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What preclinical cancer types have shown sensitivity to ivermectin in vitro and in vivo?
Executive summary
Preclinical studies report ivermectin activity—both in vitro (cell lines) and in vivo (xenografts or mouse models)—across a wide range of cancer types, most repeatedly in breast, ovarian, gastric, esophageal, colon/CRC, glioma, pancreatic, cholangiocarcinoma, lung (NSCLC models) and hematologic models such as leukemia; several papers also emphasize reversal of chemotherapy resistance in vivo (e.g., leukemia and NSCLC models) [1] [2] [3] [4] [5] [6] [7] [8] [9] [10]. Coverage in reviews and experimental reports suggests both single‑agent antiproliferative effects and drug‑sensitizing roles have been demonstrated at preclinical doses considered clinically reachable [6] [1] [11].
1. Which cancer types show in vitro sensitivity to ivermectin — a catalogue from the literature
Multiple primary research studies and reviews list cancer cell lines that are inhibited by ivermectin in culture: breast cancer lines including MDA‑MB‑231, MDA‑MB‑468 and MCF‑7 showed marked sensitivity in screening and mechanistic work [1] [6]; ovarian cancer lines such as SKOV‑3 and other ovarian models responded and showed synergy with cisplatin [1] [2]; gastric cancer lines MKN1 and SH‑10‑TC were identified as ivermectin‑sensitive versus MKN7/MKN28 [12] [3]; esophageal squamous cell carcinoma lines responded in multiple cell‑based assays [4]; colon cancer/ WNT‑TCF–dependent cell models responded in vitro and were mechanistically linked to WNT‑TCF blockade [5]; glioma cell lines displayed antiproliferative effects [6]; pancreatic MiaPaCa‑2 cells were sensitive in vitro in combination studies [7]; cholangiocarcinoma lines including gemcitabine‑resistant KKU214GemR showed sensitivity in vitro [8]; and non‑small cell lung cancer models showed effects on P‑gp and paclitaxel resistance in cell systems [9]. Reviews aggregate still broader lists [6]. Where specific lines are named, they are cited above [1] [3] [8].
2. Which cancer types show in vivo (animal xenograft or mouse) sensitivity to ivermectin
Several studies moved from cell culture to animal models. Breast xenografts (lines above) showed antitumor effects in vivo [1] [13]. Ovarian tumor xenografts plus combination cisplatin experiments demonstrated augmented efficacy in mice [2]. Gastric cancer xenograft models (MKN1/SH‑10‑TC) showed growth suppression in mice [3] [12]. Esophageal squamous cell carcinoma xenografts had reduced Ki‑67 and tumor size after ivermectin treatment [4]. Colon cancer WNT‑TCF–sensitive xenografts were repressed in vivo by ivermectin in the EMBO study [5]. Leukemia models — notably NOD/SCID mice injected with K562 cells — showed ivermectin reversed adriamycin resistance in vivo [11] [10]. Reviews and preclinical reports state glioma in vivo models responded as well [6]. Authors repeatedly state these in vivo effects occurred at doses claimed to be pharmacologically feasible [6] [1].
3. Ivermectin as a chemosensitizer: evidence and cancer types
Multiple studies highlight ivermectin’s ability to increase sensitivity to chemotherapies or reverse multidrug resistance in vitro and in vivo. The EGFR/ERK/Akt/NF‑κB pathway work shows ivermectin reversed chemoresistance and increased efficacy of agents such as adriamycin in leukemia mouse models [10] [11]. Ovarian cancer work reports ivermectin augmented cisplatin efficacy in cell lines and animal models [2]. NSCLC in vitro research indicates ivermectin can abrogate P‑gp–mediated paclitaxel resistance [9]. Reviews summarize ivermectin’s interactions with MDR proteins and cancer stem‑like populations as a general mechanism for chemosensitization [6].
4. Mechanisms invoked and why different cancers respond differently
Authors link ivermectin activity to multiple mechanisms: inhibition of PAK1 and downstream Akt/mTOR signaling (implicated across breast, ovarian and other tumors) [13] [2], blockade of WNT‑TCF signaling in TCF‑sensitive colon cancer [5], inhibition of YAP1 in gastric cancer [3], modulation of MDR/P‑gp and EGFR/ERK/Akt/NF‑κB pathways in chemoresistance models [10] [9], and effects on RNA helicases/miR‑21 in glioma [6]. This multiplicity helps explain why sensitivity appears tumor‑type and even cell‑line specific [12] [6].
5. Limitations, gaps and cautionary context
All evidence cited is preclinical (cell lines and animal models); clinical efficacy and safety as a cancer therapeutic in humans are not documented in these sources (available sources do not mention definitive clinical trial results). Responses are cell‑line and model dependent (e.g., MKN1 vs MKN7 in gastric cancer) and mechanisms differ by context, so translational uncertainty remains [3] [6]. Some reports emphasize dose‑feasibility, but human pharmacokinetic and toxicity in oncology settings require formal testing [6] [1].
Summary judgment: preclinical literature shows ivermectin has demonstrable antiproliferative and chemosensitizing activity in a range of cancers — notably breast, ovarian, gastric, esophageal, colon (WNT‑TCF sensitive), glioma, pancreatic, cholangiocarcinoma, lung models and leukemia — with both in vitro and in vivo supportive experiments, while clinical efficacy and safety for cancer treatment remain unestablished in the sources provided [1] [2] [3] [4] [5] [6] [7] [8] [9] [10].