cells, where they release the encapsulated drug (6, 16 -18). For anticancer agents encapsulated in liposomes to be an effective treatment in patients with solid tumors, the active form of the anticancer agent must be released from the liposome into the tumor ECF and then penetrate into the cell (6,18).…”

mentioning

confidence: 99%

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Plasma, Tumor, and Tissue Disposition of STEALTH Liposomal CKD-602 (S-CKD602) and Nonliposomal CKD-602 in Mice Bearing A375 Human Melanoma Xenografts

Zamboni

Strychor

Joseph

et al. 2007

Clinical Cancer Research

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108

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Purpose: S-CKD602 is a STEALTH liposomal formulation of CKD-602, a camptothecin analogue. The cytotoxicity of camptothecin analogues is related to the duration of exposure in the tumor. STEALTH liposomal formulations contain lipid conjugated to methoxypolyethylene glycol and have been designed to prolong drug circulation time, increase tumor delivery, and improve the therapeutic index. For STEALTH liposomal formulations of anticancer agents to achieve antitumor effects, the active drug must be released into the tumor extracellular fluid (ECF). Experimental Design: S-CKD602 at 1 mg/kg or nonliposomal CKD-602 at 30 mg/kg was administered once via tail vein to mice bearing A375 human melanoma xenografts. Mice (n = 3 per time point) were euthanized at 0.083 to 24 h, 48 h, and 72 h after S-CKD02 and from 0.083 to 24 h after nonliposomal CKD-602. Plasma samples were processed to measure encapsulated, released, and sum total (encapsulated plus released) CKD-602, and tumor and tissue samples were processed to measure sum total CKD-602. Microdialysis samples of tumor ECF were obtained from 0 to 2 h, 4 to 7 h, and 20 to 24 h after nonliposomal CKD-602 and from 0 to 2 h, 24 to 27 h, 48 to 51 h, and 72 to 75 h after S-CKD602. A liquid chromatographymass spectrometry assay was used to measure the total (sum of lactone and hydroxyl acid) CKD-602. The area under the concentration-versus-time curves (AUC) from 0 to infinity and time >1ng/mL in tumor were estimated.Results: For S-CKD602, the CKD-602 sum total AUC in plasma and tumor and the CKD-602 AUC in tumor ECF were 201,929, 13,194, and 187 ng/mL h, respectively. For S-CKD602, 82% of CKD-602 remains encapsulated in plasma. For nonliposomal CKD-602, the CKD-602 AUC in plasma and tumor and the CKD-602 AUC in tumor ECF were 9,117, 11,661, and 639 ng/mL Á h, respectively. The duration of time the CKD-602 concentration was >1ng/mL in tumor ECF after S-CKD602 and nonliposomal CKD-602 was >72 and f20 h, respectively. For S-CKD602, the CKD-602 sum total exposure was 1.3-fold higher in fat as compared with muscle. The ratio of CKD-602 sum total exposure in fat to muscle was 3.8-fold higher after administration of S-CKD602 compared with nonliposomal CKD-602. Conclusion: S-CKD602 provides pharmacokinetic advantages in plasma, tumor, and tumor ECF compared with nonliposomal CKD-602 at 1/30th of the dose, which is consistent with the improved antitumor efficacy of S-CKD602 in preclinical studies. The distribution of S-CKD602 is greater in fat compared with muscle whereas the distribution of nonliposomal CKD-602 is greater in muscle compared with fat.These results suggest that the body composition of a patient may affect the disposition of S-CKD602 and released CKD-602.

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supporting

confidence: 67%

mentioning

confidence: 99%

Plasma, Tumor, and Tissue Disposition of STEALTH Liposomal CKD-602 (S-CKD602) and Nonliposomal CKD-602 in Mice Bearing A375 Human Melanoma Xenografts

Zamboni

Strychor

Joseph

et al. 2007

Clinical Cancer Research

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108

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“…However, there was a poor therapeutic effect in three murine tumor models owing to the slow release rate of cisplatin from liposomes. A similar result was observed by Zamboni et al (2004) after mice bearing melanoma tumors were administered cisplatin loaded PEG-modified liposomes.…”

Section: Pegylated Liposomal Vincristinesupporting

confidence: 69%

Are PEGylated liposomes better than conventional liposomes? A special case for vincristine

Wang

Song

et al. 2015

Drug Delivery

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Cancer poses a significant threat to human health worldwide, and many therapies have been used for its palliative and curative treatments. Vincristine has been extensively used in chemotherapy. However, there are two major challenges concerning its applications in various tumors: (1) Vincristine's antitumor mechanism is cell-cycle-specific, and the duration of its exposure to tumor cells can significantly affect its antitumor activity and (2) Vincristine is widely bio-distributed and can be rapidly eliminated. One solution to these challenges is the encapsulation of vincristine into liposomes. Vincristine can be loaded into conventional liposomes, but it quickly leak out owing to its high membrane permeability. Numerous approaches have been attempted to overcome this problem. Vincristine has been loaded into PEGylated liposomes to prolong circulation time and improve tumor accumulation. These liposomes indeed prolong circulation time, but the payout characteristic of vincristine is severer, resulting in a compromised outcome rather than a better efficacy compared to conventional sphingomyelin (SM)/cholesterol (Chol) liposomes. In 2012, the USA Food and Drug Administration (FDA) approved SM/Chol liposomal vincristine (Marqibo Õ ) for commercial use. In this review, we mainly focus on the drug's rapid leakage problem and the potentially relevant solutions that can be applied during the development of liposomal vincristine and the reason for conventional liposomal vincristine rather than PEGylated liposomes has access to the market.

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“…However, in Phase I and II studies, SPI-077 exhibited essentially no antitumor activity in patients [42][43][44]. A subsequent study in tumor-bearing mice indicated that although more SPI-077 distributes into tumors, it releases less Pt into the tumor, and forms fewer Pt-DNA adducts, as compared with free cisplatin [45].…”

Section: Liposomal Formulations Of Platinum Drugsmentioning

confidence: 99%

Nanocapsules: A Novel Formulation Technology For Platinum-Based Anticancer Drugs

Hamelers¹,

Kroon²

2007

Future Lipidology

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Systemic and tumor disposition of platinum after administration of cisplatin or STEALTH liposomal-cisplatin formulations (SPI-077 and SPI-077 B103) in a preclinical tumor model of melanoma

Abstract: This study suggests that more SPI-077 and SPI-077 B103 distribute into tumors, but release less Pt into tumor ECF, and form fewer Pt-DNA adducts than does cisplatin.

Cited by 149 publications

References 31 publications

Plasma, Tumor, and Tissue Disposition of STEALTH Liposomal CKD-602 (S-CKD602) and Nonliposomal CKD-602 in Mice Bearing A375 Human Melanoma Xenografts

Plasma, Tumor, and Tissue Disposition of STEALTH Liposomal CKD-602 (S-CKD602) and Nonliposomal CKD-602 in Mice Bearing A375 Human Melanoma Xenografts

Are PEGylated liposomes better than conventional liposomes? A special case for vincristine

Nanocapsules: A Novel Formulation Technology For Platinum-Based Anticancer Drugs

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