Pair Name	Sanguinarium, Bortezomib
Partner Name	Bortezomib
Disease Info	[ICD-11: 2A83]	Multiple myeloma		Investigative
Biological Phenomena	Induction-->Apoptosis
Gene Regulation	Up-regulation	Expression	BAX	hsa581
	Down-regulation	Expression	BCL2	hsa596
	Down-regulation	Expression	BCL-xL	hsa598
	Down-regulation	Activity	CASP3	hsa836
	Down-regulation	Activity	CASP9	hsa842
	Down-regulation	Expression	CCND1	hsa595
	Down-regulation	Expression	JAK2	hsa3717
	Down-regulation	Cleavage	PARP1	hsa142
	Up-regulation	Expression	PTPN6	hsa5777
	Down-regulation	Expression	STAT3	hsa6774
	Down-regulation	Expression	XIAP	hsa331
In Vitro Model	U266B1	Plasma cell myeloma	Homo sapiens (Human)	CVCL_0566
	MM1.S	Plasma cell myeloma	Homo sapiens (Human)	CVCL_8792
Result	Our findings demonstrate that SNG induces mitochondrial and caspase-dependent apoptosis, generates oxidative stress, and suppresses MM cell lines proliferation. In addition, co-treatment of MM cell lines with sub-toxic doses of SNG and BTZ potentiated the cytotoxic activity. These results would suggest that SNG could be developed into therapeutic agent either alone or in combination with other anticancer drugs in MM.

Pair Name	Sanguinarium, Cisplatin
Partner Name	Cisplatin
Disease Info	[ICD-11: 2C73]	Ovarian cancer		Investigative
Biological Phenomena	Induction-->Blockade of cell cycle in G0/G1 phase
Gene Regulation	Down-regulation	Expression	AREG	hsa374
	Down-regulation	Expression	EGFR	hsa1956
	Down-regulation	Phosphorylation	JUN	hsa3725
	Down-regulation	Phosphorylation	MAPK8	hsa5599
	Down-regulation	Expression	MKI67	hsa4288
In Vitro Model	SK-OV-3	Ovarian serous cystadenocarcinoma	Homo sapiens (Human)	CVCL_0532
Result	Our findings demonstrate that SNG induces mitochondrial and caspase-dependent apoptosis, generates oxidative stress, and suppresses MM cell lines proliferation. In addition, co-treatment of MM cell lines with sub-toxic doses of SNG and BTZ potentiated the cytotoxic activity. These results would suggest that SNG could be developed into therapeutic agent either alone or in combination with other anticancer drugs in MM.

Pair Name	Sanguinarium, Doxorubicin
Partner Name	Doxorubicin
Disease Info	[ICD-11: 2C60]	Breast cancer		Investigative
Biological Phenomena	Induction-->Apoptosis
Gene Regulation	Up-regulation	Expression	CASP3	hsa836
	Down-regulation	Expression	CCND1	hsa595
	Up-regulation	Expression	CDKN1A	hsa1026
In Vitro Model	MCF-7	Invasive breast carcinoma of no special type	Homo sapiens (Human)	CVCL_0031
	MCR-5	Healthy	Homo sapiens (Human)	CVCL_0440
Result	Cellular and molecular studies suggested adjuvant chemosensitizers SA and SN to reverse MDR in breast cancer cells.

Pair Name	Sanguinarium, Cisplatin
Partner Name	Cisplatin
Disease Info	[ICD-11: 2C73]	Ovarian cancer		Investigative
Biological Phenomena	Induction-->Apoptosis
In Vitro Model	A2780	Ovarian endometrioid adenocarcinoma	Homo sapiens (Human)	CVCL_0134
	A2780/CP70	Ovarian endometrioid adenocarcinoma	Homo sapiens (Human)	CVCL_0135
Result	These findings suggest that sanguinarine could reverse cisplatin resistance in A2780/R cells through GSH reduction,sanguinarine can be used as one of the potent adjuvants for ovarian cancer chemotherapy.

Pair Name	Sanguinarium, Gefitinib
Partner Name	Gefitinib
Disease Info	[ICD-11: 2C25]	Lung cancer		Investigative
Biological Phenomena	Induction-->Redox imbalance
Gene Regulation	Up-regulation	Expression	BAX	hsa581
	Down-regulation	Expression	BCL2	hsa596
	Down-regulation	Expression	BCL-xL	hsa598
	Up-regulation	Expression	NOX3	KEGG ID N.A.
In Vitro Model	NCI-H1975	Lung adenocarcinoma	Homo sapiens (Human)	CVCL_1511
In Vivo Model	The mixture of 1×10⁶ H1975 cells was resuspended in 100 μL of RPMI 1640 medium and 50 μL of Matrigel and injected into the armpit of the right forelimb of 6- to 8-week-old nude mice. Five days later, the mice with tumor formation were administered with sanguinarine via i.p. injection and afatinib via intragastric administration 5 days/week 32 for consecutive days. The tumor growth was monitored every 3–4 days using calipers.
Result	Targeting EGFR by elevating ROS and redox imbalance is a potential new strategy to develop a new EGFR inhibitor for TKI-resistant patients with a wide therapeutic window between EGFR(T790M) and EGFR(WT)